Importance Definitions of sepsis and septic shock were last revised in 2001. Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination. Objective To evaluate and, as needed, update definitions for sepsis and septic shock. Process A task force (n = 19) with expertise in sepsis pathobiology, clinical trials, and epidemiology was convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine. Definitions and clinical criteria were generated through meetings, Delphi processes, analysis of electronic health record databases, and voting, followed by circulation to international professional societies, requesting peer review and endorsement (by 31 societies listed in the Acknowledgment). Key Findings From Evidence Synthesis Limitations of previous definitions included an excessive focus on inflammation, the misleading model that sepsis follows a continuum through severe sepsis to shock, and inadequate specificity and sensitivity of the systemic inflammatory response syndrome (SIRS) criteria. Multiple definitions and terminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepancies in reported incidence and observed mortality. The task force concluded the term severe sepsis was redundant. Recommendations Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%. In out-of-hospital, emergency department, or general hospital ward settings, adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following clinical criteria that together constitute a new bedside clinical score termed quickSOFA (qSOFA): respiratory rate of 22/min or greater, altered mentation, or systolic blood pressure of 100 mm Hg or less. Conclusions and Relevance These updated definitions and clinical criteria should replace previous definitions, offer greater consistency for epidemiologic studies and clinical trials, and facilitate earlier recognition and more timely management of patients with sepsis or at risk of developing sepsis.

https://jamanetwork.com/journals/jama/articlepdf/2492881/jsc160002.pdf

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

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

Context Infection is a major cause of morbidity and mortality in intensive care units (ICUs) worldwide. However, relatively little information is available about the global epidemiology of such infections. Objective To provide an up-to-date, international picture of the extent and patterns of infection in ICUs. Design, Setting, and Patients The Extended Prevalence of Infection in Intensive Care (EPIC II) study, a 1-day, prospective, point prevalence study with follow-up conducted on May 8, 2007. Demographic, physiological, bacteriological, therapeutic, and outcome data were collected for 14 414 patients in 1265 participating ICUs from 75 countries on the study day. Analyses focused on the data from the 13 796 adult (>18 years) patients. Results On the day of the study, 7087 of 13 796 patients (51%) were considered infected; 9084 (71%) were receiving antibiotics. The infection was of respiratory origin in 4503 (64%), and microbiological culture results were positive in 4947 (70%) of the infected patients; 62% of the positive isolates were gram-negative organisms, 47% were gram-positive, and 19% were fungi. Patients who had longer ICU stays prior to the study day had higher rates of infection, especially infections due to resistant staphylococci, Acinetobacter, Pseudomonas species, and Candida species. The ICU mortality rate of infected patients was more than twice that of noninfected patients (25% [1688/6659] vs 11% [ 682/6352], respectively; P  Conclusions Infections are common in patients in contemporary ICUs, and risk of infection increases with duration of ICU stay. In this large cohort, infection was independently associated with an increased risk of hospital death.

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International Study of the Prevalence and Outcomes of Infection in Intensive Care Units

Objective:To better define the incidence of sepsis and the characteristics of critically ill patients in European intensive care units.Design:Cohort, multiple-center, observational study.Setting:One hundred and ninety-eight intensive care units in 24 European countries.Patients:All new adult admissi

Sepsis in European intensive care units: results of the SOAP study.

Objective: The aim was to formulate clinical practice guidelines for pheochromocytoma and paraganglioma (PPGL). Participants: The Task Force included a chair selected by the Endocrine Society Clinical Guidelines Subcommittee (CGS), seven experts in the field, and a methodologist. The authors received no corporate funding or remuneration. Evidence: This evidence-based guideline was developed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to describe both the strength of recommendations and the quality of evidence. The Task Force reviewed primary evidence and commissioned two additional systematic reviews. Consensus Process: One group meeting, several conference calls, and e-mail communications enabled consensus. Committees and members of the Endocrine Society, European Society of Endocrinology, and Americal Association for Clinical Chemistry reviewed drafts of the guidelines. Conclusions: The Task Force recommends that initial biochemical testing for PPGLs shou...

/pdf/pheochromocytoma-and-paraganglioma-an-endocrine-society-4ij7m1t7fo.pdf

Pheochromocytoma and paraganglioma: An endocrine society clinical practice guideline

Mortality after surgery in Europe

Effect of L-arginine on endothelial injury and hemostasis in rabbit endotoxin shock. J Appl Physiol

Hamzaoui and colleagues [1] recently reported the eff ects of early norepinephrine for septic shock with lifethreatening hypotension. Th eir observations fi rst answer ‘yes’ to the question ‘Can norepinephrine alone restore mean arterial pressure (MAP) in septic shock?’ Second, as an answer to ‘How does norepinephrine alone restore MAP?’, they confi rm that norepinephrine restores MAP despite minimal fl uid administration through ‘recruiting’ unstressed volume while allowing increased contractility despite increasing afterload. Th e most critical question that remains unanswered, however, is ‘Should nor epinephrine alone be used to restore MAP in septic shock?’ If the price of fl uid resuscitation may be edema and organ failure, what may be the price of norepinephrine resuscitation? Th e fear is that the very same eff ects that allow norepinephrine to recruit unstressed volume, through alpha adrenergic eff ects on venous and arterial vasculature, might recruit volume to the macrovas culature, all the while decreasing fl ow in previously critically collapsible microvascular beds. Answers to this crucial question are still unclear. In two previous confl icting studies showing benefi cial [2] or detrimental [3] eff ects on microvascular blood fl ow, the discrepancies may have been due to diff erences in prior fl uid therapy and ensuing preload reserve. In order to determine the optimal use of norepinephrine, future studies of microcirculation and perfusion should either optimize on an indicator of fl uid responsiveness during the fl uid therapy preceding norepinephrine treatment or rapidly wean the inevitable early norepinephrine infusion rate once the targeted MAP is obtained by screening for and addressing preload dependency during infusion rate decrements [4].

/pdf/early-norepinephrine-resuscitation-of-life-threatening-1tbw7m6hde.pdf

Early norepinephrine resuscitation of life-threatening hypotensive septic shock: it can do the job, but at what cost?

In the anesthetized dog infused with endotoxin, cardiac output falls and a hypodynamic shock state ensues (Cain and Curtis, 1992). If supportive therapy, boluses of donor red cells and dextran, is given then this can be converted to the hyperdynamic and hypermetabolic condition so often observed in human sepsis with adequate volume resuscitation (Cain and Curtis, 1991). Other evidence from experimental animals indicated that endotoxin infusion caused arterial conductance increases and venous constriction with consequent pooling in capillary beds of muscle (Bond et al., 1992) and the splanchnic bed (Abel and Beck, 1992). The decrease in venous return to the heart was one of the reasons that volume treatment was necessary to reverse the shock state. Other consequences of the powerful cytokines liberated by endotoxin infusions can be capillary plugging and endothelial damage so that microcirculatory function and peripheral oxygenation are adversely affected (Cain, 1986). As a result, even with adequate or elevated levels of cardiac output, the potential for severe tissue hypoxia in peripheral organ systems has been postulated to be very high as O2 consumption becomes markedly flow-dependent (Rackow and Astiz, 1991).

Resuscitation of Dogs from Endotoxic Shock by Continuous Dextran Infusion with and without Perflubron Added

l s prospectively staslied 15 septic (P) tifio rxptirecl a basal Ibperrire infusion and the addition of a 2nd CH. Initial and final values for PAJP, I-AP, CI, SR, D02 amyl 402 trure assessed before and after tta second drug had started. 311 15 P rere on Lbomrdne (Dl mean close 8,3 t / g/ndn) infusion. Dobutanitle (Le) sea a:kieci in 7 P (group I nenn dose 11,3 ug/Kg/min, rortality 14%) atzt epinelisine (03) in 8 (group II mean close 0,7 ug/lcghttin, mortality 87) ). The trnnrlyrtamic responses are sisal in the table:

Benoit Vallet

Papers

Mortality after surgery in Europe

Effect of L-arginine on endothelial injury and hemostasis in rabbit endotoxin shock. J Appl Physiol

Early norepinephrine resuscitation of life-threatening hypotensive septic shock: it can do the job, but at what cost?

Resuscitation of Dogs from Endotoxic Shock by Continuous Dextran Infusion with and without Perflubron Added

Septic shock treatment