Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

GRADE guidelines: 15. Going from evidence to recommendation-determinants of a recommendation's direction and strength.

Coronary artery disease

ガイドライン解説 AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease : 2011 update

Postoperative pulmonary complications (PPCs) are common, costly, and increase patient mortality. Changes to the respiratory system occur immediately on induction of general anaesthesia: respiratory drive and muscle function are altered, lung volumes reduced, and atelectasis develops in > 75% of patients receiving a neuromuscular blocking drug. The respiratory system may take 6 weeks to return to its preoperative state after general anaesthesia for major surgery. Risk factors for PPC development are numerous, and clinicians should be aware of non-modifiable and modifiable factors in order to recognize those at risk and optimize their care. Many validated risk prediction models are described. These have been useful for improving our understanding of PPC development, but there remains inadequate consensus for them to be useful clinically. Preventative measures include preoperative optimization of co-morbidities, smoking cessation, and correction of anaemia, in addition to intraoperative protective ventilation strategies and appropriate management of neuromuscular blocking drugs. Protective ventilation includes low tidal volumes, which must be calculated according to the patient's ideal body weight. Further evidence for the most beneficial level of PEEP is required, and on-going randomized trials will hopefully provide more information. When PEEP is used, it may be useful to precede this with a recruitment manoeuvre if atelectasis is suspected. For high-risk patients, surgical time should be minimized. After surgery, nasogastric tubes should be avoided and analgesia optimized. A postoperative mobilization, chest physiotherapy, and oral hygiene bundle reduces PPCs.

Postoperative pulmonary complications

Background: Patients with chronic obstructive pulmonary disease (COPD) have increased postoperative morbidity and mortality. Epidural analgesia (EDA) improves postoperative outcome but may worsen postoperative lung function. It is unknown whether patients with COPD benefit from EDA. The objective of this study was to determine whether patients with COPD undergoing major abdominal surgery benefit from EDA in addition to general anesthesia. Methods: This cohort study included 541 consecutive patients with COPD who underwent major abdominal surgery between 1995 and 2007 at a university medical center. Propensity scores estimating the probability of receiving EDA were used in multivariate correction. The primary outcome was postoperative pneumonia and 30-day mortality. Results: There were 324 patients (60%) who received EDA in addition to general anesthesia. The incidence of postoperative pneumonia (16% vs. 11%; P = 0.08) and 30-day mortality (9% vs. 5%; P = 0.03) was lower in patients who received EDA. After correction EDA was associated with improved outcome for postoperative pneumonia (OR 0.5; 95% CI: 0.3-0.9; P = 0.03). The strongest preventive effect was seen in patients with the most severe type of COPD. Conclusion: This study provides evidence that in patients with COPD who are scheduled for major abdominal surgery, epidural analgesia decreases postoperative pulmonary complications. Copyright

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Epidural Analgesia Is Associated with Improved Health Outcomes of Surgical Patients with Chronic Obstructive Pulmonary Disease

Background: Intraoperative hypotension has been associated with postoperative morbidity and early mortality. Postoperative hypotension, however, has
been less studied. This study examines postoperative hypotension, hypothesizing that both the degree of hypotension severity and longer durations would
be associated with myocardial injury.
Methods: This single-center observational cohort was comprised of 1,710
patients aged 60 yr or more undergoing intermediate- to high-risk noncardiac surgery. Frequent sampling of hemodynamic monitoring on a postoperative high-dependency ward during the first 24 h after surgery was recorded.
Multiple mean arterial pressure (MAP) absolute thresholds (50 to 75 mmHg)
were used to define hypotension characterized by cumulative minutes, duration, area, and time-weighted-average under MAP. Zero time spent under
a threshold was used as the reference group. The primary outcome was
myocardial injury (a peak high-sensitive troponin T measurement 50 ng/l or
greater) during the first 3 postoperative days.
Results: Postoperative hypotension was common, e.g., 2 cumulative hours
below a threshold of 60 mmHg occurred in 144 (8%) patients while 4 h less
than 75 mmHg occurred in 824 (48%) patients. Patients with myocardial
injury had higher prolonged exposures for all characterizations. After adjusting for confounders, postoperative duration below a threshold of 75 mmHg
for more than 635min was associated with myocardial injury (adjusted odds
ratio, 2.68; 95% CI, 1.46 to 5.07, P = 0.002). Comparing multiple thresholds,
cumulative durations of 2 to 4 h below a MAP threshold of 60 mmHg (adjusted
odds ratio, 3.26; 95% CI, 1.57 to 6.48, P = 0.001) and durations of more
than 4 h less than 65 mmHg (adjusted odds ratio, 2.98; 95% CI, 1.78 to 4.98,
P < 0.001) and 70 mmHg (adjusted odds ratio, 2.18; 95% CI, 1.37 to 3.51,
P < 0.001) were also associated with myocardial injury. Associations remained
significant after adjusting for intraoperative hypotension, which independently
was not associated with myocardial injury.
Conclusions: In this study, postoperative hypotension was common and
was independently associated with myocardial injury

Postoperative Hypotension after Noncardiac Surgery and the Association with Myocardial Injury

Epidural Analgesia Is Associated With Improved Health Outcomes of Surgical Patients With Chronic Obstructive Pulmonary Disease

The incidence of postoperative stroke ranges from 0.08% to 0.7% in noncardiac surgery. Recently, the PeriOperative ISchemic Evaluation (POISE) study reported an incidence of postoperative stroke of 1% in patients scheduled for noncardiac surgery when β blockers were initiated immediately before surgery. To assess the association between chronic β-blocker use and postoperative stroke in noncardiac surgery, we undertook a case-control study among 186,779 patients who underwent noncardiac surgery from 2000 to 2008 at the Erasmus Medical Centre. Patients who were undergoing intracerebral surgery or carotid surgery or who had head and/or carotid trauma were excluded. The case subjects were 34 patients (0.02%) who had experienced a stroke within 30 days after surgery. Of the remaining patients, 2 controls were selected for each case and were stratified according to calendar year, type of surgery, and age. For cases and controls, information was obtained regarding β-blocker use before surgery, the presence of cardiac risk factors, and the use of other cardiovascular medication. The use of β blockers was as common in the cases as in the controls (29% vs 29%; p = 1.0). The adjusted odds ratio for postoperative stroke among β-blocker users compared with nonusers was 0.4 (95% confidence interval 0.1 to 1.5). Similar results were obtained in the subgroups of patients stratified according to the use of cardiovascular therapy and the presence of cardiac risk factors. In conclusion, the present case-control study has shown no increased risk of postoperative stroke in patients taking chronic β-blocker therapy.

Effect of chronic beta-blocker use on stroke after noncardiac surgery.

-blocker therapy was associated with an improved car- diac outcome, overall mortality was increased in the metoprolol-treated group. This was partially related to the increased incidence of postoperative stroke occur- ring early after surgery. These findings might have im- portant implications on perioperative -blocker use, not only for initiation of therapy before surgery in -blocker naive patients but also whether or not to continue ther- apy throughout surgery. This commentary reviews the incidence and pathophysiology of perioperative stroke and the relation of -blockers and perioperative stroke, focusing on noncardiac surgery. The risk of clinically apparent perioperative brain in- jury such as stroke varies widely among different types of surgery. Whereas patients undergoing general surgery appear to be at low risk (0.08 - 0.7%), those undergoing heart valve surgery and aortic arch repair have a high incidence of perioperative stroke (8 -10%). 2 In Europe, 40 million general surgical procedures are performed annually. Therefore, it is estimated that 32,000 -280,000 patients suffer from postoperative stroke. However, the true incidence of cerebral complications is probably underestimated because subtle forms of brain injury are commonly classified as delirium that may only be de- tected by rigorous neuropsychological testing. The knowledge of the pathophysiology of postopera- tive cerebral complications is predominantly based on cardiothoracic surgery patients. It is estimated that 62% of strokes in this population have an embolic origin, 10% are related to hypoperfusion, and 10% have multiple causes. 2 Importantly, only 1% of strokes are caused by intracerebral hemorrhage. However, it should be ac- knowledged that the true pathophysiological basis of perioperative stroke is not as straightforward as it might seem. Embolic and hypoperfusion cerebral infarction most likely do not occur in isolation. 3 Impaired clear- ance of emboli (washout) seems to be the link between hypoperfusion, embolism, and ischemic stroke. 4 Intra- operative microemboli and low middle cerebral artery blood flow velocity are additive in predicting develop- ment of cerebral ischemic events after carotid endarter- ectomy. 5 Second, newer data wherein sensitive diffusion weighted magnetic resonance imaging (MRI) was per- formed suggest that as many as two-thirds of postcardiac surgery strokes have watershed or hypoperfusion pat- tern. 6 Finally, what appears to be occurring in cardiac surgery patients is that there is a rising prevalence of mostly unrecognized cerebral vascular disease concur- rent with the rising age of our population. In fact, one study (that interestingly excluded patients with known cerebral vascular disease) found that as many as 75% of patients had evidence of impaired cerebral perfusion based on single photon emission computed tomography (SPECT) imaging before coronary artery bypass grafting (CABG) surgery. 7 Approximately 45% of perioperative strokes are iden- tified within the first day after surgery. The remaining 55% occur after uneventful recovery from anesthesia, from the second postoperative day onward. Early embo- lism results especially from manipulations of the heart and aorta or release of particulate matter from the car- diopulmonary-bypass pump. Delayed embolism is often attributed to postoperative atrial fibrillation, myocardial infarction resulting from an imbalance between myocar- dial oxygen supply and demand, and coagulopathy. Compared to stroke after cardiac surgery, the pathophys- iology of stroke after noncardiac surgery is ill defined. Perioperative hemodynamic instability and cardiac events, such as myocardial infarction and arrhythmias, likely play a major role. Recently, the POISE study identified a new risk factor for perioperative ischemic strokes: high-dose meto- prolol succinate initiated for cardiac protection in patients undergoing noncardiac surgery.

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Felix van Lier

Papers

Epidural Analgesia Is Associated with Improved Health Outcomes of Surgical Patients with Chronic Obstructive Pulmonary Disease

Postoperative Hypotension after Noncardiac Surgery and the Association with Myocardial Injury

Epidural Analgesia Is Associated With Improved Health Outcomes of Surgical Patients With Chronic Obstructive Pulmonary Disease

Effect of chronic beta-blocker use on stroke after noncardiac surgery.

Perioperative strokes and β-blockade