Principles of environmentally-sustainable anaesthesia: a global consensus statement from the World Federation of Societies of Anaesthesiologists.

The Earth's mean surface temperature is already approximately 1.1°C higher than pre-industrial levels. Exceeding a mean 1.5°C rise by 2050 will make global adaptation to the consequences of climate change less possible. To protect public health, anaesthesia providers need to reduce the contribution their practice makes to global warming. We convened a Working Group of 45 anaesthesia providers with a recognised interest in sustainability, and used a three-stage modified Delphi consensus process to agree on principles of environmentally sustainable anaesthesia that are achievable worldwide. The Working Group agreed on the following three important underlying statements: patient safety should not be compromised by sustainable anaesthetic practices; high-, middle- and low-income countries should support each other appropriately in delivering sustainable healthcare (including anaesthesia); and healthcare systems should be mandated to reduce their contribution to global warming. We set out seven fundamental principles to guide anaesthesia providers in the move to environmentally sustainable practice, including: choice of medications and equipment; minimising waste and overuse of resources; and addressing environmental sustainability in anaesthetists' education, research, quality improvement and local healthcare leadership activities. These changes are achievable with minimal material resource and financial investment, and should undergo re-evaluation and updates as better evidence is published. This paper discusses each principle individually, and directs readers towards further important references.

Towards high-quality peri-operative care: a global perspective.

Article 25 of the United Nations' Universal Declaration of Human Rights enshrines the right to health and well-being for every individual. However, universal access to high-quality healthcare remains the purview of a handful of wealthy nations. This is no more apparent than in peri-operative care, where an estimated five billion individuals lack access to safe, affordable and timely surgical care. Delivery of surgery and anaesthesia in low-resource environments presents unique challenges that, when unaddressed, result in limited access to low-quality care. Current peri-operative research and clinical guidance often fail to acknowledge these system-level deficits and therefore have limited applicability in low-resource settings. In this manuscript, the authors priority-set the need for equitable access to high-quality peri-operative care and analyse the system-level contributors to excess peri-operative mortality rates, a key marker of quality of care. To provide examples of how research and investment may close the equity gap, a modified Delphi method was adopted to curate and appraise interventions which may, with subsequent research and evaluation, begin to address the barriers to high-quality peri-operative care in low- and middle-income countries.

Anaemia and red blood cell transfusion in intracranial neurosurgery: a comprehensive review.

Both anaemia and blood transfusion are associated with poor outcomes in the neurosurgical population. Based on the available literature, the optimal haemoglobin concentration for neurologically injured patients appears to be in the range of 9.0-10.0 g dl-1, although the individual risks and benefits should be weighed. Several perioperative blood conservation strategies have been used successfully in neurosurgery, including correction of anaemia and coagulopathy, use of antifibrinolytics, and intraoperative cell salvage. Avoidance of non-steroidal anti-inflammatory drugs and starch-containing solutions is recommended given the potential for platelet dysfunction.

Covert stroke after non-cardiac surgery: a prospective cohort study.

BACKGROUND: Overt stroke after non-cardiac surgery has a substantial impact on the duration and quality of life. Covert stroke in the non-surgical setting is much more common than overt stroke and is associated with an increased risk of cognitive decline and dementia. Little is known about covert stroke after non-cardiac, non-carotid artery surgery. METHODS: We undertook a prospective, international cohort study to determine the incidence of covert stroke after non-cardiac, non-carotid artery surgery. Eligible patients were ≥65 yr of age and were admitted to hospital for at least three nights after non-cardiac, non-carotid artery surgery. Patients underwent a brain magnetic resonance study between postoperative days 3 and 10. The main outcome was the incidence of perioperative covert stroke. RESULTS: We enrolled a total of 100 patients from six centres in four countries. The incidence of perioperative covert stroke was 10.0% (10/100 patients, 95% confidence interval 5.5-17.4%). Five of the six centres that enrolled patients reported an incident covert stroke, and covert stroke was found in patients undergoing major general (3/27), major orthopaedic (3/41), major urological or gynaecological (3/22), and low-risk surgery (1/12). CONCLUSIONS: This international multicentre study suggests that 1 in 10 patients ≥65 yr of age experiences a perioperative covert stroke. A larger study is required to determine the impact of perioperative covert stroke on patient-important outcomes. CLINICAL TRIAL REGISTRATION: NCT01369537.

Definition, evaluation, and management of brain relaxation during craniotomy.

The term 'brain relaxation' is routinely used to describe the size and firmness of the brain tissue during craniotomy. The status of brain relaxation is an important aspect of neuroanaesthesia practice and is relevant to the operating conditions, retraction injury, and likely patient outcomes. Brain relaxation is determined by the relationship between the volume of the intracranial contents and the capacity of the intracranial space (i.e. a content-space relationship). It is a concept related to, but distinct from, intracranial pressure. The evaluation of brain relaxation should be standardized to facilitate clinical communication and research collaboration. Both advantageous and disadvantageous effects of the various interventions for brain relaxation should be taken into account in patient care. The outcomes that matter the most to patients should be emphasized in defining, evaluating, and managing brain relaxation. To date, brain relaxation has not been reviewed specifically, and the aim of this manuscript is to discuss the current approaches to the definition, evaluation, and management of brain relaxation, knowledge gaps, and targets for future research.

Clinical diagnostic tools for screening of perioperative stroke in general surgery: a systematic review.

Perioperative stroke is a devastating complication that carries high mortality and functional disability. Unfortunately, residual anaesthesia and analgesia may obscure important warning signs and may lead to a delay in the assessment and treatment of major stroke after surgery. The purpose of this review is to examine the utility of existing stroke scales, for the recognition of perioperative stroke in the general surgical population. A total of 21 stroke scales have been described in the literature. Diagnostic performance was reported in 17 scales. The majority of the stroke scales were designed to evaluate current neurological deficits after an established stroke event. Recent abbreviated stroke test, such as the Face, Arm, Speech Test (FAST), were developed to facilitate stroke identification in the emergency department. Only two stroke scales have been applied in the perioperative setting after cardiac, carotid and neurological surgeries. The modified National Institutes of Health Stroke Scale appears to be useful in detecting new subtle neurological deficits in critical care, or high dependency units after surgery. However, in the general postsurgical wards, given the concern about the workload required, abbreviated stroke tests may be more appropriate for routine regular stroke surveillance. It is hoped that these tests will provide rapid assessment of global neurological function to facilitate timely diagnosis and treatment of perioperative stroke.

Flurbiprofen and hypertension but not hydroxyethyl starch are associated with post-craniotomy intracranial haematoma requiring surgery.

BACKGROUND: Post-craniotomy intracranial haematoma is one of the most serious complications after neurosurgery. We examined whether post-craniotomy intracranial haematoma requiring surgery is associated with the non-steroidal anti-inflammatory drugs flurbiprofen, hypertension, or hydroxyethyl starch (HES). METHODS: A case-control study was conducted among 42 359 patients who underwent elective craniotomy procedures at Beijing Tiantan Hospital between January 2006 and December 2011. A one-to-one control group without post-craniotomy intracranial haematoma was selected matched by age, pathologic diagnosis, tumour location, and surgeon. Perioperative blood pressure records up to the diagnosis of haematoma, the use of flurbiprofen and HES were examined. The incidence of post-craniotomy intracranial haematoma and the odds ratios for the risk factors were determined. RESULTS: A total of 202 patients suffered post-craniotomy intracranial haematoma during the study period, for an incidence of 0.48% (95% CI=0.41-0.55). Haematoma requiring surgery was associated with an intraoperative systolic blood pressure of >160 mm Hg (OR=2.618, 95% CI=2.084-2.723, P=0.007), an intraoperative mean blood pressure of >110 mm Hg (OR=2.600, 95% CI=2.312-3.098, P=0.037), a postoperative systolic blood pressure of >160 mm Hg (OR=2.060, 95% CI= 1.763-2.642, P=0.022), a postoperative mean blood pressure of >110 mm Hg (OR=3.600, 95% CI= 3.226-4.057, P=0.001), and the use of flurbiprofen during but not after the surgery (OR=2.256, 95% CI=2.004-2.598, P=0.005). The intraoperative infusion of HES showed no significant difference between patients who had a haematoma and those who did not. CONCLUSIONS: Intraoperative and postoperative hypertension and the use of flurbiprofen during surgery are risk factors for post-craniotomy intracranial haematoma requiring surgery. The intraoperative infusion of HES was not associated with a higher incidence of haematoma.

Pharmacological perioperative brain neuroprotection: a qualitative review of randomized clinical trials.

Perioperative cerebral damage may be associated with surgery and anaesthesia. Pharmacological perioperative neuroprotection is associated with conflicting results. In this qualitative review of randomized controlled clinical trials on perioperative pharmacological brain neuroprotection, we report the effects of tested therapies on new postoperative neurological deficit, postoperative cognitive decline (POCD), and mortality rate. Studies were identified from Cochrane Central Register and MEDLINE and by hand-searching. Of 5904 retrieved studies, 25 randomized trials met our inclusion criteria. Tested therapies were: lidocaine, thiopental, S(+)-ketamine, propofol, nimodipine, GM1 ganglioside, lexipafant, glutamate/aspartate and xenon remacemide, atorvastatin, magnesium sulphate, erythropoietin, piracetam, rivastigmine, pegorgotein, and 17ß-estradiol. The use of atorvastatin and magnesium sulphate was associated with a lower incidence of new postoperative neurological deficit. The use of lidocaine, ketamine, and magnesium sulphate was associated with controversial results on POCD. The POCD did not differ between treated patients and control group for other tested drugs (thiopental, propofol, nimodipine, GM1 ganglioside, lexipafant, glutamate/aspartate, xenon, erythropoietin, remacemide, piracetam, rivastigmine, pegorgotein, and 17ß-estradiol). None of the tested drugs was associated with a reduction in mortality rate. Drugs with various mechanisms of action have been tested over time; current evidence suggests that pharmacological brain neuroprotection might reduce the incidence of new postoperative neurological deficits and POCD, while no benefits on perioperative mortality are described. Of importance from this review is the need for shared methodological approach when clinical studies on pharmacological neuroprotection are designed.

Changes in cerebral tissue oxygen saturation during anaesthetic-induced hypotension: an interpretation based on neurovascular coupling and cerebral autoregulation.

There is currently no consensus regarding how to intervene in anaesthetic-induced hypotension. Whether or not the balance between cerebral oxygen supply and demand is maintained lacks adequate elucidation. It is thus intriguing to explore how cerebral tissue oxygen saturation is affected by anaesthetic-induced hypotension. Thirty-three patients scheduled for elective non-neurosurgical procedures were included in this study. Physiological measurements were performed immediately before induction with propofol and fentanyl and after tracheal intubation. Mean (SD) Bispectral index decreased from 84.3 (9.3) to 24.4 (8.0) (p<0.001). Mean arterial pressure decreased from 84.4 (10.6) mmHg to 53.6 (11.4) mmHg (p<0.001). However, cerebral tissue oxygen saturation remained stable (67.0 (9.4) % vs 67.5 (7.8) %, p=0.6). These results imply that the fine balance between cerebral oxygen supply and demand is not disrupted by anaesthetic-induced hypotension. An interpretation based on neurovascular coupling and cerebral autoregulation is proposed.

Impact of stepwise hyperventilation on cerebral tissue oxygen saturation in anesthetized patients: a mechanistic study.

BACKGROUND: While the decrease in blood carbon dioxide (CO2 ) secondary to hyperventilation is generally accepted to play a major role in the decrease of cerebral tissue oxygen saturation (SctO2 ), it remains unclear if the associated systemic hemodynamic changes are also accountable. METHODS: Twenty-six patients (American Society of Anesthesiologists I-II) undergoing nonneurosurgical procedures were anesthetized with either propofol-remifentanil (n = 13) or sevoflurane (n = 13). During a stable intraoperative period, ventilation was adjusted stepwise from hypoventilation to hyperventilation to achieve a progressive change in end-tidal CO2 (ETCO2 ) from 55 to 25 mmHg. Minute ventilation, SctO2 , ETCO2 , mean arterial pressure (MAP), and cardiac output (CO) were recorded. RESULTS: Hyperventilation led to a SctO2 decrease from 78 ± 4% to 69 ± 5% (Δ = -9 ± 4%, P < 0.001) in the propofol-remifentanil group and from 81 ± 5% to 71 ± 7% (Δ = -10 ± 3%, P < 0.001) in the sevoflurane group. The decreases in SctO2 were not statistically different between these two groups (P = 0.5). SctO2 correlated significantly with ETCO2 in both groups (P < 0.001). SctO2 also correlated significantly with MAP (P < 0.001) and CO (P < 0.001) during propofol-remifentanil, but not sevoflurane (P = 0.4 and 0.5), anesthesia. CONCLUSION: The main mechanism responsible for the hyperventilation-induced decrease in SctO2 is hypocapnia during both propofol-remifentanil and sevoflurane anesthesia. Hyperventilation-associated increase in MAP and decrease in CO during propofol-remifentanil, but not sevoflurane, anesthesia may also contribute to the decrease in SctO2 but to a much smaller degree.

Impact of phenylephrine administration on cerebral tissue oxygen saturation and blood volume is modulated by carbon dioxide in anaesthetized patients.

BACKGROUND: Multiple studies have shown that cerebral tissue oxygen saturation (Sct(O(2))) is decreased after phenylephrine treatment. We hypothesized that the negative impact of phenylephrine administration on Sct(O(2)) is affected by arterial blood carbon dioxide partial pressure (Pa(CO(2))) because CO(2) is a powerful modulator of cerebrovascular tone. METHODS: In 14 anaesthetized healthy patients, i.v. phenylephrine bolus was administered to increase the mean arterial pressure ~20-30% during hypocapnia, normocapnia, and hypercapnia. Sct(O(2)) and cerebral blood volume (CBV) were measured using frequency domain near-infrared spectroscopy, a quantitative technology. Data collection occurred before and after each treatment. RESULTS: Phenylephrine caused a significant decrease in Sct(O(2)) during hypocapnia [ΔSct(O(2)) =-3.4 (1.5)%, P<0.001], normocapnia [ΔSct(O(2)) =-2.4 (1.5)%, P<0.001], and hypercapnia [ΔSct(O(2)) =-1.4 (1.5)%, P<0.01]. Decreases in Sct(O(2)) were significantly different between hypocapnia, normocapnia, and hypercapnia (P<0.001). Phenylephrine also caused a significant decrease in CBV during hypocapnia (P<0.01), but not during normocapnia or hypercapnia. CONCLUSION: The negative impact of phenylephrine treatment on Sct(O(2)) and CBV is intensified during hypocapnia while blunted during hypercapnia.

Cerebral blood flow during orthostasis: role of arterial CO2.

Reductions in end-tidal Pco(2) (Pet(CO(2))) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in Pet(CO(2)) reflected decreases in arterial Pco(2) (Pa(CO(2))) and their relation to increases in alveolar ventilation (Va) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. Pa(CO(2)), Va, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in Pet(CO(2)) and Pa(CO(2)) (-1.7 +/- 0.5 and -1.1 +/- 0.4 mmHg, P < 0.05) during minute 1 of HUT were associated with a significant increase in Va (+0.7 +/- 0.3 l/min, P < 0.05). However, further decreases in Pa(CO(2)) (-0.5 +/- 0.5 mmHg, P < 0.05), from minute 1 to the last minute of HUT, occurred even though Va did not change significantly (-0.2 +/- 0.3 l/min, P = not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (-7 +/- 2 and -8 +/- 2%, P < 0.05) from minute 1 to the last minute of HUT, despite minimal changes in Pa(CO(2)). These data suggest that decreases in Pet(CO(2)) and Pa(CO(2)) during upright posture are not solely due to increased Va but could be due to ventilation-perfusion mismatch or a redistribution of CO(2) stores. Furthermore, the reduction in Pa(CO(2)) did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in Pa(CO(2)) play a role in the CBF response to orthostatic stress.

Circulating norepinephrine and cerebrovascular control in conscious humans.

BACKGROUND: Cerebral vasoconstriction without concurrent changes in systemic arterial blood pressure has been observed in both normal individuals and those with idiopathic orthostatic intolerance following several minutes of postural stress when circulating catecholamines are elevated. Therefore, we tested the hypothesis that alpha-adrenergic activation with and without elevated circulating norepinephrine (NE) directly affects cerebrovascular tone in healthy individuals. METHODS: Mean arterial pressure (MAP; tonometry) and cerebral blood flow velocity (MFV) in the middle cerebral artery (transcranial Doppler) were measured in seven healthy individuals during 15 min periods of saline and of 50 (low NE) and 100 (high NE) ng kg(-1) min(-1) infusions of NE. Following this, phentolamine (PHO) was administered to return MAP back to baseline while high NE infusion continued (high NE+PHO). Finally, NE infusion was stopped allowing the persistent effects of PHO to dominate. RESULTS: Circulating NE caused a dose-dependent increase in MAP (P<0.05). During combined high NE+PHO, blood pressure was initially reduced to baseline levels but then increased a second time (P<0.05) during the final approximately 5 min of this phase. MFV remained constant during both low NE and high NE. In contrast, the secondary increase in BP during the late high NE+PHO phase was associated with elevated MFV. Cerebral vascular resistance (CVR) increased during high NE but was reduced to baseline during both early and late portions of the combined high NE+PHO phase (i.e. despite the late-phase increase in blood pressure). CONCLUSIONS: The increase in CVR during NE infusion was explained by an autoregulatory response to the increased blood pressure and not an alpha-mediated constriction. However, PHO appeared to interfere with the normal autoregulatory response to increasing blood pressure.

Detection of awareness in surgical patients with EEG-based indices--bispectral index and patient state index.

BACKGROUND: Patient state index (PSI) and bispectral index (BIS) are values derived from the EEG, which can measure the hypnotic component of anaesthesia. We measured the ability of PSI and BIS to distinguish consciousness from unconsciousness during induction and emergence from anaesthesia and a period of awareness in surgical patients. METHODS: Forty unpremedicated patients were randomized to receive: (1) sevoflurane/remifentanil (< or =0.1 microg kg(-1) min(-1)), (2) sevoflurane/remifentanil (> or = 0.2 microg kg(-1) min(-1)), (3) propofol/remifentanil (< or =0.1 microg kg(-1) min(-1)), (4) propofol/remifentanil (> or = 0.2 microg kg(-1) min(-1)). Every 30 s after the start of the remifentanil, patients were asked to squeeze the investigator's hand. Sevoflurane or propofol were given until loss of consciousness (LOC1). Tunstall's isolated forearm technique was used during neuromuscular block with succinylcholine. After tracheal intubation, propofol or sevoflurane were stopped until return of consciousness (ROC1). Propofol or sevoflurane were re-started to induce LOC2. After surgery, drugs were discontinued and recovery (ROC2) was observed. PSI and BIS at LOC (LOC1 and LOC2) were compared with those at ROC (ROC1 and ROC2) (t-test). Prediction probability (P(k)) was calculated from values at the last command before and at LOC and ROC. Values are mean (SD). RESULTS: At non-responsiveness, BIS (66 (17)) and PSI (55 (23)) were significantly less than at responsiveness (BIS, 79 (14); PSI, 77 (18); P<0.05). The wide variation with both BIS and PSI measurements of the 80 'awareness' values led to an erroneous classification as unconscious in some cases (BIS, six patients; PSI, nine patients). P(k) was 0.68 (0.03) (BIS) and 0.69 (0.03) (PSI). CONCLUSIONS: Despite significant differences between mean values at responsiveness and non-responsiveness for BIS and PSI, neither measure may be sufficient to detect awareness in an individual patient, reflected by a P(k) less than below 70%.