Critical Care, GI, Improving Outcomes, Mythbusting

Less transfusions, the better, platelet style.

Over 4 years, the Mayo clinic reviewed over 40,000 ICU patients, and sought to determine if prophylactic platelets for critically ill thrombocytopenics matter.

Of these 40,000 ICU patients, they excluded anyone who received RBCs within 24 hours prior to the PLT count that triggered transfusion “to minimize the risk of including those with active bleeding” … The primary outcome was essentially to determine if transfusing platelets led to more RBC transfusions, and, secondarily, all-cause mortality, ICU and hospital free days (among others). Seems backwards, but whatever.

So what falls out of this data?

For all comers, in a propensity matched cohort, one transfusion begets another – (46.3 % of those with platelet transfusions also had an RBC transfusion vs 10.4% of those without platelet transfusions who had an RBC transfusion). Interestingly, those transfused platelets had less ICU free days (22.7 vs 20.8), more hospital free days (15.8 vs 13). When you look specifically at the ~5000 patients with <50k platelet counts and compare those who were/were not transfused platelets, there was no change in ICU mortality, 30 day mortality, ICU-free days, or hospital free days. While this was underpowered to determine statistical significance for those with platelet counts <50k, it is not hard to imagine a larger study to suggest similar benefits of not transfusing these patients- particularly since this study saw fewer hospital free days and fewer ICU free stays (10.2 vs 7.8 days and 19.9 vs 18.3 days respectively) – favoring a more restrictive transfusion strategy (but again, not meeting statistical significance, perhaps due to so few patients with <50k PLT).

This is not the first study I have seen suggesting empiric transfusion or outright canceling of procedures based on platelet counts between 50k and 150k is essentially bunk, and that prophylactic platelet therapy is of little benefit, if not outright harmful. There is even a flicker of a signal that prophylactic platelet transfusions >20k may not be beneficial – but this has yet to be definitively shown true -yet.

I can not agree more with the last words to the authors, “Finally, it must be acknowledged that while clinical trajectories did not improve for the cohort as a whole after platelet transfusion, it is possible that certain subpopulations may indeed benefit from the intervention, though these subgroups have yet to be identified.”

Improving Outcomes, Improving Throughput, Radiology

Parting the SEA with the almighty H&P (& rapid MRI).

Necessity is the mother of invention, and sometimes, necessity comes in the form of hospital administration after a bad outcome. The authors of this paper, essentially developed a rapid MRI protocol for suspected spinal epidural abscess after “several cases of SEA associated with delayed diagnoses and poor outcomes prompted the chairs of the departments of emergency medicine, neurosciences, medicine, and radiology, and members of the Division of Healthcare Quality, to develop a multidisciplinary, clinical decision support tool and imaging protocol with the goal of facilitating early recognition of SEA.”

Wow. Talk about moving mountains. If you’re department is anything like mine, it takes hours to agree on where we’re getting take out from; I cant imagine adding in 4 entire departments into the lunch-ordering mix, let alone all agree on a protocol.

They took a relatively simple approach – if you have new or worsening back/neck pain AND a history of spinal abscess or current/recent (6 months) bacteremia, straight to MRI. I think the recent bacteremia often gets lost in the work up, so I appreciate that they put this front and center. If there is no recent spinal infection or recent/current bacteremia, They looked at risk factors- and I’ll make this simple and break it into 2 categories: people putting things where they dont belong (IVDA, vascular catheters, spinal procedures/injections) and the recurrently ill: ED visit or antimicrobial treatment within 30 days or an infectious process elsewhere. If yes, head to MRI.

I’m torn a bit on this- while I want to applaud the authors for not dwelling on a variety of risk factors that only a small portion of the population has – alcoholism, HIV, severe COPD, the undomiciled, HepC, oncology patients, transplant patients, etc; to say that this group is pretty much captured in the recent ED visit category probably misses a fair amount of patients on the first go-round. And here is the problem of trying to find a needle in the haystack – its hard to increase sensitivity and specificity without causing a delay at some other portion of the food chain – every stat MRI for so many additional back pain patients pushes out another patient and potentially extends at least 1 other patients length of stay.


Despite an increase from 56 MRI’s in the 7 months pre-intervention to 147 in the 7 months post-intervention, yield for a positive MRI (defined solely as SEA and not vertebral osteomyelitis or infectious discitis), went from 16.1% to 17.7%.

On first glance, that’s not a lot of improvement in yield, but they screened 3 times as many patients without losing yield! This is rather impressive. However, they tripled their ED MRI rate, and, even though they drastically cut turn around times from 8.6 hours to 4.4 hours from time of MRI order to radiology report, thats still well over 4 hours for patients with back pain in a highly optimized system. And while yes, they missed fewer SEAs, they probably still have a good percentage that they missed on first visit – the various forms of immunocompromised – the severe COPDer on repeated steroid prescriptions, the HepC patient, the elderly – these are likely missed on the first go round.

I think this is a great step towards creating a policy towards SEA workup. It needs some refinement, but is the best I’ve seen yet. It poses some issues for smaller facilities that do not have 24/7 MRI capabilities, as well as for consultants (neurology essentially becoming a house officer for ID and neurosurgery), and poses a big time crunch for the ED (again, neurology took control of these cases once the decision to MRI was performed, which the hospitalists must be thankful for!). In the end, there is no such thing as zero miss, but Baystate, with this study, demonstrates that, at least for one day, the H&P is not dead.

Critical Care, Mythbusting

Even Pharma is getting in on Vanco-PipTazo AKI

This was an entertaining 9 page meta-analysis espousing the therapeutic harm of vancomycin and pip-tazo in the form of acute kidney injury.  With a conflict of interest page that reads like a pharmaceutical mutual fund (The Medicines Company, Cubist, Pfizer, Merck, Forest/Allergan, Melinta), it’s no wonder that they infer increased mortality due to AKI, yet conveniently COMPLETELY ignore that the same papers they reference show no mortality difference – and if anything a trend towards mortality benefit for vanco-PipTazo.  Likewise, with dialysis rates <2%, the induced kidney injury is less likely to cause harm than a suboptimal drug that wont kill your bug.

They also fail to mention cefepime neurotoxicity.

There are other ways to go about this. Like, say, reviewing the damn cultures.

But in the end, since The Medicines Company and Melinta have new broad spectrum antibiotics on the market or on the way, it probably behooves them to run a slight smear campaign on current treatment regimens. Therefore, forgive me for considering the possibility that the authors intentions may not be pure.

Improving Outcomes

Review the damn cultures.

This is a multi-center observational cohort study performed over 5 years at two hospital systems. They reviewed over 1800 cases of gram negative bacteremia. About 20% of patients with a prior gram negative bacteremia (within the year) received antibiotics to which their prior cultures were resistant.

This is embarrassing. Just review the prior damn cultures. The answer isnt VancoPime reflexively for everyone. Hell, add on a dose of gentamicin, or whatever the prior cultures are sensitive to. Just write a note in the chart and explain it to the oncoming team.

Side note: bout 25% of admits within the last 90 days were resistant to ceftriaxone and cipro, with an 80% or better percentage for resistance (for ceftriaxone, ceftazidime, meropenem, cipro, or gentamicin – 61% for pip-tazo) to the same antibiotic if the same organism was isolated.

Regardless, blaming the surviving sepsis guidelines or the federal government, or whoever is simply trying to pin your own laziness on someone else. It takes no fewer than 5 minutes – and probably closer to 30 seconds – to review prior cultures. In the critically ill, this is utterly and completely unacceptable.

GI, Improving Outcomes, Mythbusting

NG tubes. just. wont. die.

My angst for the NGT has been explained in a previous post, and while this study adds to said angst, it sadly comes short of putting a nail in the coffin in the debate with surgical colleagues.
This is a retrospective single center study which enrolled 181 ED patients with SBO from September 2013 to Sept 2015, and essentially grouped patients according to whether or not a nasogastric tube was placed (49% of patients did not receive the dreaded NGT). Looking at a multitude of factors, they attempted to tease out items associated with nasogastric tube placement, and if there were any appreciable benefits to NGT placement.

Ultimately, if you are over age 70 (37% NGT+ vs 19% NGT-),  have a malignancy (30% NGT+ vs 17% NGT-), or had a prior SBO (56% NGT+ vs 32% NGT-) you’re more likely to have an NGT because, hey, one good NGT deserves another.  NGT+ patients were also less likely to have “likely / early SBO” (19% NGT+ vs 40% NGT-) on CT imaging as well.

All in all, while I’d love to point at the mean length of stays (7 days for NGT+ vs 4.2 days for NGT-; median 5 days vs 3 days), and non-statistically significant resection rates of 13% vs 9% as indications that the NGT is not needed…. well, we’re not exactly comparing apples to apples. The NGT+ patients were sicker- they were older, had higher malignancy rates, had a slightly higher surgical rate, and were more likely to have “definite SBO” on CT. Sadly, this is not the paper to put the NGT argument to rest.  We still need a larger study, preferably with matched controls, to fully put this dinosaur to rest.


Someone?  please? … anyone? please?

Improving Outcomes

Optimizing the Quinsy

So a few days ago, we discussed management of a peritonsillar abscess; while admit rates from 2012 were roughly 22% with transfer rates at 5.9%, and its probably a tough sell that rates of transfer for on-call specialties such as ENT are down significantly from, say, this 2008 paper from EMRAP paper-chaser Mike Menchine (among others).

So what can we do to optimize these patients?

For one, choosing amoxicillin-clavulanate or cefuroxime/flagyl over amoxicillin might help; as it is associated with decreased failure rates, and a decreased rate of requiring additional procedures.

Likewise, this study, found that despite having more ominous clinical findings (more likely to have trismus, peritonsillar bulges, muffled voice, uvular deviation, dysphagia, etc), as well as having radiographically larger abscesses (2.6cm vs 1.3cm), surgically treated patients were less likely to be admitted (20% vs 11%) –  with high levels of success (97% surgical success vs 95% for those treated medically). Now, perhaps this was because of more aggressive treatment in the surgical arm – they were more likely to have antibiotics in the ED (and yes, they were more frequently dosed with IV antibiotics), as well as steroids (yep, more likely to have IV steroids too), as well as fewer repeat visits. Admittedly, repeat visits were quite high (20% medical treatment vs 14% surgical treatment) – which was higher than in the previous paper discussed, which estimated a 5% repeat visit rate nationally.

So who should stay, who should go, and what to do?  I think to avoid an admission or transfer, it’s my belief that we should be maximally aggressive with Quinsy’s – IV fluids, steroids (10mg dexamethasone seems to be a reasonable), antibiotics (likely a dose of either ceftriaxone or clindamycin), and some form of analgesia (ketorolac, opiates, etc).  While medical management has significant success, it still appears somewhat suboptimal compared to surgical treatment (ie, aspiration or I&D).  Generally, I have not been a believer in IV treatments being better than PO treatments, but this seems to be one of those rare instances where it might matter; particularly if you’re trying to stave off a transfer or admission. Likewise, the immunocompromised, those with poor airways (think those with sleep apnea), the extremes of age (with older than 40 years of age having a prolonged disease course in one study!) , intractable pain, vomiting, or persistent bleeding all should be considered for observation.

Improving Outcomes, Mythbusting, Neurology

Early vs late meningitis diagnosis: capturing the needle in the haystack

Needle in the haystack, infectious pathway, take 6.

This is a retrospective study looking at early vs late diagnosis of bacterial meningitis from three hospitals in Denmark (one looking at data from 1998-2014; the other two from 2003-2014). To be eligible, patients had to be >15 years of age, and, obviously, had to be hospitalized with a clinical presentation consistent with possible community acquired meningitis (any combination of headache, neck stiffness, fever, altered mental status, petechiae) with no alternative diagnoses made during or after admission. Furthermore, all patients also had to have a proven bacterial etiology by either: positive CSF culture, positive blood culture and CSF with >10 wbcs, bacteria seen on CSF gram stain, or bacteria in CSF by PCR or antigen analysis.

So what is early and what is late diagnosis? They define “early diagnosis” as being recognized in the ED (1.3 hours to antibiotics median), and “late diagnosis” as, well, not diagnosed in the ED (ie, diagnosed on the wards- 13 hours to antibiotics median). Over roughly 15 years, they saw 358 cases of bacterial meningitis, (~8 cases per year per institute – seems a bit high? They do not mention total number of annual ED visits), with 32% being classified as diagnosed “late.” … so, probably 2-3 cases a year of “late” diagnosis – a true needle in the haystack.

Why the late diagnosis? They tended to be older (65 years of age vs 56), less likely presenting with headache (58% vs 82%), less likely with neck stiffness (36% vs 78%), less likely with fever (59% vs 78%), with the classic triage of AMS, fever, and neck stiffness was only present 20% of the time in the late diagnosis group vs 50% in the early diagnosis…. So, it wasn’t an easy catch.

Why does this matter?  Welp, with early antibiotics having a positive effect on mortality (18% vs 36%) as well as unfavourable outcome (which they do not actually define, 37% vs 66%, in favor of early antibiotics).  This is a HUGE difference in mortality and unfavourable outcomes if you do not catch it early!  … Then again, do we do more harm by giving 1-2g of ceftriaxone to everyone who is a bit altered?  Would the risk of cdiff then outweigh the 2-3 annual misses? I’m not so sure.  What about the recurrent headaches and repeat visits for post-LP headaches?

If you really want to tease out the data a bit, 53% of late diagnosis patients vs 26% or earlier diagnosis patients had a head CT before the LP. 72% of “late diagnosis” patients tentatively had a non-infectious etiology- so let’s explore some of the tentative diagnoses:

loss of consciousness (19 patients)

stroke (12 patients)

intracranial / subarachnoid hemorrhage (7 patients)

impaired mental status (6 patients)

headache (5 patients)

back pain (5 patients)

seizures (5 patients)

loss of vision (2 patients)

(among others)


What I’m seeing here is a a trend towards a neurologic issue (a CT scan, a diagnosis of syncope / seizures, AMS, etc) – which may indicate that the thought of meningitis (or even endocarditis) may not have been entertained. Cant make the diagnosis if you dont think about it. In a similar vein, this diagnosis is rare and runs across a spectrum – on one end, the febrile, meningeal and altered, on the other, the vaguely unwell.  And that, surprisingly, even a 12 hour delay to antibiotics can wreck havoc on the patient.

The take home points?  Be vigilant, entertain the spectrum of disease for meningitis, but remember that every decision you make has consequences, including the decision to, and not to, perform an LP, not to mention the decision to indiscriminately give antibiotics for those “altered”.  Choose wisely, and remember there is no such thing as zero risk.