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February 2010 Journal Watch

1 A major step forward: guidelines for the management of cardiac patients for non-cardiac surgery - the art of anaesthesia. Editorial: Münter Sellevold OF et al. Eur J Anaesthesiol. 2010 Feb;27(2):89-91

Guidelines for pre-operative cardiac risk assessment and perioperative cardiac management in non-cardiac surgery: the Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management in Non-cardiac Surgery of the European Society of Cardiology (ESC) and endorsed by the European Society of Anaesthesiology (ESA). Poldermans D et al. Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management in Non-cardiac Surgery of European Society of Cardiology (ESC); European Society of Anaesthesiology (ESA). Eur J Anaesthesiol. 2010 Feb;27(2):92-137

Inspired by the AHA/ACC guidelines for the management of patients with cardiac disease having non-cardiac surgery, the European society of cardiology (ESC) has formulated guidelines that have been endorsed by the European Society of Anesthesiology (ESA). The author of the accompanying editorial justifies the need for the European guidelines because the American health system is significantly different to that dominating in large parts of Europe (?Australia). The new ESC/ESA guidelines are comprehensive and show both similarities and differences to the well-established US guidelines. Each recommendation is accompanied by a (subjective) class of recommendation and an (objective) level of evidence. The taskforce starts with discussion about the increasing burden of cardiovascular disease. The section about preoperative evaluation recommends an assessment of the surgical risk and patient risk including functional capacity, presence or 6 risk factors (IHD, surgical risk, CCF, CVA/TIA, DM and renal dysfunction) and the use of the Lee clinical risk index for risk stratification. Recommendations for resting echocardiography are restricted to patients undergoing high-risk surgery and stress testing is only recommended strongly for patients with ≥3 risk factors having high-risk surgery. Interestingly, the taskforce recommends consideration of BNP measurement in high-risk patients. Emphasis is placed on the restricted use of prophylactic coronary revascularization, as this is rarely indicated simply to ensure the patient survives surgery. In contrast, optimization and initiation of medical therapy is recommended for all patients in having intermediate/high risk surgery in the presence of CAD and/or patients with poor functional capacity or risk factors. The main messages re beta-blockers are: (1) they should not be stopped preoperatively, (2) they are recommended in high risk surgery or any surgery if the patient has known IHD or ischaemia on preoperative testing. In comparison the AHA/ACC focused update on perioperative beta-blockade (Circ, Nov, 2009) restricts recommendations to patients with risk factors having vascular surgery or intermediate risk surgery if multiple risk factors. Both sets of guidelines emphasise initiation of therapy well in advance of surgery (at least 1 week) and strict titration to both HR and BP parameters. The taskforce views statins as an important intervention for high risk patients and recommends that they should started in high-risk patients 1-4 weeks prior to surgery and continued perioperatively in patients with chronic prescriptions. Likewise, perioperative continuation of ACEI and diuretics are recommended in patients with LV dysfunction. The evidence of perioperative aspirin therapy (in the absence of coronary stenting) is more limited. Detailed recommendations are given for management of anticoagulation therapy. Specific disease states are also analysed in detail by the taskforce with practical suggestions given for management of these conditions. Notable recommendations for intraoperative monitoring include 12-lead ECG monitoring for all patients undergoing surgery. Recommendations for TOE are much more limited except in the setting of acute, sustained, severe haemodynamic disturbances. The authors also undertake an analysis of the evidence for perioperative glycaemic control and recommend targeting ≤ 10 mmol/L in high-risk surgery or surgery requiring post-operative critical care. The guidelines make it clear that strong evidence remains to be gathered of the influence of intra-operative anaesthetic management on short and long-term postoperative outcome. The taskforce summarises their recommendations with a one-page algorithm for pre-operative cardiac risk evaluation and perioperative management. The obvious emphasis on optimal medical therapy suggests a pressing need for anaesthetists to refer readily to physicians/cardiologists well in advance of surgery or to act as a perioperative physician themselves. Finally, the accompanying editorial raises the vexed question of whether the anaesthetist should play a role in recommending to the patient whether or not a surgical intervention should be performed.

Take home question: Are the new ESA/ESC or the AHA/ACC guidelines for cardiac patients having non-cardiac surgery more relevant to the Australian health system?

See also: Nov 2009 Journal Watch (1); Jun 09 Journal Watch (9)

2 Breathe deeply the sweet air: ruminations on glycemic control. Editorial: Keegan MT et al. Anesth Analg. 2010 Feb;110(2):296-8

Scientific principles and clinical implications of perioperative glucose regulation and control. Akhtar S et al. Anesth Analg. 2010 Feb;110(2):478-97.

This review discusses the evidence that hyperglycaemia after major operations is very common and associated with poor outcomes in critically ill and postsurgical patients. The author gives a summary of the physiology of glycaemic control prior to explaining why patients are prone to hyperglycaemia in the perioperative period. Chiefly, the perioperative stress response leads to insulin resistance. This may be modulated by many factors, including anaesthetic technique, perioperative medications, surgical location and extent, and operative duration and technique. Insulin secretion is also directly affected by anaesthetics and various vasoactive medications. There is an outline of the evidence gained from retrospective studies to suggest that preoperative, intraoperative and postoperative hyperglycaemia is associated with sub-optimal outcomes. However, from retrospective data it remains poorly understood whether hyperglycaemia mediates poor operative outcomes or whether it is simply an “innocent bystander.” It is also mentioned that, given approximately 40% of patients with prediabetes/diabetes are unaware of their disease, perioperative evaluation provides a unique opportunity to screen patients for hyperglycaemia. The author then analyses the prospective evidence for intensive glycaemic control (IGC-target glucose <5.5 mmol/l) concluding that, although the association between perioperative hyperglycaemia and poor outcomes is strong, IGC cannot be advocated for perioperative patients at the present time, especially in view of the NICE-SUGAR (Finfer et al, NEJM, 2009) results. However, this does not imply that glucose control should be totally abandoned and that any hyperglycaemic levels are acceptable. In conclusion, there is neither a universally appropriate therapeutic glycaemic target or consensus of the true efficacy of perioperative glycaemic control, so glycaemic targets must err on the side of caution, mainly to reduce the risk of inadvertent hypoglycaemia. The author feels that insulin therapy should preferably be administered IV in the perioperative period and should always be accompanied by close glucose monitoring. The accompanying editorial highlights the May 2009 consensus statement on inpatient glycaemic control from the American Diabetes Association (ADA) which recommends initiation of insulin, preferably by continuous infusion, in critically ill patients with glucose concentrations of >10 mmol/l, aiming for a target value of between 7.8-10 mmol/l. For non-critically ill patients, the AACE/ADA recommend a premeal blood glucose target of <7.8 mmol/l and random sugars of < 10mmol/l. The editorialist states: “rather than abandoning glycaemic control in 2009, we have simply ‘moved the goal posts’ to provide a greater margin of safety (and avoid hypoglycaemia).

Take home message: According to this review, it is prudent to maintain glucose levels <10 mmol/l in the perioperative period and glycaemic control should always be accompanied by close glucose monitoring.

See also: April 09 Journal Watch (6);

For related reading this month: Bagshaw SM et al. Best evidence in critical care medicine. Intensive vs conventional blood glucose control in critically ill patients. Can J Anaesth. 2010 Feb;57(2):172-5

3 Postoperative noninvasive ventilation. Jaber S et al. Anesthesiology. 2010 Feb;112(2):453-61. [Article]

This review article provides a rationale for use of postoperative non-invasive ventilation (NIV). The author discusses the main respiratory modifications induced by surgery and anaesthesia that justify postoperative NIV use. Regardless of the presence of complications, thoracic and/or abdominal surgery necessarily and profoundly alters the respiratory system for long periods. The two main NIV techniques are CPAP and BiPAP (PSV+PEEP/CPAP). Bi stands for bilevel. CPAP used alone essentially helps to provide satisfactory gas exchange through changes in ventilation/perfusion ratio and increase in oxygen partial alveolar pressure. BiPAP provides a better physiologic response in terms of muscle unloading and dyspnoea relief.

The article provides some recommendations to safely apply postoperative NIV. When initiating CPAP therapy, pressures of 7-10 cm H2O are required to keep tracheal pressure positive during the entire respiratory cycle. When initiating BiPAP, patient comfort and interface acceptance may be gained by starting with PEEP alone and then slowly increasing the PSV level once the mask is applied. The authors recommend starting with PSV of 3-5 cm H20 and increasing in increment of 2 cm H20 to achieve a 6-10 ml/kg expiratory tidal volume, a decrease in the patient’s respiratory rate, and a comfort improvement. The PEEP, is started at 3-5 cm H20 and increased as needed to improve oxygenation without adverse haemodynamic effects up to 10 cm H20. Ultimately PSV is usually 10-15 cm H20 with PEEP of 5-10 cm H20. Individual titration should be performed and periods of use may alternate with lengthy ventilator-free periods. Caution must be exercise in patients with upper digestive stitching and lack of patient co-operation or deteriorating mental status are contraindications to NIV use. The author feels that the optimal location for patients receiving NIV is ICU or recovery room.

The author then presents the available evidence to support the use of NIV. Postoperative NIV can be proposed in two ways. The first is a preventative or ‘prophylactic’ application to prevent postoperative acute respiratory failure (ARF) from developing in patients at risk (elderly, obese, COPD, IHD) and the second consists of a ‘curative’ application, once ARF has occurred, to alleviate respiratory failure while aiming to avoid tracheal intubation, a cause of increased morbidity. Preventive use of NIV in a pre- and postoperative manner has been shown to significantly reduce pulmonary dysfunction after lung resection. Likewise, preventive NIV has been used favourably in upper abdominal surgery, bariatric surgery and AAA surgery. Curative use of NIV has been used to avoid intubation in lung transplant patients, other thoracic surgery abdominal surgery including oesophagectomy.

Take home message: NIV has proven to be an effective strategy to reduce intubation rates (and associated morbidity), nosocomial infections, ICU and hospital lengths of stay and morbidity and mortality in patients with either hypercapnic of non-hypercapnic ARF.

4 Development and validation of a postoperative nausea and vomiting intensity scale. Wengritzky R et al. Br J Anaesth. 2010 Feb;104(2):158-66.

This study sought to develop a measurement tool for PONV intensity in order to identify clinically important PONV, as opposed to minor, transient PONV episodes that have minimal impact on postoperative recovery. The study was divided into two phases. The first phase was the ‘development’ phase. After a literature review, the investigators constructed a questionnaire exploring the intensity, pattern and duration that defines severe PONV and surveyed 122 patients/relatives and 58 medical/ nursing staff. Based on these results, a PONV scale was developed. In the ‘validation’ phase, the investigators then evaluated the scale in a further 163 patients reporting PONV. Psychometric techniques were used to prospectively validate and test the reliability and responsiveness of the PONV Intensity Scale in a broad surgical setting. The authors found that a PONV Intensity Scale ≥50 defined clinically important PONV and correlated with a group of patients who required more antiemetic therapy, had higher rates of complications associated with severe PONV, and took longer to recover from their surgery. PONV Intensity Scale ≥50 also was associated with a poor quality of recovery. The scale identified 29 patients of 163 patients evaluated in the ‘validation’ phase (18%) as having clinically important PONV. Of note, 96% of these patients had an Apfel score of ≥2 however only 66% were administered ≥1 prophylactic antiemetic and only 35% received double- or triple-antiemetic prophylaxis. The scale was revised to a simpler version after 100 patients and it was found to be essentially interchangeable with the original PONV Intensity Scale. It was also found to be superior to the nausea VAS≥75 in detecting clinically significant PONV.

Take home message: The PONV Scale can be used to identify clinically important PONV.

For related reading this month:

Editorial: Apfel CC et al. Can central antiemetic effects of opioids counter-balance opioid-induced nausea and vomiting? Acta Anaesthesiol Scand. 2010 Feb;54(2):129-31.

Johnston KD. The potential for mu-opioid receptor agonists to be anti-emetic in humans: a review of clinical data. Acta Anaesthesiol Scand. 2010 Feb;54(2):132-40.

Chaparro LE et al. Effectiveness of combined haloperidol and dexamethasone versus dexamethasone only for postoperative nausea and vomiting in high-risk day surgery patients: a randomized blinded trial. Eur J Anaesthesiol. 2010 Feb;27(2):192-5.

5 The effect of an anatomically classified procedure on antiemetic administration in the postanesthesia care unit. Ruiz JR et al. Anesth Analg. 2010 Feb;110(2):403-9.

Postoperative nausea and vomiting: we don't know everything yet. Editorial: Glass PS. Anesth Analg. 2010 Feb;110(2):299. -

PRO: Anatomical classification of surgical procedures improves our understanding of the mechanisms of postoperative nausea and vomiting. Scuderi PE. Anesth Analg. 2010 Feb;110(2):410-1

CON: Postoperative nausea and vomiting database research: limitations and opportunities. Habib AS et al. Anesth Analg. 2010 Feb;110(2):412-4.

This retrospective observational study (n=18,109) investigated the effect the type of surgical procedure (categorized and compared anatomically) has on antiemetic therapy within 2 hours of admission to PACU, using an oncology anaesthesia database. The authors classified the types of surgical procedure anatomically into seven categories, with the integumentary musculoskeletal and superficial surgeries chosen as the reference group. Compared the reference group, patients undergoing neurological, head or neck and abdominal surgeries were administered PACU antiemetic statistically significantly more often, whereas patients undergoing thoracic surgeries were administered PACU antiemetic significantly less often. Breast or axilla and endoscopic procedures did not differ from the reference category. Apfel PONV factors as well as intraoperative and postoperative opioid administration were significantly associated with antiemetic administration. 79% of patients received prophylactic ondansetron and 24% of patients received prophylactic dexamethasone. A major limitation of this study is that PONV was not directly assessed-the investigators relied on a surrogate endpoint, namely, the antiemetic administration within the PACU. Also, a large proportion of the neurological patients were excluded because they were admitted directly to ICU. The study is accompanied by an editorial and 2 commentaries: the one by Scuderi supporting the study results and the one by Habib et al. questioning the validity of the study conclusions. Scuderi feels that the paper offers insight into heretofore unappreciated risk factors of PONV. He also supports routine administration of up to 3 antiemetics. Habib et al feels that the paper is not valid because the method of grouping surgical procedures by anatomical location makes no sense. He also suggests that the observed results could be confounded by the influence of aggressive antiemetic prophylaxis in specific procedures ie. breast/axilla surgery. The editorial invites researchers to prospectively, validate or refute the findings.

Take home message: This observational study found the type of surgery, categorized by anatomical site, was a significant predictor of antiemetic administration. These results need to be validated in a prospective RCT.

6 Anesthetic neurotoxicity: it's not just for children anymore. Editorial: Durieux ME. Anesth Analg. 2010 Feb;110(2):291-2

Anesthesia and the old brain. Tang J et al. Anesth Analg. 2010 Feb;110(2):421-6.

The young: neuroapoptosis induced by anesthetics and what to do about it. Creeley CE et al. Anesth Analg. 2010 Feb;110(2):442-8.

Isoflurane does not affect brain cell death, hippocampal neurogenesis, or long-term neurocognitive outcome in aged rats. Stratmann G et al. Anesthesiology. 2010 Feb;112(2):305-15.

Inhaled anesthetic potency in aged Alzheimer mice. Bianchi SL et al. Anesth Analg. 2010 Feb;110(2):427-30.

A collection of articles published in Anesthesia Analgesia this month focus on the potential neurotoxicity of general anaesthesia. Contrary to a long-held belief, anaesthetic drugs have potential to change structure and function of the brain permanently. Emerging evidence suggests that commonly used anaesthetics may be profoundly toxic to neurons when administered during synaptogenesis, an active process during the neonatal period of life. Even more concerning, recent finding demonstrate that relatively brief exposure to anaesthetics can have long-term effects, potentially lasting a lifetime. Researchers are actively investigating potential neuroprotection strategies (lithium treatment and hypothermia) that are considered promising. Unfortunately, much of the data relies on extrapolation of animal study results. Anaesthesia kills cells in the infantile rodent brain and causes long-term neurocognitive dysfunction, but whether there is a causal link between these finding is questionable. Likewise, existing data suggests the elderly may be susceptible to adverse effects of anaesthesia which may contribute to neurodegenerative disorders in susceptible individuals. Patients believed to be at particular risk are those with Alzheimer disease and potential histological mechanisms of neurotoxicity may involve amyloidopathy and tauopathy.

The author of the accompanying editorial cautions against abandoning well-established anaesthetic approaches because of laboratory results with unsubstantiated clinical relevance. However, he does recommend avoiding anaesthesia wherever possible until after the brain growth spurt (third trimester fetus and very young children), and to keep anaesthesia simple using the least amount of drugs required.

Take home message: There is suggestive, but not definitive, emerging evidence to support human susceptibility for potential long-term neurotoxic effects of general anaesthesia, especially in patients at the extremes of age.

See also: April 09 Journal Watch (2); Dec 09 Journal Watch (8)