Guideline fail?

What if adherence to a guideline was associated with worse outcomes? How much independent validation of guideline recommendations should occur? Is it realistic to expect guidelines to be subjected to “real-world” testing prior to adoption?

If these questions intrigue you, you’ll be interested in a Pfizer-pfunded four-center performance improvement initiative that included education around the ATS-IDSA pneumonia guidelines and a prospective assessment of outcomes. As the authors report in Lancet Infectious Diseases this week, patients who received “guideline compliant” empiric therapy were more likely to be dead at 28 days than were those who received “guideline non-compliant” therapy.

Before you submit your resignations to IDSA and ATS, you should know that there were plenty of problems with this observational study—most of them are well-summarized in an accompanying editorial. The failure of the authors to consider appropriate de-escalation of therapy in their determination of guideline compliance is an especially big problem, given that antibiotic overuse has been linked to increased mortality in the ICU.

Despite the limitations, I think this study raises important questions about guideline-driven approaches to complex infections. It is interesting, for example, that guideline non-compliant empiric therapy was equally or even more likely to cover the eventually-isolated pathogen than was compliant therapy (85% vs. 81% of the time, respectively).

And there will be prizes!

The U.S. Department of Health and Human Services just sent me an e-mail announcing two new national awards to recognize success in “reducing and eliminating central-line associated bloodstream infection and ventilator-associated pneumonia.” The awards are co-sponsored by the Critical Care Societies Collaborative.

The announcement states that the awards are intended to motivate. There should already be several potent motivators at work here (e.g. saving lives, reducing lengths of hospital stay and costs, CMS public disclosure requirements, etc.). But if the prospect of getting a plaque and a free trip to Chicago is what your organization needs to get over the hump, then by all means get to work. I’m also in favor of anything that raises the profile of HAI prevention, so it is good to see on that level.

Speaking of raising profiles, there was a very similar award presented at the Fifth Decennial, to recognize excellent team performance in infection prevention. It would have been nice to see SHEA, APIC and IDSA co-sponsoring this, too.

Award announcement here

Two new NPSGs from the Joint Commission target VAP and CAUTI

University of Iowa, Class of 2013

The Joint Commission has just released new National Patient Safety Goals for 2012-13 for full implementation by January 1, 2013.  They cover VAP and CAUTI in hospitals and LTCF and are open for public comment until 1/27/2011.  The strategies were published in the October 2008 SHEA Compendium in ICHE. 

Two comments: (1) I thought the world was going to end in December 12, 2012, so probably not much to worry about, apart from the world ending and (2) VAP may be going away in NHSN to be replaced by process measures, so I wonder how VAP outcomes will be tracked, as required, when no one can decide on a definition? I'm sure you have comments and they want to hear from you.

Note: It looks like even if the Mayans were wrong about 2012, we may still not make it through 2013.

Example for VAP, NPSG.07.06.01 in Hospitals requires 7 steps:
1) A plan
2) Hand hygiene before/after caring for ventilated patients
3) Semirecumbent position of patient
4) Regular antiseptic oral care
5) Daily weaning assessment
6) Daily sedation interruption
7) Measure VAP process measures and outcomes

Hospital Program draft versions of NPSG.07.06.01 (VAP) and NPSG.07.07.01 (CAUTI) (PDF)
LTC Program versions (PDF)
JC page that provides links for submitting comments.

h/t Marc Wright

Happy Weekend: VALORI or Volaré?

Remember those 1979 Plymouth Volaré ads?  Remember how the Volaré was the car that brought bankruptcy Chrysler's way?  Me neither.  Well, when I see the the acronym VALORI (Ventilator Associated Lower Respiratory Infection) like in Dan's recent VALORI post, I start singing Volare in my head.  Now, perhaps, the same thing will happen to you. For that, I'm truly sorry. To apologize, I bring you Dean Martin, the pride of Steubenville, Ohio.

My new VAP definition is unstoppable!

As we have blogged on numerous occasions, existing ventilator-associated pneumonia (VAP) definitions (for both clinical and surveillance purposes) are craptastic. In Mike’s recent post about this problem, he calls for CDC to collaborate with IPs and hospital epidemiologists to help develop better definitions. Well, the CDC is doing just that. They have been working with critical care and ID physicians, as well as with some of the CDC Epicenters, to develop and assess a new definition for “VALORI” (Ventilator Associated Lower Respiratory Infection). A simple algorithmic summary of the approach is below, courtesy of Dr. Shelley Magill, who gave an excellent talk at a recent CDC/HHS meeting I attended in DC:

The major objection voiced to the draft VALORI definition is that by removing some aspects that introduce subjectivity, the definition becomes more of a severity of illness measure than a description of what we know clinically to be VAP. The definition also retains some elements that are subjective (or hinge on clinician behavior, such as use of antibiotics), so it isn’t clear if it will have better performance characteristics than the current NHSN definitions.

In my view, we should not use VAP as a quality measure, period. VAP rates should not be compared across hospitals, publicly disclosed, or used in any pay-for-performance schemes. For as soon as they are, hospitals will quickly learn to reduce their rates without doing anything that actually improves patient outcomes (e.g. by narrowly interpreting clinical signs or CXR findings, by seeking consensus among multiple IPs for each case, or by incorporating clinician’s opinions regarding the diagnosis).

In the meantime, we can probably agree on some practices that could be selected for public reporting and benchmarking (i.e. process measures). The practices chosen should be those that are demonstrated to improve meaningful patient outcomes in controlled clinical trials. A great example is this 4-center study of spontaneous awakening + spontaneous breathing trials. The investigators, recognizing the futility of defining VAP, instead demonstrated reductions in ICU days, vent days, hospital days, and mortality in the intervention group.

Tracheotomy, VAP, p-values and death

There is a new RCT just published in JAMA by a large group in Italy looking at the benefits of early (day 6-8) vs late (day 13-15) tracheotomy completed in 12 ICUs. The primary endpoint was VAP. There is also a very nice accompanying editorial. There are several interesting findings. First, patients randomized to early tracheotomy were less likely to develop VAP by day 28, 14% vs 21%, but the p-value was 0.07. Since the p value was greater than 0.05, the authors were forced to say that there was no benefit from early tracheotomy.

Interestingly the also found significantly greater vent-free days, ICU-free days, successful weaning and ICU discharges in the early tracheotomy group. There was even a trend towards higher survival in the early vs late group, HR=0.80, 95% CI 0.56-1.15. The authors and editorial do a nice job of pointing out that 31% or early and 43% of the late group didn't even receive a tracheotomy due to impending extubation or death. The editorial even makes the point that selecting an early tracheotomy is really a strategy of more trachs. The study did not assess patient comfort, which may be associated with early tracheotomy.

What is always troubling to me is that scientists, editorialists, journals and clinicians are stuck in this p-value trap. Here we have a study, a very good randomized trial, which shows likely clinically significant reductions in VAP and potentially lower mortality, but since the study was underpowered we are forced to say "no difference." I wonder if you calculated how many patients are intubated each year in the US (or Italy) and reduced VAP rates by 33%, how many VAPs would be prevented and how many deaths would be prevented? I know this study should be repeated, but will it? You have a negative JAMA study, what's the incentive? I describe this phenomenon as "Death by p-value."

VAP: Do you know it when you see it? (Again!)

There's a new paper on the utility (or lack thereof) of CDC's definition of ventilator-associated pneumonia. In this study 4 persons reviewed 50 cases of ventilated patients with respiratory deterioration >48 hours after intubation. Two reviewers were experienced infection preventionists who applied the CDC definition. A third IP used a modification of the CDC definition that was more quantitative, and the fourth reviewer was a physician board-certified in infectious diseases and critical care who used clinical judgment to define VAP. Using the standard definition, one IP assigned the VAP diagnosis to 11 patients and the other, 20 patients. The IP using the modified definition assigned 15 cases as VAP. The physician diagnosed VAP in 7 patients. The IPs agreed on 62% of cases (kappa=0.40). All 4 reviewers agreed on the VAP diagnosis in only 4 cases. This is not the first study to show how complex assigning the diagnosis of VAP can be.

Given that public reporting has raised the stakes to high levels, the CDC can no longer ignore this issue. Consumers cannot make choices on where to receive care if inter-hospital comparisons of infection rates are not valid. There needs to be a convening of IPs and hospital epidemiologists who use the definitions on a daily basis to thoroughly assess each of the HAI case definitions and begin to work on the development of new ones that will be fair to hospitals and helpful to consumers. Otherwise, it's garbage in, garbage out, and the entire concept of public reporting is undermined.

Defining our way to zero?

Here is a quote from an Emerging Infections Network post today, regarding how we define central-line associated bloodstream infections (CLABSI):

Is it really worthwhile to adjudicate blood stream infections in patients with central lines as "primary" or "secondary"? The adjudication according to the "definition" is still subjective. For example, a Klebsiella bacteremia in a pt with a PICC and PEG was ascribed to "gastroenteritis" since the pt had some coincident diarrhea and stool fecal leukocyte+ (hence bacteremia was considered secondary). A candidemia was attributed to pneumonia since the pt was immunocompromised (on steroids for BOOP), had a fluctuating CXR and had Candida in his sputum (hence the candidemia was considered secondary). I was told that these attributions were completely reasonable since they were compatible with the definitions and that the institution regularly passes muster when audited. It is distasteful to argue but anyone looking closely would see a discrepancy between the clinical diagnosis and the adjudicated diagnosis. Since the public is taking these numbers seriously, there is a problem.

This EIN post goes to the heart of a very important issue in healthcare associated infection reporting—the subjective interpretation of National Healthcare Safety Network (NHSN) definitions. Of course we already know that ventilator associated pneumonia (VAP) rates are a load of crap (I’ll leave it to Klompas and Platt to explain why). It is less well recognized how much fiddling is going on with the CLABSI definition. The post above is a great example of what is happening across the country in hospitals that are under increasing pressure to “get to zero”, and as public reporting of infection rates becomes the norm rather than the exception. Hence those hospitals that apply the NHSN CLABSI definition very strictly are punished with higher CLABSI rates. Meanwhile, hospitals celebrating “zero” rates may in fact be no more “safe” than before they began fudging their definitions.

How to fix this? Either via an expensive and cumbersome validation system for public reporting (any ideas for CDC and state public health departments on how to do this?), or via more specific definitions from NHSN.

Decontamination: not so selective?

Remember the NEJM study from the Netherlands that compared selective digestive decontamination (SDD) vs. selective oropharyngeal decontamination (SOD) vs. placebo for infection prevention in ICU patients? The upshot, using 28 day mortality as an endpoint, was that both SDD and SOD were beneficial, but there was no evidence that one was better than another.

These investigators have now published a report on changes in antimicrobial resistance after the prophylactic use of antibiotics in this study (tobramycin, polymyxin E and amphotericin for oropharyngeal (SOD) or nasogastric (SDD) administration, and 4 days of IV cefotaxime (SDD)).

Surveillance of rectal and respiratory tract samples from patients in the 13 participating ICUs demonstrated that resistance to ceftazidime, tobramycin, and ciprofloxacin increased in GI tract flora after the SDD intervention and increased in respiratory flora after both SDD and SOD interventions.

I have to read the fine print more closely, but this confirms my view that we should stick with chlorhexidine oral care to suppress oropharyngeal flora, rather than SDD or SOD approaches that use therapeutic antibiotics.