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Summary

This comprehensive, on-demand teaching session is aimed at final year medical students or those seeking a refresher on sepsis. Detailed discussions cover sepsis and types of shock, definitions and pathophysiology of sepsis, clinical presentations seen in sepsis, and guidelines for investigation and management. Participants will have the opportunity to review high yield examples, engage in questions, and provide feedback. Upon completion, participants will receive a certificate. The session will be recorded and uploaded for future access and review. The deep dive into sepsis pathophysiology, clinical presentations, and protocols such as Sepsis Six Protocol, as well as comparison of different types of shock and their management, make this a valuable resource for all medical professionals.

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Description

Understanding sepsis, types of shock and how to effectively diagnose and manage.

Learning objectives

  1. Understand the definition of sepsis and its associated terms, along with comprehending its pathophysiology.
  2. Learn how to identify the clinical presentations of sepsis, enabling early detection and diagnosis.
  3. Learn to apply national guidelines for the investigation and management of sepsis in a real medical setting.
  4. Understand the types of shock (hypovolemic, cardiogenic, distributive, obstructive, and neurogenic), and the differences in their presentations, investigations, and management methods.
  5. Understand the components of the Sepsis Six protocol and its importance in the initial management of sepsis.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello, everyone and welcome to our teaching session on sepsis. This is targeted at final year medical students slash fy ones or those that are just hoping for a refresher on the topic. We will be going through consolidating your understanding of what sepsis and the types of shock are and then be going through some high yield examples and questions at the end next slide, please. Ok. So we've also got a feedback survey at the end of our session. Once you fit in the survey, we'll be able to provide you with certificates for completion as well. This is also going to be recorded and uploaded on our page on medal so you can watch it back on demand. I Yes. Yeah. Right. Uh So in terms of the line directors of today's session, the main aspects we'll be covering, um, we'll look at the definitions of sepsis, um and its associated terms along with its pathophysiology. Um We'll be discussing the typical clinical presentations you'll see in sepsis, um applying national guidelines to discuss investigations and management. Um And we'll have a quick look at different types of shock as well rather than just sepsis. Um And comparing how they differ in their investigation presentations and management. So, sepsis, what is sepsis? Um So the definition of sepsis itself is it's life threatening organ dysfunction um caused by dysregulated host response to infection. Um It used to be known as infection plus S or systematic systemic inflammatory response syndrome. Um It's a little bit outdated now, but we still included the criteria on the screen for you to have a look at. So it was a temperature of less than 36 or more than 38 and increased respirate tachycardia or increased heart rate and white cells below 4000 or over 12,000. Um in terms of what severe sepsis is, it's sepsis with acute organ dysfunction. So for example, renal failure, secondary to sepsis. Um and then your septic shock is when you've got a sepsis with persistent or refractory hypotension or low BP. Um and tissue hypoperfusion despite um fluid research. So, despite it kind of giving continuous fluids, that's the difference between those three. Ok. Ok. Moving on to the pathophysiology. Um this is something that's not really covered in much depth, but it helps to consolidate your understanding on why it happens in the first place. So normally there's an infection most commonly, it's a respiratory infection or in the elderly. It might also be a urinary infection that triggers an exaggerated immune response specifically by the macrophages, lymphocytes and mast cells. This then in chain causes cytokines like interleukins and TNF to be released and they increase the vascular ability through the release of a substance called nitrous oxide. Nitrous oxide is really important here because that's the triggering chemical in edema forming because it allows an increase in fluid to build up in the extracellular spaces. The more edema and the more fluid that's building up in the extracellular spaces means that there is less space between the actual blood and the tissues to be adequately perfused. So that reduces the oxygenation of the tissues. Now that we've reduced the oxygenation of the tissues. The coagulation pathway now kicks in. So it gets activated, which risks the forming of micro thrombi because there is more fibrin that gets deposited within the vessels and therefore more micro thrombi that occurs throughout the vasculature. This means that in terms of the circulation as a whole, we are running the risk of compromising organ and tissue perfusion. And it explains why um one of the sort of key criteria of sepsis is that you would see a rising lactate because when tissues have an inadequate oxygen supply, anaerobic respiration is taking place and lactic acid is a byproduct of that respiration. So, when the serum lactate is rising and metabolic acidosis is occurring, you can be pretty sure that there is a tissue hypoperfusion as a result of the initial trigger of an infection and the over response of your macrophages and lymphocytes. Ok. So, looking at the clinical features of sepsis and how it normally presents in practice. Um These features are very broad, they're very vague and they're quite nonspecific, but the generic ones that you'll get, um, are things like fever Rigas and just general malaise. Um, specifically to the cardio system, you'll get things like hypotension, tachycardia, um, especially in quite severe cases. Um, in a respiratory way, they can present with Ayia and hypoxia. Um, they can present with confusion, agitation, drowsiness, um and just kind of sleeping more sometimes as well. Uh they can present with early urea, so reduce urine production or sometimes no urine production. Um and often their skin can appear quite mottled. Um and then can be, it can kind of go either way we quite warm and flush or it can be sign those with co peripheries depending on what type of infection they've got and how severe the sepsis is. Um So in terms of sepsis six. So the sepsis six protocol is a kind of a bundle of six investigations and kind of management points that should be initiated within one hour of suspecting sepsis. So as soon as you suspect it, you start sepsis six immediately and it typically goes three out of three in. Um So the three things that you'll take out, so you will take blood cultures, try and figure out the kind of actual organism that's causing the infection, um, urine output monitoring. So that might involve catheterizing the patient or just keeping an eye on urine production, um and a BVG and lactate. Um just to check for, like we mentioned that tissue ischemia, the three in that you'll be initiating are your high flow oxygen. And that's usually if they're desaturating, you'll probably, you know, start 15 L. Um, straight away IV, broad spectrum antibiotics. Now, ideally you'd want to take cultures first. Um, but you wouldn't wait for results or anything because they can take up to 72 hours to come back. So you'd start broad spectrum antibiotics and then you can tailor those and make them more narrow once you've got the cultures back. Um and IV fluids and typically, that's a bolus first if they're hypotensive and then slower fluids um to try and rehydrate them as much as possible. I OK, moving on to septic shock. So as uh Judy explained earlier, um septic shock is where there's persisting hypotension despite ade despite adequate fluid resuscitation, and you also note a metabolic acidosis in the form of uh an elevated lactate. So this basically means that the BP isn't being maintained and oftentimes patients will get escalated to it or high dependency units because they will need vasopressor support such as with noradrenaline. Since vasopressors allow vasoconstriction to take place and that in turn will increase the systemic vascular resistance and allow the map to increase as well in an attempt to increase tissue perfusion uh moving on to investigation. So, um both in f one slash when you're on call. Um or just generally in the acute setting as part of sepsis. Six, we say you need to take bloods and cultures, but specifically the bloods that you need to be taking that F BCE and ke especially if you are expecting an organ system to be affected, such as the renal system. It's also worth checking on the clotting because sepsis can also cause thrombocytopenia. So you want to be keeping an eye on whether there is any deranged clotting present. And although very severe, you would be able to assess for whether there is any evidence of dic for the very acute IW patients in terms of imaging chest x rays. Since one of the most common sites of or causes of sepsis is respiratory CT. If you are considering something like an abscess um formation intracranially or if you're um considering some sort of abdominal perforation. So bowel ischemia, bowel perforation, you'll be doing a CT abd pelvis or if you're just very unclear as to where the cause of infection is, you'd be enduring both um others that are also relevant. So, urine, urine M CNS, so that you can target antibiotics once you've completed broad spectrum antibiotics for a couple of days and an LP, if you're thinking of meningitis or a neurological source of the septic infection, moving on to the types of shock. So, uh shock can be divided into the following categories. Hypovolemic. So that is happening because there's a reduced systemic vascular resistance as a form of fluid loss happening somewhere in the body cardiogenic. So it does it in the title. So you um ak your heart isn't functioning as well. Therefore, leading to shock, distributive shock, which is we say sepsis is a loose term. But sepsis technically comes under distributive shock when it presents as a shock obstructive. So a physical blockage. So for example, a pe and neurogenic shock. So spinal cord injuries, we'll be going into these in a bit more detail. Now. Um so a couple of key terms to consider before we kind of dive into any further scenarios and things. Um a couple of things that relate.