 Sepsis certainly keeps us going... either when treating patients on ICU or when it comes to the discussion on what actually sepsis is and how to define it. So far the SIRS (Systemic Inflammatory Response Syndrome) criteria have provided some degree of handle to cope with this syndrome but of course we weren't all quite happy with this. In fact every person with any sort of infectious disease will respond with 2 or more SIRS criteria... but doesn't necessarily have to be septic. As a matter of fact a SIRS is nothing else but a physiologic response to any sort of inflammation. The New Approach to Sepsis - The SOFA The new international consensus definitions for sepsis and septic shock try to focus on the fact that sepsis itself defines a life-threatening organ dysfunction caused by a dysregulated host response to infection. By saying this the aim is to provide a definition that allows early detection of septic patients and allow prompt and appropriate response. As even a modest degree of organ dysfunction is associated with an increased in-hospital mortality the SOFA score (Sequential or 'Sepsis-related' Organ Failure Assessment) was found to be the best scoring system for this purpose. It's well known, simple to use and has a well-validated relationship to mortality risk. Sepsis (related organ dysfunction) is now defined by a SOFA score increase of 2 points or more  The Quick Approach to Sepsis - The BAT In the out-of-hospital setting, on the general wards or in the emergency department the task force recommends an altered bed side clinical score called the quickSOFA - or alternatively 'the BAT' score:  The New Approach to Septic Shock -Vasopressors and Lactate Septic shock is now defined as a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities are associated with a greater risk of death than sepsis alone. Keeping a long story short: Septic Shock is now: - The need for vasopressors to maintain a mean arterial pressure of at least 65mmHg AND - a serum lactate level of more than 2mmol/L... after adequate fluid resuscitation  The Bottom Line: The way it looks like we are left with Sepsis and Septic Shock Severe Sepsis has vanished and the question remains, whether these new definitions will actually benefit the ones that need it most... our septic patients! Singer M et al. JAMA. 2016;315(8):801-810. Seymour CW et al. JAMA. 2016;315(8):762-774. Shankar-Hari M et al. JAMA. 2016;315(8):775-787.
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 One of the most controversial manoeuvres in anaesthesia and critical care has got some new support since the Difficult Airway Society has published their new guidelines in which they basically continue to support the use of cricoid pressure (CP) for rapid sequence induction. The authors of the Obstetric Anaesthetists' Association and Difficult Airway Society Guidelines for the Management of Difficult and Failed Tracheal Intubation also continue to recommend routine CP, which is considered level 3b evidence.
Surprised on how obstinately CP persists in current guidelines I think that following statement by Priebe HJ is an important reading. It summarises nicely why there is such a disagreement with these recommendations. He states that - not a single controlled clinical study provided convincing evidence that the use of cricoid pressure was associated with a reduced risk of pulmon ary aspiration. At the same time, there is good evidence that nearly all aspects of airway management are adversely affected by cricoid pressure - if cricoid pressure were considered a new airway device, it would not be considered for further evaluation because Level 3B evidence for its efficacy does not exist - when using cricoid pressure, we may well be endangering more lives by interfer ing with optimal airway management than we are saving lives by preventing pulmonary aspiration Priebe HJ, Anaesthesia 2016, 71, 343–351 Want to get more information on the controversy of cricoid pressure? Read here: Cricoid Pressure for RSI in the ICU: Time to Let GO? Time to let go? Remarkable article on RSI and Cricoid Pressure Difficult Airway Society DAS: New Guidelines OUT! Cricoid Pressure still IN?  The discussion on the so-called lactic acidosis and its causes have become increasingly attractive over the last couple of years as several biochemical explanations are challenged. A significant confusion persists on the various relationships between lactate, lactic acid and metabolic acidosis. Most clinicians continue to refer to the traditional understanding of impaired tissue oxygenation causing increased lactate production, impaired lactate clearance and therefore resultant metabolic acidosis. Just recently we had a discussion on our ward round on this topic when a team member presented the most recent article of UpToDate online on the causes of lactic acidosis. The authors state that 'Lactic acidosis is the most common cause of metabolic acidosis in hospitalised patients' and that 'Lactic acidosis occurs when lactate production exceeds lactate clearance. The increase in lactate production is usually caused by impaired tissue oxygenation...'... finally suggesting that lactate is no good! These statements support the classical understanding that: - Hyperlactatemia is caused by tissue hypoxemia, and - This in turn then leads to a metabolic acidosis called lactic acidosis This biochemical understanding has persisted for decades, but there are some good reasons to vigorously challenge this traditional aspect on the 'bad' lactate. Lactate turns out to be by far more complex in its characteristics and functions, so I decided to try and make a short but comprehensive overview of this molecule. What is lactate? Lactate is a small organic molecule with the chemical formula CH3CH(OH)CO2H and structurally looks like on the image to the left. It is produced in the cytoplasm of human cells mainly by anaerobic glycolysis by the conversion of pyruvate to lactate by LDH. This chemical reaction results typically in a blood lactate to pyruvate ratio of about 10:1. And while lactate is produced, NAD+ also is incurred, and this actually can accept protons itself, so does not result in acidosis itself. Lactate arises from the production of energy by consuming glycogen and glucose. 
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