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

Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."

/pdf/2020-esc-guidelines-for-the-diagnosis-and-management-of-38dpic1xu8.pdf

2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS).

Guidelines for the management of patients with invasive candidiasis and mucosal candidiasis were prepared by an Expert Panel of the Infectious Diseases Society of America. These updated guidelines replace the previous guidelines published in the 15 January 2004 issue of Clinical Infectious Diseases and are intended for use by health care providers who care for patients who either have or are at risk of these infections. Since 2004, several new antifungal agents have become available, and several new studies have been published relating to the treatment of candidemia, other forms of invasive candidiasis, and mucosal disease, including oropharyngeal and esophageal candidiasis. There are also recent prospective data on the prevention of invasive candidiasis in high-risk neonates and adults and on the empiric treatment of suspected invasive candidiasis in adults. This new information is incorporated into this revised document.

https://www.easy-immune-health.com/support-files/clin_practice_guidelines_candidiasis.pdf

Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America.

Executive Summary Introduction Methodology Used to Prepare the Guideline Epidemiology Incidence Etiology Major Epidemiologic Points Pathogenesis Major Points for Pathogenesis Modifiable Risk Factors Intubation and Mechanical Ventilation Aspiration, Body Position, and Enteral Feeding Modulation of Colonization: Oral Antiseptics and Antibiotics Stress Bleeding Prophylaxis, Transfusion, and Glucose Control Major Points and Recommendations for Modifiable Risk Factors Diagnostic Testing Major Points and Recommendations for Diagnosis Diagnostic Strategies and Approaches Clinical Strategy Bacteriologic Strategy Recommended Diagnostic Strategy Major Points and Recommendations for Comparing Diagnostic Strategies Antibiotic Treatment of Hospital-acquired Pneumonia General Approach Initial Empiric Antibiotic Therapy Appropriate Antibiotic Selection and Adequate Dosing Local Instillation and Aerosolized Antibiotics Combination versus Monotherapy Duration of Therapy Major Points and Recommendations for Optimal Antibiotic Therapy Specific Antibiotic Regimens Antibiotic Heterogeneity and Antibiotic Cycling Response to Therapy Modification of Empiric Antibiotic Regimens Defining the Normal Pattern of Resolution Reasons for Deterioration or Nonresolution Evaluation of the Nonresponding Patient Major Points and Recommendations for Assessing Response to Therapy Suggested Performance Indicators

Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia the official statement of the American Thoracic Society and the Infectious Disease Society of America (特集 救急診療ガイドライン) -- (海外のガイドライン)

BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc

Additional view of the mitral valve.

It is with great interest that we read ‘ketamine may be related to reduced ejection fraction in children during procedural sedation’ by Eken et al. At our institution, we run a procedural sedation and analgesia (PSA) service, and we have performed more than 10,000 procedures on children over the last 6 years. The vast majority of these cases are outpatients. One of the medications commonly used is ketamine in conjunction with other sedative and analgesic agents which allows us to reduce the dose of all medications, hence their potentially adverse events while maintaining spontaneous breathing in children. Adverse events do occur although rarely and they are of respiratory origin in particular. We are surprised by the significant differences between the results derived from this cohort study with both our experience and recent data from literature, suggesting that other reasons could have caused alterations in haemodynamic parameters rather than solely ketamine. It is undeniable that children belong to a population group who are prone to adverse events during PSA. All currently used sedatives aim to depress awareness, and in doing so, they may potentially inhibit centrally mediated haemodynamic control particularly with increasing doses. Ketamine is an N-methyl-D-aspartate receptor antagonist that blocks glutamate in the limbic system. However, the mechanism of receptor blockade differs based on ketamine concentration. While at low concentrations, analgesic properties are evident; at higher concentrations, ketamine causes an anaesthetic state called ‘dissociative anaesthesia’ as a result of a functional dissociation between the cortical and limbic systems. Assuming large doses are not rapidly administered, ketamine may preserve pharyngeal and laryngeal protective reflexes, lowers airway resistance, increases lung compliance and is less likely to induce respiratory depression. Furthermore, unlike other sedatives, ketamine is sympathomimetic and facilitates adrenergic transmission, which offsets its direct myocardial depressant actions. It also increases the systemic catecholamine concentrations by centrally mediated release of catecholamine and inhibition of neuronal catecholamine reuptake which is expected to result in an increased heart rate and blood pressure, hence maintaining haemodynamic stability in critically ill patients. This unique pharmacodynamic profile of ketamine makes it an appealing alternative agent for PSA overall within the paediatric population and in the emergency department (ED). However, like all drugs, ketamine is not without side effects, and a ‘single, safe and effective’ agent for paediatric PSA is yet to be determined. With increasing doses, ketamine may induce laryngospasm, respiratory depression, hypersalivation, emesis and emergence phenomena. ED is a clearly different situation where procedures performed are likely to be painful and urgent in nature, yet safety concerns while using ketamine in this setting still remain real. In their manuscript, the authors described haemodynamic changes based on blood pressure and echocardiography findings. However, measuring blood pressure and performing echocardiography prior to sedation on injured, painful and

Jan Poelaert

Papers

Additional view of the mitral valve.

Alterations in haemodynamic parameters during procedural sedation and analgesia in children: Is ketamine really to blame?

Letter to the Editor: Isolated diastolic dysfunction is associated with increased mortality in critically ill patients.

General anesthesia or phrenic nerve block for treatment of chronic hiccups? Authors' reply

Intraoperative Echocardiographic Detection of an Anomalous Left Main Coronary Artery. Authors' reply