So good afternoon again, everyone, and welcome back. Just a bit of housekeeping reminder for anyone just joining. If you do have any questions, please submit them through the app, and then we can answer them all at the Q&A session at the end.
And please do remember that the app will be closing at 5 o'clock this evening when the event finishes. So if there's anything you want to get from the app, please make sure that you do that before 5 p.m.
Today. So it gives me great pleasure to reintroduce Dan Lewis for our 3rd and final session of today. For anyone just joining us, Dan holds both the European and American diplomas in emergency and critical care, and Dan works in Vets Now's referral hospital in Glasgow and is our national clinical lead in emergency and critical care.
He's got a particular clinical interest in sepsis, which he is going to share with us now. And over to you, Dan. Thanks Laura.
Hi everybody. Right, so I guess for anybody who is in the, the earlier sessions, there will be some building on what we've, talked about already, but don't worry if you've been, at a different session, I mean, why would you? But this will stand alone as well, so hopefully, hopefully it'll be OK.
Right, antibiotics in sepsis. Here we go. What, when and how.
OK. So Whenever we talk about urs and and sepsists and mods and things like that, there's an awful lot of definitions and things being sort of bandied around, and although you never want to make these lectures too sort of dry, it's worth just sort of reminding . I guess everybody what those different definitions are, so that.
When I speak to you, you speak to me, you speak to each other. We all know that we're talking about the same thing if we say sepsis, or SIDS or mods, OK? So that my concept of sepsis is the same as yours, it's the same as Laura's, and so we all know what we're dealing with.
So SES, that systemic inflammatory response syndrome, that's a, that's a sterile global inflammatory issue. Sepsis is that global inflammatory issue that's caused by an infection, but it's also led to organ dysfunction. And multiple organ dysfunction syndrome, MODs, is that situation where you've got at least 2 organ systems that aren't working very well, and they weren't where the problem came from.
OK. So, Sepsis, what is sepsis? What the next slide is.
There we go. So, sepsis is that condition where the body's immune system reacts abnormally to an infection, with the resultant disease state. Being worse than you might necessarily expect.
But the same sort of problem, where there's an. Abnormal immune system response and we're, we're talking about the innate immune system here, so that's the neutrophils, the macrophages, the dendritic cells. The epithelium, the endothelium, but not the lymphocytes.
That same sort of problem can be caused without infection. That's our SERS. That's our SERS issue.
But sepsis is when we've got this. Abnormal immune system reacting to an infection resulting in. Organ dysfunction.
The whole thing is triggered by molecules or antigens that are associated with insult. Whether that insult is injury. We've been talking about trauma earlier today, or infection.
OK. Those molecules, those antigens are known as those pamps and damps, OK? And they trigger receptors that are found in lots and lots of different places.
That stimulates the innate immune system, those neutrophils, those macrophages, that wide range of cells to produce those pro-inflammatory mediators. And we touched on this a little bit earlier. And then those cells, once they've been switched on by those pumps or those damps, those molecules that are caused by injury.
Or in this case we're talking about infection. That then produces a cascade of events downstream. White blood cells are switched on.
The lymphocytes are switched on as well. The blood becomes more sticky. We get vasodilation and we get ongoing production of pro and anti-inflammatory mediators.
We've got local effects on the vasculature, vasodilation, increased leakiness of those blood vessels. And those effects on the vasculature. Instead of being confined to where the infection is, when we're talking about sepsis, we're talking about a global problem.
That's extended throughout the body. And so that then starts to have effects on organs that are distant to the original injury. As those vital organs are affected, that then spirals out of control and affects our other organs.
Reduce function, more cell damage. And more molecules associated with cell injury get released and cause more inflammation. If our immune system cells get affected, or maybe something like the guts, then we run the risk of secondary infections and opportunistic infections getting in.
As we talked about last time, it's important to remember that in getting in sepsis, it's the relationship between pro and anti-inflammatory processes and pro resolution or repair processes. It's the balance that's disturbed. Maybe the pro-inflammatory reaction is too big.
Maybe the anti-inflammatory reaction is too big and it lets in a secondary infection. But it's an imbalance that's the problem. The other thing I just want you to remember as well is when we're talking about infection that's driving sepsis.
We're not just talking. About bacteria. OK.
So When we're talking about sepsis. We're not really talking about one single condition. We're talking about a spectrum of disease.
OK. And you yourself will be able to identify that, the patients that you've seen. A dog with a pyometra is.
Has got sepsis. But it may well be a relatively stable animal that's with sepsis. Compare that to A 15 year old Yorkie.
That's got aspiration pneumonia. It's still sepsis, but that patient is likely to be much, much sicker. So what you need to think of it, sepsis as being, is being a spectrum.
Well we haven't just got systemic inflammation, we've got infection. Of a variety of different causes, and we might have other things that kick in and contribute to the context of the disease in that animal. And therefore we need to think about what leads one individual to become septic and not the next one.
Now we can't at the moment predict which of our patients are gonna be worst affected for any given septic injury, insult. And which ones will just be ill. But what it's worth us doing as clinicians is thinking about those factors that may influence this process.
And the PEO acronym. Is really useful in terms of that. Doesn't have to be anything quantitative.
But in all of our ill patients. Maybe even the trauma patients, but certainly our really sick patients, we ought to be thinking about this concept. Predisposition, what else might they have that makes them more likely to get properly sick?
Are they old? Are they really young? Are they immunocompromised because of either of those two things, or maybe because of drugs or other diseases like diabetes?
Hypoadrenal corticism, hyperadrenal corticism. Are they genetically predisposed to be more at risk of certain issues? Are they an Irish setter with a problem with antigen recognition?
Are they a black and tan dog with a inability to fight off parva virus very strongly? All of those things add into the mix. Of our sick patients, our septic patients.
We need to think about the degree of insult. He talks about trauma, you can talk about what's being affected, but if we're talking about sepsis, we need to consider what infection it is we're dealing with. How unpleasant is it?
Has it been acquired from the community? Has it been acquired from a hospital? Is it a multi-resistant bacteria?
Is it an organism that we can't identify? We can look at the response, is our animal mounting an appropriate response? Is that response excessive?
And this is where we will progress in terms of the future, in terms of markers of inflammation and infection. And do we have signs of organ dysfunction? Because that is the ultimate thing, that's what we really need to know, because that's the thing that we need to support.
Without treatment. But we're talking about antibiotics in sepsis. So we need to be thinking about the insult or the infection here.
So what we do about the insult, the infection. It's probably best addressed as a series of questions that we should endeavour to answer whenever we've got a septic, or even a patient with sterile Sirs, septicy or a sursy patient. We need to ask some questions.
If we think our patient's septic, where do we think the infections come from? Most of the infections we're gonna see in association with sepsis are likely to be gastrointestinal in origin. Potentially some might be dermal.
OK. But mostly they're gonna come from the gastrointestinal tract. What you also need to think about, I mean, you know, we're probably all thinking about it at the moment, but what you also need to think about is whether your infection.
Has been acquired from another animal or person? Is it a contagious pathogen, or is it self-derived? Has it come from the patient, and that includes secondary opportunistic infections.
We also need to think about whether the infection might be iatrogenic. Is it our fault? Is it a hospital acquired infection or a surgical site infection?
But again, don't forget those stuff that's not bacteria. Remember the viruses. OK.
At the moment we're all worrying about a virus that makes people very, very ill. OK, that's viral sepsis that COVID-19 causes in a lot of people. Think about things like the Apicomplexions, the Babecia species, particularly for those of you practising in the sort of the, the warmer bits of the IVC range.
Molecules like mycoplasma. Protozoans, like toxoplasma, and again, maybe going towards those sort of those warmer, wetter areas of Europe, the systemic fungal infections as well. Now, To perhaps explain this more clearly, most of the time when we talk about sepsis, we're considering.
Things like leakage from the gut, contaminating the peritoneum in the abdomen with bacteria. But remember, it's the patient's immune response to the pathogen. That is the bigger problem than the pathogen itself.
So do remember that those viral infections like parvovirus, like COVID-19, that are causing organ dysfunction, are causing sepsis even before any secondary infections get in there. Right. But we're gonna ignore those other things for the moment.
We're gonna talk about bacterial or things that are like bacteria anyway, in terms of causing sepsis. What we need to do, our second question. After where has it come from, is what kind of bugs we might find.
With that source of infection in sepsis. The majority of our dermal infections. Are going to be mainly gramme positive focused.
Our our gastrointestinal infections. Are gonna be gramme positive and gramme negative. But most of the time they're gonna be aerobic.
For both of those two things. However, if we've got an infection that's originating from the mouth or from the colon. So either end of the gastrointestinal tract.
That's more likely to have anaerobic bacteria in there. May seem strange, but that's the way it is. Now, you might be able to make an educated guess.
Based on where the infections come from, as to what kind of bugs you might have in there, but you're not gonna know. So what you probably ought to be doing. Is when we're thinking about using antibiotics in septic patients.
He's thinking about covering each of those four quadrants on the screen there. Until we know better. What we're dealing with.
So we need to make sure that we're gonna kill our gramme positive bacteria, whether they're aerobic or anaerobic. And our gramme negative bacteria, whether they're aerobic or anaerobic again. The next question is, can you actually get a sample of those bugs?
Before you start your antibiotics. Can you quickly get an aspirate from a chest or an abdominal cavity, a cystocentesis sample, a sample for blood culture, or maybe even perform a trans tracheal wash, or maybe a bronchoalveolar lavage or an endotracheal wash. These should all be straightforward procedures that don't require much equipment or much time.
Once you've got your sample, You know that's gonna take 2 to 3 days to get a result back from the lab. But once you've got your sample, you can start your antibiotics, your broad spectrum antibiotics that are gonna cover all four quadrants. Consider what you've got.
Consider your equipment, your technical ability, the financial implications. Of taking these samples. And also remember those temporal aspects, it is gonna take you time to get the results back.
Sampling before antibiotic use would be the gold standard. But we need to remember that you don't want to be delaying. Your treatment of antibiotics too long in order to get your sample.
The next question. Is what are we actually trying to achieve? Are you trying to control your primary disease pathogen?
Are you trying to stop secondary bacterial infections? Or are you trying to sort of damp down or restrict a primary disease pathogen prior to surgical. Definitive control.
Let's think of some examples there. You Control your primary disease pathogen. An example of that might be treating a septic pneumonia.
There is no surgical solution for that. You have to kill the infection with antibiotics. Preventing secondary bacterial infection, well, that might be the reason to use antibiotics in a parvovirus puppy.
Because it's likely to be immunologically naive. It's got sepsis because of the parvovirus. But as part of that part of the virus infection, it's also taking out.
The neutrophils. Meaning that puppy is at risk of a secondary infection. And then for the 3rd 1, that middle example there, restriction of primary disease pathogen prior to surgical source control.
Well, Lots of possible examples of that, but aseptic peritonitis would be a classic example. We're not gonna withhold antibiotics until we're able to go in surgically because we may not be able to go in surgically straight away. What we need to do is we need to give some antibiotics to try and reduce the number of bacteria reproducing in their abdomen.
To help make our patient more stable for its anaesthetic. The next thing, what do you need to think about? What virulence factors, how nasty a bug?
Is it? Has it come from the environment, has it come from your hospital? And don't forget that a lot of the bugs that we see that are multi-resistant organisms will often have originated in human healthcare environments.
Remember that human healthcare environments aren't just. Doctor's clinics or hospitals. They may well be care homes.
Is your infection hospital acquired or community acquired? Have you got local? Resistant bugs that haunts your clinics or haunts one of your neighbour's clinics or seems to be going round the area at the moment.
Things like Klebsella, Pseudomonas, Staph aureus are really good at becoming resistant. Don't forget your other clinics. Think about what may have come to you from somewhere else.
And consider whether your patient's been exposed to antibiotics recently. If your animal's been, if your patient's been exposed to antibiotics in the last 3 months, then you should expect a degree of bacterial resistance to that antibiotics. That's 3 months.
That's longer than we would normally think about, but it will affect the bacteria. The next thing, and probably the most important thing you need to think about. Is what kills what?
And what is appropriate to use. Now that's deliberately blurred because there's far too much information on there. But what we need to think about again is those four quadrants.
The gramme positives, the gramme negatives, and whether they're each aerobic or anaerobic in nature. OK. There's an awful lot of bacteria, there's an awful lot of bacteria on there, there's an awful lot of drugs on there.
It's too confused a picture. Instead, Let's have this Now this is the scheme I have in my head when I'm thinking about treating my septic patients. OK, to give them antibiotics.
I've got those drugs that will kill both gramme negative and gramme positives, and I've got those drugs that will kill anaerobes and aerobes. Some drugs will do everything. Comoxiclav, so potentiated amoxicillin, will kill.
Everything from every quadrant. Doxycycline will kill pretty much everything from pretty much every quadrant as well, but it's really difficult to get injectable form of it. Cephalosporin's not quite so good at curing anaerobes.
The quinolones, the fluoroquinolones, terrible at killing anaerobes. So if we're using one of those drugs, if we want to cover all four quadrants, we might need to use a combination. Metronidazole and clindamycin, both.
Work really, really nicely in combination with either a 2nd generation cephalosporin or a fluoroquinolone. Maybe we shouldn't be using fluoroquinolones as a first choice in. Veterinary patients.
But remember that these are very sick animals. I agree, we shouldn't be using them, reaching for them. Immediately, but these are individually very sick animals, and so using a fluoroquinolone may still be indicated, but I want you to be thinking about it first.
We probably oughtn't ever to be using 3rd or 4th or 5th generation cephalosporins. But remember some of our older and more simple drugs as well, ampicillin, pretty good. Trimethoprim sulfonamides.
Pretty good drugs. And remember those antibiotics that also kill some of the weird things. Those mycoplasmas.
Yeah. OK. What other factors do you need to consider?
Where is the infection? Fluoroquinolones are great at getting into exudates. But they don't kill anaerobes, and in certain gramme positive dermal infections, they're actually contraindicated.
OK, necrotizing fasciitis, don't give it a fluoroquinolone, you'll make it worse. Beta lactams, your penicillins, your cephalosporins, they're pretty good for the upper respiratory tract. They're not so good for the lower respiratory tract, but they're very good for the urinary tract.
Except the prostate. They're not so good at the prostate. So think about where your infection is.
And the best drug to get there as well. Think about host factors as well. Are there other considerations you need to consider?
And logistical factors as well. OK. Can you administer them appropriately?
Automatically for our sick patient, that means that we need to have access to the intravenous injection. And that intravenous injection needs to be safe in the species we're talking about. So to a great extent, that may well influence your choices.
Hopefully everybody's got intravenous coamoxi clav, potentially the amoxicillin, on the shelf. Hopefully you've all got access to maybe a 2nd generation cephalosporin. Or metronidazole.
And you've probably all got access to a fluoroquinolone as well. If you don't have access to at least one of those things. In a licenced product that can be given intravenously or something that we know is safe.
Then maybe you need to change that in your clinic. But the other thing about logistics. The other things that we need to consider is we need to think about pharmacokinetics.
Yeah, only kidding, we don't need to do that. We need to do a little bit of it. The pharmacokinetics we're gonna talk about.
Is clinical pharmacokinetics, it's what actually matters to your patients. And when we're talking about antibiotics, what we can do is we can divide our antibiotics up into two types. Those that are time dependent.
The penicillins, the cephalosporins, and clindamycin. And those that are concentration dependent, the fluoroquinolones, metronidazole, maybe aminoglycosides. OK.
And there's a difference in how we should use those antibiotics. To give us the biggest effect on the infections that we're dealing with. And that can be summed up by that bottom line there.
The time dependent antibiotics, the more often we give them, the more bacteria we kill. For the concentration dependent antibiotics, the bigger the dose we give, the more bacteria we kill. So, Our penicillins, our cephalosporins.
We give them more frequently, you can see from that little graph on the the right there. We give them more frequently, we get a longer period of time over that dotted line, that's the minimum inhibitory concentration, that's the concentration where the bacteria are killed, OK? The more time we spend over that line, the more bacteria die.
If you took that to its ultimate, then. A CRI, a continuous infusion of a penicillin or a cephalosporin, would give us the greatest killing effect. And that's been shown in human ICUs.
And the odd case report in veterinary medicine, that that is probably the most effective way of using those bacteria, those antibiotics, sorry, but. That's not always achievable in veterinary practise. But more doses, more frequently, more kill.
Remember that. Quite often in our clinic, we'll be giving. Our Comoxylas, our cephalosporins every 4 or 6 hours.
Certainly every 8 hours, very rarely we would give it as infrequently as every 12 hours. In our sick patients. For our concentration dependent antibiotics.
It's the size of the peak of plasma concentration over that MIC line. It gives us more kill. So a big dose once a day is more effective than lots of little doses.
Frequently. OK. So for a concentration dependent antibiotic, we want that black.
Line On the top, that black trace. OK, bigger dose, more kill. So, let's make it real.
What do we actually want to be reaching for? What can we reach for? Well, The first line, the first choice should always probably be coamoxicillin clavilanaclavi clavulanic acid, clavilanate.
Augmentin, potentiated amoxicillin, call it what you want. It's broad spectrum, it covers all four quadrants, and we ought to be giving it a 20 to 25 migs per gig every 6 to 8 hours in our sick patients. If we haven't got that, or maybe because our patient's been exposed to that previously, the next one down my list is gonna be cefuroxime, that's a 2nd generation cephalosporin.
It's called Zinoceph is the trade name. Same dose, same frequency. It doesn't kill my anaerobes quite as effectively as amoxicillin does.
So I'm gonna add in metronidazole. The metronizole's either gonna be twice a day or one big dose once a day. If I can't use either of those two, if I can't use a penicillin or a beta lactam, then I'm gonna reach for a quinolone, for a fluoroquinolone.
That's only the time I'm gonna reach for a fluoroquinolone. My preference is gonna be marbafloxacin, but I'm also gonna give it to the higher, Dose Than is recommended. The dosing regime would be 2 mg per kg, but we've got really strong evidence that that isn't always enough.
That 4 migs per gig is a better dose to use, and that's what I'm gonna give. Once a day, And that's gonna have a pretty good effect. Again, my fluoroquinolones, my marbfloxacin, maybe my Nrefloxacin is not gonna kill any anaerobic bacteria.
So I need to combine it with either metronidazole or clindamycin. What if you haven't got any of those? What if you're in a mixed practise of farm animal practise?
Simple benzyl penicillin, penicillin G is actually much more effective than we give it credit for, particularly if we combine it with a couple of other drugs. In our septic patients. It will actually kill most things if we combine it with amiccain.
And metronidazole. I haven't given doses for those because. You're not gonna be using them very often, and actually the one that you want to be reaching for is that potentiated amoxicillin.
But you've got alternatives. And they're all being given IV. Because if we've got sepsis, then we need to kill that infection quickly.
Start as soon as you can. Don't forget to stabilise your major body systems. Don't forget to try and identify the source of the infection, get a sample of it if you can.
But time undoubtedly matters. If antibiotics are gonna help your septic patient and bacterial infection is contributing to their organ dysfunction, then the sooner they're killed, the better, right? Makes sense?
Well, Current human recommendations are to administer appropriate ant antimicrobials within an hour of diagnosis of sepsis or septic shock. Evidence supports this in septic shock, but it's less compelling in milder forms of sepsis. It's unclear when the administration of appropriate antibiotics is most beneficial and when it should be considered essential.
But very evidence is a little bit less clear. However, In your septic patients, you should be aiming to administer early and appropriate antibiotics. And in a sense that's probably, if you can do that, that's a measure of the quality of your practise rather than necessarily affecting prognosis.
Because if you can do that, if you're thinking about it, if you're switched on enough to get antibiotics into your septic patients early. Then you're probably doing lots of other things well that will improve the prognosis of your patients. Just as important to think about when we shouldn't give antibiotics.
We know that antibiotic stewardship is vital for the future of, well, everybody. And so we don't want to be splashing it around when we don't need to. Non-infectious SERS is probably more common than sepsis in cats, although cats are quite good at hiding sepsis.
So this is one of those things where. If they don't appear septic at the start. Have another look later.
Have another look with that point of care ultrasound. Make sure they haven't produced an exudate that you need to tap, identify and then give antibiotics to treat. But it is extremely likely that a systemic inflammatory response will progress to sepsis if you don't get all of the other things sorted out, the hypo perfusion, the oxygenation, the support of the organ function.
Should you always give broad-spectrum antibiotic cover to serve patients? Well. Maybe it depends on the quality of your other aspects of your care.
Maybe some of those things that we talked about earlier in the previous lecture about stabilising our major body systems and improving perfusion. Go back to your animal. Think about those other things that you may well need to consider.
Are there predisposing factors? Your diabetic patient may not be septic because of its diabetes, but it does make complications such as pyelonephritis more likely. Has your poly trauma.
Cat that's got systemic inflammation been hit by a car. Or has it been hit by a Staffordshire bull terrier? One of those is gonna be more likely to get infected, because bites, wounds, and bacteria will be involved.
Think about what organs are dysfunctional. Bearing in mind that the hypo perfused of a septic body is predisposed to secondary infections, an escalation of a systemic inflammatory response, a sterile one. Tends to occur for one of the two main reasons.
Either because The innate immune system stops working very well. Or because of injury to the gut. Now innate immune system cell is, is, is sort of twofold.
Some are taken out by infection and damage control, and some are taken out by those cytokines that we mentioned before. Sometimes the pro-inflammatory drive is so profound. That the bone marrow can't keep up with demand.
That might influence the need to give antibiotics sooner. Then in another case. Do a neutrophil can.
What about the gut? Well, Exactly what role the gut has in sepsis is unclear, but it's important in driving that pro-inflammation forward. Think about the gut It's consisting of two of three things.
It's a barrier with a strong epithelium. It's got a lot of immune system components associated with it. And it's got an awful lot of bacteria in there.
It's pretty likely in our sickest patients, particularly those with poor perfusion, that at least one of those components will not be working well. And what that can result in is the release of bacteria, yes, but probably not as often as we think. Some of those molecules, molecules associated with bacteria that cause damage, so bacterial toxins, but also some of those cell associated, those host associated markers of injury.
And cytokines getting into the circulation. And remember we don't need bacteria in the, in the blood. To cause sepsis, we just need those inflammatory mediators.
All of those things get into the circulation via the lymphatic system. Up through the thoracic duct into the great veins. And then into the circulation, so the first thing they hit tends to be the lungs.
So, quickly now, how does sepsis progress to that multiple organ dysfunction syndrome? Well, Multiple organ systems are gonna be affected if we've got either impairment of one of our vital body systems. Significant impairment of that vital organ system, or mild impairment of several vital organ systems.
And remember that our patients may have come into the clinic with mild impairments of several vital systems because of their age or because of other diseases. So remember that. That's gonna cause a domino effect on our other organ systems.
Again, remember it's the dysregulation of the balance between pro and anti-inflammatory processes. But to really progress from sepsis, to make things worse, there are 3 probable reasons. We might have the one hit approach where that initial injury or infection is so bad that causes organ failure.
For human patients, particularly human trauma patients, they often see. 2 instances of, of, of multiple organ failure. Either because of the initial injury or because of poorly timed anaesthetic interventions, surgical interventions, poor resuscitation, inappropriate fluid therapy.
So that initial injury is significant, but we then as clinicians do something that doesn't fix them, maybe even makes them worse. Those are the patients to be careful about, about when you take them to surgery, about how you resuscitate them. And then we've got that sustained hit which probably comes from that ongoing inflammation in the GI tract.
We talked about source control. You may have a sepsis that you need surgery to fix it. And again, going back to my previous talk earlier this afternoon, we want to get our patient as stable as possible first.
OK. Surgeons don't kill people, anaesthetists do. Avoid prolonged anaesthesia.
Be quick. Consider control surgery, damage control surgery rather than definitive surgery in your really sick patient. Get as many things as you can do ready before you anaesthetize a patient.
Be prepared for things going wrong in anaesthesia, have a plan, have a plan for hypotension. Have a plan for resuscitation, have a plan for bradycardia. Have a plan maybe even for ventilation and fluids and blood.
Think about what might go wrong before it goes wrong. Think about what your patient might need when it comes out of surgery. You don't go into surgery with sepsis and come out.
Happy and fixed. You're sick for a few days, so think about what else your patient might need, a feeding tube, a central line, maybe nasal oxygen cannulae, a urinary catheter to reduce abdominal discomfort. Think about all that before you need it.
And think about it, can you do something temporarily to assist in reducing that septic drive prior to anaesthesia in surgery? The last lecture I talked about, this patient, which, no I don't, didn't show it there, the slide on the left shows a big liver abscess that was making this patient so septic, so cardiovascularly unstable, that even with norepinephrine and plasma transfusions, we could not get its blood pressure above, it's mean arterial blood pressure above about 75. I knew that as soon as we took that to anaesthesia to surgery, that blood pressure would crash and the patient would probably die.
So instead, under ultrasound, we've put a big tube into that abscess. And drained Some of the rubbish out. There's less puss in there, that is definitely gonna be making my patient feel less rubbish, and it definitely is gonna be making my patient become more physiologically stable.
We did this, we drained this abscess for about, well, it was overnight really, it was about 18 hours, gave the antibiotics, gave the fluids, gave everything else, and it meant that that patient when he went to surgery was much, much more stable than he would have been otherwise. Maybe he would have lived Even if we haven't done this. But I'm certain that he did better because we did.
Can you do source control? In stages, temporarily assisting things before you go to anaesthesia. Right.
Last couple of slides. With using antibiotics in sepsis, we also need to think, the final question is when do we stop? Do we stop them when our signs of inflammation go?
Do we stop them when everything goes back to normal? Can we stop them, let's say for septic pneumonia, when the lungs look normal on ultrasound or X-ray? That might take weeks.
Do we just stop when the client runs out of money or when we get the blood tests back? Most of the time, if we're using antibiotics. To treat sepsis, and we can do effective source control, maybe with surgery, maybe with something else.
Then using short courses of very aggressive antibiotics, so those doses I talked about. For 5 to 7 days is enough. You don't need to carry on for 4 to 6 weeks.
Right. So last slide, in summary. You need to be identifying your patients that have got sepsis or those that are at risk of sepsis.
Once you've done that, try and get a sample if you can. But don't mess about. Start an appropriate antibiotic promptly, because it probably improves patient survival.
Use a good intravenous antibiotic at a sensible dose and think about those regimes. Comoxy la, 20 metres per gig every 6 or 8 hours. Marbasil at 4 mgs per gig every 24 hours with something to kill your anaerobic bacteria.
If you can remove some of the pus, some of the gunk, some of the rubbish that's sitting in your patient's body cavities, causing sepsis. If you can remove some With a needle or a tube or a drain, before you take them to surgery, there will be a better surgical candidate. Don't carry on your antibiotics for weeks and weeks and weeks.
Look at your patient, Use things like biomarkers like CRP in dogs to help you decide when it's appropriate to de-escalate your antibiotics, and use your culture results to help you as well. But hit them hard, hit them fast and then stop. And that It's me.
