 The topic we're going to be going over today is sepsis. By definition, sepsis is bacteria in your blood. Oh my goodness, what are you talking about? Yeah, that is the last place you want a bacteria to be. You don't want bacteria in your blood and not supposed to be there. That's why we have mucosal defenses, defense, right? To prevent bacteria from going into our bloodstream. But once they get in there, we develop sepsis. But before we go forward, we need to understand the sepsis pathway. Because before the bacteria gets into the blood, we're going to get a little wink, wink from the body, telling us, watch out, watch out. So what are we going to start with? We're going to start with a systemic, the entire system is affected. Inflammatory response syndrome, which we're going to talk about. What is the definition of SIRS? Well, you have to meet at least two criteria of the following, what? We got to meet two of all these criteria to meet SIRS syndrome? Yeah, but before we explain, we need to explain what SIRS really is. We are, that's going to start with a pathophysiology of sepsis. Here, down below. Don't laugh, that's my funny little neutrophils. And those are the microfragments. They got guns, yeah, I tell you, they have real big guns and that is bacteria. So that is a bacteria who has a suicide mission, so we're going to start with a nice little story. So a bacteria was sent to go blow up stuff inside our body. You know bacteria doesn't, they love to destroy things. So they wrapped them up in a bomb and guess which bacteria it was? It was E. coli, Escherichial coli. And it's all the friends, aside from E. coli, it's all the bacteria that cause sepsis. We're going to go over that in a minute, we're going to just pick E. coli and around E. coli has all these endotoxins. Now, when bacteria take a sneak peek into the bloodstream, guess what's going to be activated? Ah, neutrophils are going to be activated, monocytes are going to be activated through interleukins, cytokines, telling them, I smell problem, that's an intruder. When the invader comes in, they put out their guns and they're about to go shut them down. So the neutrophils and the macrophages they rush inside the bloodstream. And this is the beginning of the pathophysiology of sepsis. However, this patients are usually going to start up with a fever, a fever. All right, so here's the story with fever. I told the story before, I'm going to tell it again. In medicine, right? Anytime you have fever in a location, always remember, for you to have a fever, I'm going to show you my nice little chimney house. Okay, that's the chimney house and that's the kitchen. So back in the days, they used to have chimneys. You probably see houses that have chimneys and it's always smoke. So that's when you're cooking here inside the kitchen and you burn stuff or there's so much smoke, it has to go through the chimney. Well, as an observer, when you see the chimney and the smoke coming out, you're like, I think something is burning inside the house. Well, I don't want to go check it out. Wait, guys, the signal the body sends out, the smoke is the fever. Oh, you start to shake. Oh, you get fever, you get warm, you get chills. Well, that's the smoke, that's the fever. That's the body's response telling you there's something going on. But the kitchen is the location. Because guess what? It's the bacteria that's causing you to have the fever. So check this out, guys. Fever and the headache. I might have a intracellular abscess or meningitis. Oh, look at that, sepsis man. If I have fever and meningitis, fever, headache, rigid neck, ah, guess what? The fever is telling me what's going on. It's a bacterial infection and it's going inside the head to have a headache. Ah, it's irritating my meninges. Ooh, what about if I have a fever and I have cough and I'm short of breath and I have productive cough? Well, it's coming from the lungs. Fever, lungs, fever, lungs. Pneumonia, cough, right? Because I was just junk made up by the bacteria, cooking and cropping and scraping every single little parenchymo inside my lungs. And all of you are like, I'm not too happy about that. Check this out, fever and flank pain. Flank pain, ah, I might have pylonephritis. Really? Yeah, because it just told you the fever gave it away. But this is flank pain, just gave it away. That's where the bacteria is. If I have fever and redness and rhythm pain, ah, look at that, look up on the skin. It's red, it's painful, cellulitis, staph strap. Ooh, you see? How about fever, radical quadrant pain. Fever, radical quadrant pain. Ah, I might have an ascending colonitis. Can you see how it's giving it away? They literally give it away. Absolutely genius. So, these patients at the beginning of systemic inflammatory response, they will have a temperature greater than 38 or less than 36. Now, the second thing is their heart rate is going to go up. Being, they're gonna be tachycardic. They're gonna have heart rate greater than 90 beats per minute. You need to memorize this. Tachypnea. Why is the patient tachypnea? And their respiratory rate is greater than 20 beats per minute. Let's check this out. The patients is developing systemic inflammatory response syndrome and they start to develop hypertension. Slowly, what happens is they develop metabolic acidosis. Metabolic acidosis compensation requires you to do what? Blow out the CO2 through your lungs. Look at that. So, because you have all these acids that build up in your body because what? You're undergoing metabolic acidosis because you're what? Going back to going to sepsis. Because there's a bacteria that's about to cause a problem. You have to be tachypneic. Guess what? That explains why your PSCO2 is less than 32, right? Because that's the only way you can get rid of the CO2. Normal CO2 is 40, where you hyperventilate. You're gonna blow out most of the CO2 and it's gonna be low. Get it? Good. White count. Now the white count can either be 12,000, which makes sense, right? Because you have a lot of what? Neutrophils and monocytes. Microphone is running, running to the spot. You're about to go kill the bacteria. So a lot of them are gonna what? Flow inside your bloodstream. They're gonna find the source of the infection. However, you might also have less than 4,000 if you're immunocompromised, right? So if you're immunocompromised, have HIV or you're on chemotherapy, drugs, your white count might be really low. You might be leukopenic. So you might develop a leukocytosis or you could be leukopenic. See greater than 10% bands? Bands, that's a left shift. Usually the neutrophils are being rushed out and pushed out. And so you're gonna see bandemia. Literally, immature neutrophils try to get out. Try to buy their own guns to go start shooting and killing the bacteria. So what is the definition of SARS again? Before we lose track, you need two. Two of this. If the patient has just a fever, grin on 38 and the heart is up, that is systemic inflammatory response syndrome. Got it? Two. So you gotta memorize this. Please memorize this. They will ask you one day in the hospital you will be pimped. I guarantee you that. This is high, super high yield. Well, so when does the patient become septic? Well, when the patient becomes septic they develop sepsis, sepsis. Now, septic, sepsis, when they meet two of this and then we know where the infection is. Remember my story? Here's the sepsis man, fever, headache. So if the patient has meningitis and they have temperature of 38 and the heart is 90 or temperature of 38 and the white count is high, guess what? Now they have sepsis. Get it? Get it? Two of the systemic inflammatory response plus we found the infections. We looked at you, we found you. Huh, you got pneumonia. Oh, you're coughing up a lot of yellow, you know, brown stuff out of your lungs. Lo and behold, pneumonia plus one or two of this. Sepsis, got it? So now let's break down the pathophysiology of sepsis. When the bacteria sneaks into the blood, the antigens on the bomb that these guys wrapped around, right, gram positive bacteria, they have what? They have a thick cell made out of what? Peptidoglycan, peptidoglycan, the gram negatives, they have lipopolisaccharides and also the gram positive lipothaquic acid. So the bacteria has different endotoxin surrounding the bacteria. So this is where I think of sepsis in English. So the bacteria's got a lot of junk. Yeah, call it whatever you want. Peptidoglycan, who cares? But these are toxins because the body doesn't want it. These toxins are gonna damage the endothelial cell walls. Right, the endothelial walls inside the blood vessels are gonna be damaged. This is gonna eventually activate the presence of this endotoxin, it's gonna activate your neutrophils and it's also gonna activate your microfigures. Cytokines, interleukinins, they're all gonna be flushed into the system. This effect overall will lead to systemic vasodilitation. That's all you really need to know. So all you need to think of from right now, these guys are gonna start shooting and killing the bacteria. The content of the bacteria is gonna leak out. The neutrophils and the microfigures are gonna basically eat up the bacteria in the process to nasty war and the war is not gonna cause systemic vasodilitation from our cytokines and you were interleukins and all this chemical cascade but the end result is you now get systemic vasodilitation. So all your blood vessels in your side, your body, they're gonna be huge and big, huge and big. That is called systemic vasodilitation. When your blood vessels open up and they end up visoconstricting and divisor dilating, you develop hypotension, hypotension. What happens to your blood pressure? It's gonna flush down the drain and it's gonna be really, really low. Does that make sense? Because now all the blood vessels are visoconstricting and they're like, oh, whatever, right? Nitric oxide is gonna contribute to that cause of systemic vasodilitation. Then if I have systemic vasodilitation, what's gonna happen to my tissues? They're not gonna be perfused, uh-huh, yeah. Now they can't get their nutrient. They can't get oxygen. They can't get glucose. And what's gonna happen? You're gonna develop lactic acidosis from anaerobic respiration, right? Because the tissues can get perfusion cause hypotension will lead to what? Hyper perfusion, which will lead to organ failure, but also you will develop coagulopathy. So do we have to think of it, coagulopathy? The toxins are damaging the walls of the endothelial cells. When you damage the endothelial cells, what's gonna happen? Oh, von Willebrand factor. Platelet is gonna bind. Platelet aggregation, this platelet aggregation are gonna form micro thrombi, right? You're gonna use up your platelets. You're gonna use up all the coagulation cascade and all of it so you can develop DIC, too. So that is serious. That's coagulopathy. That's one of the complications of sepsis. That's just how I remember it. It's pretty, pretty easy. So damaging the endothelial wall just again, endothelial wall damage. Eventually you're gonna have von Willebrand and von Willebrand with platelet, platelet with fibrin. Fibrin, they're gonna block, they're gonna block the blood vessel and now we can't get any perfusion. And what happens to the organ? Or organ is gonna get damaged. And that's it. But this is sepsis. That is the pathophysiology. Key, hypotension, systemic vasodilitation. Hypotension, systemic vasodilitation. Now let's come back to our sepsis pathway. We were right here, right? We said CERS plus infection source, we know where the infection, if it's in the lung, we know where it is. It's sepsis. Now, to develop severe sepsis, let's see what's gonna happen. You have to have at least one organ failure. One organ failure. Well, let's find out which organ. Let's see here, right? So I'm not gonna erase the sepsis, man. Let's talk about severe sepsis. By the way, just before we move on, before I forget, there are different kind of bacteria that can actually cause sepsis. We keep saying E. coli, but there's other friends. Aside from E. coli, because E. coli causes a lot of pneumonia, right? Following the Fridays, Staph, aureus, strep, right? Causing cellulitis. We also have klepsiella. Klepsiella, ella, ella, eh eh eh. Pseudomonas can cause, so you can get Pseudomonas pneumonia that can give you also to develop sepsis. Another bacteria that we probably don't strep pneumonia, we already talked about. So these are all of his friends that can cause you to develop sepsis. Okay, so don't forget, these are the bacteria so that we make sure for completion's sake, those are the bacteria that causes you to develop sepsis. Now, let's talk about severe sepsis. In severe sepsis, we said you need one organ. One, just one organ to be filling. Now let's talk about what are we gonna see? Well, when you develop hyperprofusion and you develop lactic acidosis, huh, let's check your lactic level. Lactate, it's usually gonna be graded on four milli moles per deciliter. That is key. Lactate will be coming from your tissues because they're hyperprofused and they're converting pyruvate, right? You detect glucose and convert it to pyruvate, which is now converted into what? Lactate. This lactate is the lactic acid that's produced, lactic acid, and from the formula, pH equals to bicarb, right? That's the formula we used to calculate. Acid-based disturbances, lactic acid is gonna be a lot of what? Hydrogen ions, which is gonna decrease your bicarb, decrease your bicarb because they try to buffer all this acid produced by your tissues. That, in return, will decrease the pH of the blood, make you develop lactic acidosis. So you always wanna check the patient's lactate that's telling your tissues it's been affected. Well, also oligouria, huh. Let's talk about that. Oligouria, oligouria, right? And what do we mean by oligouria? Decrease urine output. Usually it's less than 0.5 milliliters per hour. That, per kilograms per hour, per kilogram per hour. That means you have so much systemic visitation, right? So this is your yarder coming from your heart and this is your kidneys. Everything is so big, the kidneys is not getting enough perfusion because systemic visitation is the key, is severe in sepsis, right? So you develop oligouria and the kidney can really filter stuff out and you're not picking up enough urine. What about, you're gonna develop an abrupt change in mental status. Change in mental status. You're gonna be confused, you're gonna be lethargic, you're not gonna know what you're doing. Why? Because the systemic visitation is decreasing perfusion to your brain. So this patient also might develop, they might have motile skin or delayed capillary refill. Motile skin or delayed cap refill. Let's explain that. It's all from systemic visitation It's all from systemic visitation, right? So if I try to check your capillary refill, it should be nice and red when I press, it should be white when I let it go. It should feel back within two seconds and be pinked up again. The problem is because they have so much visitation when you check for a cap refill, you're not gonna get it back. It's gonna be delayed, it's gonna take longer. The patient also might be thrombocytopenic. Thrombocytopenic. Less than 100,000. Usually platelet count is between 150 to 400,000. This patient, if the platelet count is going down, that's explaining coagulopathy. Coagulopathy, because they're using up all their platelets as you're damaging the endothelial wall, causing the platelets to stick to the von Willebrands. The fibrin is being made from the coagulation cascade and eventually the platelet count is going to drop. This is systemic, the entire body. This patient can also develop acute lung injury, which is ARDS, or acute lung injury. That's another complication, because if the lung is affected, that's one organ, right? If the brain is affected, that's also mental status. The kidney is affected. So what did we say the definition of severe subsist? Wait a minute. They have sepsis with one organ failure will give us severe sepsis. If they meet any of this, this patient is in severe sepsis. Well, we're not done. The story continues. Severe sepsis is now gonna eventually go into septic shock. Well, we're gonna go over and stop talking about what septic shock entails.