Welcome to the presentation on Ventilator-Associated Pneumonia, Diagnosis, Management, and Prevention. My name is Robert Bulk. I'm at Rush University Medical Center in Chicago, and we're going to spend the next 40 or 45 minutes reviewing the definitions, risk factors for the development of ventilator-associated pneumonia. We'll discuss common organisms that are responsible for ventilator-associated pneumonia and the guidelines for initial antibiotic treatment of ventilator-associated pneumonia. We'll also describe the prognosis and strategies for prevention of ventilator-associated pneumonia. Ventilator-associated pneumonia is part of hospital-acquired pneumonia, and hospital-acquired pneumonia is defined as development of pneumonia after 48 hours or more of being in the hospital. That helps us exclude pulmonary infections that were incubating or brewing at the time of admission. We think that hospital-acquired pneumonia occurs 5 to 10 times per every 1,000 U.S. admissions. It's the second most common nosocomial infection, and it certainly increases the risk six to 20-fold for ventilatory support, and is associated with increased morbidity, mortality, cost of care, and length of stay. Now if we go back to the 2005 ATS IDSA guideline that defined healthcare-associated pneumonia, the 2016 guideline from the same organization eliminated healthcare-associated pneumonia. Since we're in a window of only 5 years from that new guideline, I want to at least emphasize that healthcare-associated pneumonia was brought out to help identify those patients who may have multidrug-resistant pathogens, and those individuals were people who had been hospitalized in the preceding 90 days, who were nursing home or extended care facility residents, who were on home infusion therapy, including antibiotics, were receiving chronic dialysis, home wound care, or had family members with multidrug-resistant pathogens. The thinking in 2016 was that not all these factors are associated with a high risk for multidrug-resistant pathogens, and using the HCAP definition actually promoted a lot of unnecessary antibiotic usage, which may be worsening antibiotic stewardship. And that introduces the topic of ventilator-associated pneumonia. And there's a variety of definitions out there for ventilator-associated pneumonia. I think the important thing for this discussion is people who are sick enough to be on the ventilator often have abnormal chest X-rays and abnormal hemodynamics and vital signs. So what we're looking for is a new or expanding infiltrate that occurs in a patient who is more than two days after hospital admission and has been on the ventilator for at least two days, and they should have some clinical features suggesting a worsening of their situation and that go along with pneumonia, such as fever, elevated white count or low white count, purulent sputum, and worsening oxygenation. This usually occurs at least three to four days after intubation, has a prevalence that's thought to be about 9% of ventilated patients, and like hospital-acquired pneumonia, this also increases ICU and hospital length of stay, increases mortality, although there's a lot of debate as to how much more it increases mortality as opposed to the underlying condition that put the patient on the ventilator. It certainly keeps them on the ventilator longer and increase hospital care costs. Some say it will double that. Now, if this wasn't confusing enough, we're going to throw out the topic of ventilator-associated tracheobronchitis. Since a lot of times people are receiving endotracheal tube aspirates that are sent for culture, there may or may not even be an associated new infiltrate, but there may be a clinical scenario that looks like there could be an infection, and the term ventilator-associated tracheobronchitis was coined, and this may be a prelude to ventilator-associated pneumonia or could just reflect colonization of the tracheobronchial tree. When you have the positive cultures along with fever, leukocytosis, purulent sputum, and no infiltrate, you will find that a lot of these patients may have pathogens like Pseudomonas, Acinetobacter, MRSA, and this may occur in two to ten percent of our intubated population. At Wash U in St. Louis, they actually surveyed for one year their surgical and medical intensive care population, and they found that the frequency of ventilator-associated tracheobronchitis was 1.4 percent versus 4 percent of ventilator-associated pneumonia in this population. What is very interesting is that the incidence was felt to be similar, that the VAT progressed to VAP about a third of the time. VAT was caused by multi-drug resistant organisms about a third of the time, and very interesting, the two groups had no significant difference in hospital mortality, which would suggest that ventilator-associated tracheobronchitis may have similar repercussions to ventilator-associated pneumonia. So as we approach our patient who is in the ICU, has this new infiltrate, whether on the vent or not, we have to approach them like we would any potential infected or septic patient, and first think, does this patient need to be isolated for a pathogen such as TB or other communicable disease? We need to go back to history, physical exam, get our lab, get our x-rays, get cultures, and don't forget that we may have to expand from just sputum and sample the pleural fluid with a thoracentesis if it's amenable to either access to the lower airway by bronchoscopy with using protected specimen brush or BAL, or a transcutaneous lung aspirate, or a deep tracheal aspirate. All of these may give us some indication of what the underlying cause is, and these are folks who you might send a urinary antigen for legionella or for pneumococcus to help make a diagnosis. The clinical manifestations are part of the definition. We're looking for purulent sputum, fever or hypothermia, leukocytosis or left shift, new or expanding infiltrate on chest x-ray, and it's always questionable how much stock to put in positive lower airway cultures because we never know what's a colonizer, a contaminant, or a true pathogen. All of this requires our clinical acumen. The microbiology of ventilator associated pneumonia seems to change around day five. So day two to four of being intubated on the ventilator, if you have a patient acquire a ventilator associated pneumonia, it's typically with communique acquired pneumonia organisms. But the late onset, day five and beyond, ventilator associated pneumonia is typically caused by enteric gram-negative bacteria, the so-called spastic, serratia, pseudomonas, acinetobacter, citrobacter, entrobacter, and klebsiella. About 10 to 20 percent will be pseudomonas, 15 to 20 percent will be staph aureus, and about 50 percent actually turn out to be polymicrobial causes of ventilator associated pneumonia. The kind of COVID pandemic that we've been faced with now has brought out that there are some patients who have had severe pneumonias, get a secondary infection that looks like another ventilator associated pneumonia, and we've been surprised to find that aspergillus is among those new organisms. So the aspergillus will potentially have big impact on the required management and treatment as well as outcome of patients who are on the ventilator and being treated for critical illness. Another controversy that was reigning mostly in the 90s and early 2000s in ventilator associated pneumonia was whether to use an invasive diagnostic approach versus just empiric treatment using guideline-based recommended antibiotics. Part of the fuel for controversy was that there really wasn't a good gold standard diagnosis of ventilator associated pneumonia, so we're left with questionable data supporting survival benefit with early invasive diagnosis as well as concern that if we are using unnecessary antibiotics, we may be fueling our continual problem with multi-drug resistant organisms, we are potentially increasing the cost of care, and we put the patient at risk to other super infections and to worse outcomes from antibiotic associated complications. To help us, we're going to review a couple of studies that have been done to either support or refute the benefit of invasive diagnosis. Using the clinical diagnosis of ventilator associated pneumonia, people felt that it was very nonspecific, and studies have shown that there's a false positive diagnosis in up to 70% of episodes of ventilator associated pneumonia. Using protected specimen brush or BAL with quantitative or semi-quantitative cultures actually was felt to help secure the diagnosis and direct treatment such that in Rello's study, he was able to then change the initial antibiotic regimen in 43% of the patients because of the new data that came around, and he also was able to eliminate unnecessary antibiotics which led to cost savings and decreased the risk to the patient and the potential for development of resistance. In a multi-center randomized uncontrolled trial in 413 patients with suspected ventilator associated pneumonia conducted by the French where they had on site someone to do bronchoscopy with protected specimen brush or BAL at the diagnosis of possible ventilator associated pneumonia, they were able to show that this invasive strategy decreased mortality at day 14, improved SOFA score on day 3 and day 7, and ended up decreasing antibiotic use and increased the number of antibiotic-free days. Unfortunately, at day 28, mortality between the two strategies was the same, which could reflect the impact of the underlying disease, but many quarreled with this investigative approach because it did not improve 28-day mortality. And those same individuals argued for empiric treatment. They came out and said, bronchoscopic results are available too late and they're actually only valuable in identifying your treatment failures, that many people don't do bronchoscopic invasive diagnosis in the same fashion. So reproducibility is questionable and the arbitrary cutoff nature of the thresholds for defining positive culture at 10 to the 3 on protected specimen brush and 10 to the 4th colonies per mil for BAL may or may not be adequate to separate out a true infection from a colonizer. They also felt that despite that last study, there was no proof that outcome is improved by this aggressive diagnostic approach and argued that we do need better studies to evaluate the impact of the two strategies on survival, length of stay, cost of care, and emergence of resistance. Looking at the ability to split the difference and just do an endotracheal aspirate and comparing that to BAL in a Canadian study, it was found that both seem to perform about the same as far as being able to differentiate the ventilator-associated pneumonia patients from non-infected people and this was irrespective of whether they had culture positivity or negativity and the pretest likelihood of pneumonia or not. The problem with this study was that they eliminated people from the study who were already colonized or infected with resistant organisms or who were immunocompromised and I would argue that those are exactly the population that you would like additional information to know. Are these colonized or infected people infected with the same organism or is there something else? You would like to go to something more than just a deep tracheal aspirate here and certainly in the immunocompromised host, we're interested in all types of organisms, not just bacterial infections that could be causing a ventilator-associated pneumonia. They also did not emphasize de-escalation based on culture and sensitivity results, so you lost the potential impact and benefit of that maneuver in antibiotic stewardship. So let's go to a question. We have a 67-year-old man with cellulitis and a diabetic foot ulcer. He's admitted for IV levofloxacin treatment. On day four, he has worsening renal function. He has respiratory distress and actually requires intubation and ventilatory support. Four days later, he develops a new right lower lobe infiltrate, fever, elevated Y count, and decreased blood pressure. At this time, would you begin empiric broad-spectrum antibiotic coverage, begin heparin and send the patient for PE protocol chest CT, perform bronchoscopy and BAL for quantitative culture, or await culture results prior to starting antibiotic therapy? I would suggest the best answer is number one, begin empiric broad-spectrum antibiotic coverage. And I would look at this as the 2005 guideline would suggest that here we have a patient who meets the definition of at least hospital-acquired pneumonia, I would say ventilator-associated pneumonia. He's been on for at least four days and this is late onset and we are worried because he's been on prior antibiotic therapy that he may have an antibiotic-resistant organism. And that would be the person to start broad-spectrum antibiotic therapy directed against multidrug-resistant pathogens. So now, which regimen would we choose for this patient? Would we continue levofloxacin and add amikacin, start ceftriaxone and azithromycin, begin lenazolid and meropenem, or initiate ampicillin and cefepine? The answer I would suggest is begin lenazolid and meropenem as we're targeting multidrug-resistant organisms developing in this patient who has been on antibiotic therapy and is worsening. And appears to be critically ill since he's now hypotensive and on the ventilator. So now we have to sort of fudge our discussion a little bit in that I don't know how the boards are framing questions. So they may indeed ask you about the prior recommended ATS IDSA guideline on risk factors for multidrug-resistant pathogens that came out in 2005, which are similar to some of the issues we just talked about with the old concept of healthcare-associated pneumonia. So patients who have been on antimicrobial therapy in the preceding 90 days, who have been hospitalized for five days or more, there's a high frequency of antibiotic resistance in the community or the specific hospital unit, or have the presence of risk factors for HCAP, which we don't talk about anymore, but we've reviewed earlier, or they are immunosuppressed or on immunosuppressive therapy. And the 2005 guidelines for treatment would suggest that if we are talking about hospital-acquired pneumonia or ventilator-associated pneumonia with no known risk factors for multidrug-resistant pathogens, if it's early onset and with any disease severity, then we would be talking about a ceftriaxone or a respiratory fluoroquinolone or ampicillin-sulbactam or erdapenem antibiotic regimen. If, however, we do have risk factors for late-onset disease or risk for multidrug-resistant pathogens, then we're gonna look for the combination antibiotic regimen with an anti-pseudomonas cephalosporin or anti-pseudomonas carbapenem or anti-pseudomonas beta-lactam, beta-lactam-based inhibitor, plus an anti-pseudomonas fluoroquinolone or aminoglycoside. Plus, if we're concerned about methicillin-resistant staph, we would add lenazolid or vancomycin. And an important concept from that 2005 review is that if we are diagnosing somebody with HAP or VAP and we obtain our initial cultures, we start our initial therapy, and then we check our patients, check the cultures, see their clinical progress over the next 48 to 72 hours, and if we find that they have improved and their cultures are positive, we should de-escalate the antibiotics, if possible, and treat them for a course of seven to eight days, continually reassessing. If the cultures, however, are negative and they've improved, we might consider stopping antibiotics unless we have an indication that there truly is an infection. Maybe we were treating something else that was non-infectious and antibiotics are not needed. On the other hand, if the patient is not clinically improved, the cultures are positive, we should adjust our antibiotic therapy based on that culture and sensitivity data and hopefully determine whether or not just a change in antibiotics is sufficient or if we have to be looking for closed-space pus or have to do some sort of source control in order to have improvement in our patient. And if the patient is not clinically improved, all our cultures are negative, we have to start our search over again and figure out what is going on with the patient and what have we missed in order to yield a good outcome for that patient. We have lots and lots of data that says if we choose the wrong antibiotic and even if we change later on to the appropriate effective antibiotic, the initial wrong antibiotic is associated with poor outcome and higher mortality. Many studies have documented that. And if we look at a prospective observational study in 115 patients with ventilator-associated pneumonia, mortality was unacceptably high, survival was much better if you got the right antibiotic from the start. So choosing the right antibiotic helps out. And in this study, they used BAL culture and sensitivity results to help them ensure they chose the right antibiotic. And because of having culture and sensitivity data, they were able to deescalate the antibiotic therapy in 42% of the patients, which was part of a good antibiotic stewardship protocol. A lot of times we discuss with patients with staff whether to treat with lenazolid or vancomycin. And if the patient has MRSA, using lenazolid may be associated with better clinical cure and better outcome as opposed to continuing with vancomycin alone. This is a meta-analysis of two prospective randomized controlled trials of lenazolid versus vancomycin in over 1,000 patients with staff infections. In reviewing patients who have Pseudomonas aeruginosa, ventilator-associated pneumonia, there is data that suggests that starting more than one anti-pseudomonal agent will lead to better survival compared to starting with just one anti-pseudomonal antibiotic. And this is purely playing the odds of making sure you guessed correctly. So we'll talk about what the guidelines say in just a minute. But here's at least data that says, if nothing else, start with two. Once you get your culture and sensitivity data back, deescalate therapy to just the one agent that is needed to help resolve the pseudomonal ventilator-associated pneumonia. So now that we've defined our patient as having ventilator-associated pneumonia and we started antibiotic therapy, how long should we treat? Three days, seven days, 14 days, or 21 days? And of course, we're assuming a good clinical response. And the answer is seven days. And I'll show you the data for that. And we really just have this one study that the French group did. It was prospective multi-center randomized trial. They actually studied eight versus 15 days of treatment for ventilator-associated pneumonia, all confirmed by quantitative cultures. So they are big on the invasive diagnostic approach. And they showed that there was similar mortality at 28 days, similar recurrence rates, but there were more antibiotic-free days with the short duration of therapy. And that's, of course, what you would think. There was a trend for more microbiologic failure when you're dealing with non-fermenting gram-negative bacteria, such as Pseudomonas, with the short course therapy. But overall, if you're looking at just outcome and survival, and the eight days was just as good as 15 days for treatment of ventilator-associated pneumonia. And that has, I think, become pretty much the standard. So I mentioned the 2016 new guidelines from the IDSA-ATS for HAP and VAP. And the first thing you'll notice is they eliminated HCAP as a way to help improve antibiotic stewardship. They emphasized that every hospital should generate their own antibiogram. It should be unit-specific, if possible. And this will help guide antibiotic therapy, particularly related to MRSA and the need for dual coverage of gram-negative organisms. They recommend short courses of therapy and de-escalation as possible. As far as microbiologic methods to diagnose hospital or ventilator-associated pneumonia, they actually recommend against non-invasive sampling with semi-quantitative cultures for both. They recommend non-invasive sampling, not against that, against invasive sampling. And this is a weak recommendation with very low quality data. If you're gonna do invasive sampling, they feel that the benefit is to help you discontinue unnecessary antibiotics. They did not recommend using procalcitonin, soluble triggering receptor expressed on myeloid cells, CRP, or clinical pulmonary infection scores to help you determine who needs antibiotics. This is a clinical decision. If you think they need it, start it, start it early. Use guideline-based therapy and treat then for seven days or till you have additional information to warrant a change in that. They recommend treating ventilator-associated tracheobronchitis. The hospitals should regularly generate and disseminate the local antibiogram and should encourage treatment that's informed by the local distribution of the pathogens and their antimicrobial susceptibility as you could glean from your local antibiogram. They would suggest using treatment algorithms for empiric coverage of Staph aureus and Pseudomonas. Encourage the use of pharmacokinetic and pharmacodynamics rather than routine manufacturer prescribing information to ensure that you give the proper dosing for patients. So where possible, check levels and make sure that you're not underdosing people who have augmented renal clearance or who have a large volume of distribution. The 2016 guideline also looks at risk factors for multidrug-resistant pathogens and they're very similar. Prior intravenous antibiotic use within 90 days, septic shock at the time of ventilator-associated pneumonia, ARDS preceding ventilator-associated pneumonia, five or more days of hospitalization prior to the occurrence of VAP, acute renal replacement therapy prior to VAP onset. The risk factors for multidrug-resistant HAP is prior intravenous antibiotic use within 90 days. Risk factors for MRSA in either VAP or HAP is again the antibiotic use within 90 days. And same thing for multidrug-resistant Pseudomonas in VAP and HAP, it's intravenous antibiotic use within 90 days. And the treatment algorithms in the 2016 guideline are pretty well in line with the prior guidelines. Again, we're trying to ascertain what is the risk level for multidrug-resistant organisms and the likelihood of either MRSA or Pseudomonas. And I will leave you with these recommendations. And same thing for empiric ventilator-associated pneumonia treatment when MRSA is suspected. Again, here we have our treatment algorithms. And we also bring up gram-negative antibiotics with anti-pseudomonal activity and which organisms you want to target. The IDSA-ATS 2016 guidelines even goes as far as to suggest using inhaled antibiotics in addition to systemic antibiotics for ventilator-associated pneumonia due to gram-negatives that are only susceptible to aminoglycosides or polymyxin. And this is a weak recommendation with very low quality data. They would equilibrate the vancomycin-linazolid choices for MRSA in either HAP or VAP. And as far as HAP or VAP with Pseudomonas, they think the antibiotic should be based on culture and sensitivity data, but use monotherapy if the patient is not in shock or have a high risk of death, but combination therapy should be used when the patient presents in shock or has a high risk of death. In patients who have HAP or VAP caused by ESBL gram-negative bacilli, treat based on susceptibility testing and patient characteristics, and if you're treating a patient who you suspect or have evidence is caused by a carbapenemase-resistant enterobacteraceae, treat with IV polymyxin as a strong recommendation with moderate quality, and inhaled colistin as a weak recommendation with low quality of the data. With HAP or VAP caused by Acinetobacter, treat with carbapenem or ampicillin-sulbactam, and if sensitive only to polymyxin, use IV polymyxin, and again, think about adjunctive inhaled colistin as a way to treat the Acinetobacter. The duration of treatment, again, just like our one study, should be seven days, strong recommendation, very low quality, recommend de-escalating rather than fixed duration of initial treatment based on clinical response. Procalcitonin and clinical data may be better than clinical data alone to guide early discontinuation of antibiotics, but they would not recommend using the clinical pulmonary infection scale to guide discontinuation of antibiotic therapy. Now, you may just say, well, the easiest approach is just given empiric carbapenem to anybody I suspect as having hospital or ventilator-associated pneumonia, and at least here we have some data from a large meta-analysis that actually would suggest there could be a mortality benefit by using just such an approach, which relative risk reduction of 0.84 and absolute reduction of mortality of 2.68%. However, the cost is you have an increased risk of developing resistance of 2.74%. So it seems to be a wash, and I don't think anyone's gonna go for empiric carbapenems just to simplify our guessing game. So now we're gonna move into prevention of ventilator-associated pneumonia, and which of these strategies will help prevent ventilator-associated pneumonia? Maintaining the head of the bed at less than 30 degrees, changing ventilator tubing every other day, starting prophylactic inhaled colistin, or providing daily oral care, and providing daily oral care has been shown to be beneficial at preventing ventilator-associated pneumonia. I'm sure you all have your ventilator bundle, which is designed to prevent ventilator-associated pneumonia. First thing about preventing ventilator-associated pneumonia is extubate the patient, even if you have to put them on non-invasive face mask ventilation, trying to avoid re-intubation. If you can avoid routine ventilator circuit changes, use closed endotracheal suctioning, maybe even use subglottic secretion drainage, shorten the duration of time you're on the ventilator, keep them in the semi-erect position, anything over 30 degrees. And if you can use computerized order sets, rounding checklists, compliance assessments, all sorts of good stewardship to help you avoid ventilator-associated pneumonia as a way to have a quality outcome. Instead, getting them off the ventilator will reduce nosocomial, hospital-acquired pneumonia by using non-invasive ventilation. But it turns out that putting people on non-invasive ventilation actually reduces urinary tract infection and catheter-related infection. So multiple benefits for being off the ventilator. And in this retrospective cohort study of non-invasive positive pressure ventilation, as non-invasive ventilation use went up, nosocomial infections went down, and intensive care unit mortality also went down. We all strive to keep the head of the bed at 30 degrees or higher, but is it really feasible? And looking at 109 supine and 112 semi-recumbent patients that were followed, trying to keep them either at 10 versus 30 degrees, what they found for the two groups is 85% of the time, neither of these groups were able to achieve what they were for head position. So while it's obviously a goal to try and keep the head of the bed at 30 degrees or higher to prevent ventilator-associated pneumonia, in actuality, it's hard to accomplish. Maybe if we alter our endotracheal tube. So having the tube in place leads to a colonizing biofilm in about 84% of patients. And it's more likely to happen the longer the tube is in place. There are devices to clear the inside of the endotracheal tube, but very difficult to do anything on the outside of the endotracheal tube. Turns out that polyurethane cuffs are preferred and seem to have less colonization compared to polyvinyl cuffs. Low volume, low pressure tapering cuffs seem to have less chance of being colonized. Treating ventilator-associated tracheobronchitis may actually reduce. Here's at least one study showing that when they were treated with vancomycin and genomycin, there was a 71% reduction in ventilator-associated pneumonias at 14 days. So still a controversial area and one I don't think you'll actually be tested on the exam. Continuous aspiration of subglottic secretions has been shown, but you have to have a special endotracheal tube, which is more costly and often not put in at the start and taking out the routine endotracheal tube to put in the new endotracheal tube for subglottic secretion removal may put the patient at increased risk of a subsequent pneumonia. So the risk benefit needs to be considered for that. Same thing with silver-coated endotracheal tubes, which have been shown to have decreased colonization rates, but they're more expensive and not often used. Something that is easy to do and should be part of routine care is oral care, mouth care using chlorhexidine and even brushing the teeth will reduce oropharyngeal colonization and decrease ventilator-associated pneumonia. And following the ABCDEF treatment bundle, which the Society of Critical Care Medicine Collaborative put forward, will hopefully not only get the patient better quality care while they're on the ventilator, but get them off the ventilator faster and reduce the risk of having ventilator-associated pneumonia and ventilator-associated complications. And that brings us to the final part of our quality discussion of trying to deal with hospital-acquired infections, which are common, which are hopefully preventable. Whether we can eradicate that is a topic of great discussion but we know since the 1999 report from the Institute of Medicine that to err is human and a lot of unfortunate things happen to our patients who are critically ill and in the hospital. And ventilator-associated pneumonia is one of those conditions and we've been putting forward plans and we've just been discussing some of the preventive strategies to reduce the incidence of ventilator-associated pneumonia and see if that leads to better outcomes for our patients. And over the past two decades, we've seen a big decrease in the number of ventilator-associated pneumonias. But is this really a decrease or is there a definition problem? Because this is sometimes difficult to score. And even looking at the chest x-ray, there's a lot of variability as observers interpret the chest x-ray. There's really no specificity of an x-ray to say this is ventilator-associated pneumonia and the infection preventionists who screen and code for ventilator-associated pneumonia have a lot of trouble interpreting chest x-rays. They also have trouble looking at the usual signs and symptoms that we've talked about for ventilator-in-hospital-acquired pneumonia because they also lack sensitivity and specificity, very subjective, and documentation is quite variable. And even our cultures may not be as sensitive and specific because we have colonizing bacteria and controversies over how to interpret some of the results that we see. Is this a colonizing culture or is this a true contaminant or is this a true pathogen that we're dealing with that potentially is causing the infiltrate clinical situation? So CMS put together a group of clinicians and said we need to come up with a strategy that will identify patients who are on the ventilator, who develop complications, and we'll call this ventilator-associated events. And we look to see if we can pick out in a patient who is on the ventilator for two days and has a period of stability, if there is a period or an episode of worsening manifested by worsening oxygenation that requires a change in oxygen delivery or PEEP, and we're not putting in a chest x-ray now, so we're just saying we have a patient on the ventilator, something happens that you have to go up after a period of stability on the FIO2 or the PEEP that we think there's some sort of ventilator-associated condition going on, and then we have to figure out with that change in FIO2 or PEEP if there is evidence of infection or inflammation, because if there is, maybe we have an infection-related ventilator-associated complication. So we can look for changes in temperature, white blood cell count, along with the administration of a new antimicrobial agent and say, that sounds like an infection-related ventilator-associated complication, and if we then have a positive result on either microbiologic testing or a positive laboratory evidence of possible infection, we can say, is there possible or probable ventilator-associated pneumonia? So looking at our algorithm, these may become and are at least talked about as future quality indicators to look to say, how are we doing with preventing ventilator-associated pneumonia? So what is out there is you have a patient who baseline period of stability or improvement on the ventilator, so for over two calendar days, the FIO2 or PEEP are decreasing or stable, and then after the period of stability, there's an increase in either the FIO2 of 0.2 or for more than two calendar days, or an increase in the PEEP level of three centimeters of water pressure or more for more than two calendar days, then the patient meets the criteria for a ventilator-associated complication, and then we have to see, is the temperature high or low, the Y-cell count high or low, and did somebody start a new antimicrobial agent that is gonna be continued for more than four calendar days? In this window, then we're starting to think, okay, we got a ventilator-associated complication that seems to be infectious, now we can look and see, is there a purulent respiratory secretion? One or more specimens that's defined as, is there a lung, a bronchus, or tracheal infection such that we have more than 25 neutrophils, less than 10 squamous epithelial cells per low-power field, and are there semi-quantitative culture results that could direct us to this possibly being a true infection? And then we get to, if we have positive cultures of endotracheal aspirate, bronchoalveolar lavage, positive culture of lung tissue, or a protected specimen brush, then we may be talking about the patients as having possible or probable ventilator-associated pneumonia. So what we've done over the last 40 minutes is talk about ventilator-associated pneumonia, which is common and associated with increased cost of care, length of stay, morbidity, and mortality, probably. We've talked about how to begin empiric guideline-based therapy as soon as possible based on clinical status and the known unit hospital antibiogram, to use good antibiotic stewardship and tailor and deescalate treatment based on clinical response, and treat for seven days in the setting of a good clinical response. And we've got to have strategies to prevent ventilator-associated pneumonia, and I would encourage you to follow those strategies and the ABCDEF.

Ventilator-Associated Pneumonia

VAP

Hospital-Acquired Pneumonia

ATS IDSA Guidelines

Nosocomial Infection

Diagnostic Criteria

Microbiology of VAP

Preventive Strategies