Mythbusting

Does the Quinsy need draining?

Local cultures are interesting, and variety is the spice of life. So let’s look at the ripened Quinsy fruit, shall we?

It is entirely imaginable that local practice at one tertiary care center is to perform an ED needle aspiration under endocavitary ultrasound guidance for a peritonsillar abscess and discharge the patient, while another within 100 miles may consult ENT to perform an aspiration at bedside and admit the patient.  Likewise, one community center may perform aspiration, admit the patient overnight and consult ENT in the AM, while another community ED may transfer to a nearby tertiary care center because “this patient needs ENT.”

Ultimately, none of the above is necessarily wrong, it just depends on your level of comfort; but perhaps an understanding of the patients likely disease course may change your sentiment a bit.

This is a review of data from multiple sources – the National Ambulatory Health Care Survey of Emergency Departments, the national Emergency Department Sample, and the National Inpatient Sample – to evaluation the treatment outcomes of patients with a Quinsy – also known as a peritonsillar abscess. Ultimately, they find that only 20% of patients had an incision and drainage in the ED, 73% of ED patients were discharged, (5.9% transfer, 21.6% admit) yet, only a 5% revisit rate.

Importantly, medical failure occurred only 12.4% of the time, and surgical failure (a needle aspiraton was considered a surgical intervention) occurred only 3.5% of the time. There was a 2% re-admit rate, with a <2% complication rate for both medically and surgically treated patients.

Rather than transferring patients for ENT evaluation, and providing them with quite the bill for an ambulance, its entirely reasonable to attempt ED aspiration given the low likelihood of surgical failure.  Likewise, its also reasonable to have a risk benefit discussion and explain to the patient that they have about a 10-15% chance of medical failure if they elect to not undergo an invasive procedure, provided you’ve adequately explained indications for returning to the ED; 90% likelihood of success is still quite high and you dont even have to get stabbed in the throat!

In the next post, we’ll discuss ways to optimize your patient, and red flags that aught to trigger an overnight stay.  But for now, you should feel comfortable either medically treating the patient or attempting aspiration before considering transfer.

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Mythbusting

Staph bacteremia: a riddle, wrapped in a mystery, inside an enigma.

Whew! It’s been awhile! Back to it today, with a personal favorite topic- infectious disease.

This study, in particular, is a reminder that medicine is an incredibly humbling career.

All patients with staph aureus bacteremia at Radboud University Medical Center in the Netherlands between January 2013 and April 2016 were retrospectively examined, with primary outcome being newly diagnosed metastatic infection by 18F‐FDG‐PET/CT (here on out referred to as FDG-PET). Subsequent treatment modifications and mortality outcomes were also examined.

There were 148 high-risk staph aureus bacteremic patients, of which 99 underwent FDG-PET. “High risk” characteristics are associated with metastatic infection, and those characteristics are: community acquisition, signs of infection >48 hours before initiation of antibiotics, fever after 72 hours of appropriate antibiotic therapy, positive blood cultures more than 48 hours after initiation of appropriate antibiotics, or already confirmed metastatic foci at the time of presentation.

Of these 99 staph aureus bacteremic patients that underwent FDG-PET, 73.7% had metastatic focus (73 of 99); 71.2% of these patients with metastatic disease had no sign or symptom of this new focus of disease (52 of 73); and of all 73 patients with metastatic infection, 47 patients (64.4%) were diagnosed with metastatic foci in more than one organ system.

That is, 47% of all high-risk staph bacteremic patients have at least 2 organ systems infected (47/99), many of whom had no signs or symptoms. Wow.

Well, ok, but does this really matter? Maybe we just extend their antibiotics longer?

That is just partially correct. Antibiotics were prolonged 15% of the time, 10% of the time a second antibiotic was added on. 25% of time treatment duration was shortened due to no metastatic focus seen.  But…. Some form of pus drainage occurred 19% of the time (ie, 19% of all patients who underwent an FDG-PET had an otherwise unplanned drainage).

Some other pearls:

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So while I typically focus on EM articles, why do I bring up this paper? It’s not terribly uncommon for us to have the “sepsis bounceback.”  The previously critically ill who now re-presents with fever.  We’re getting a second chance to find the other foci of infection – and frankly, these are not easy diagnoses to make.  Lastly, this paper is a good serving of humble pie- with 71% of patients with a metastatic focus of infection for which they had no sign or symptom.

Staph bacteremia:  trust no one.  Believe nothing.

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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.

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Critical Care, Improving Outcomes, Mythbusting

FOAMed: embracing the skeptics, push dose edition.

Embrace the skeptics. Seek them out. They’re actually your greatest allies.  Even when they express concerns over FOAM’s beloved push-dose pressors.

This paper reviews three cases of push dose pressor usage at their institution over an unnamed time period.

1) A post-op patient (“with known blood loss”) with hypotension in transport (no BP or MAP measurements given), and rather than optimize the slurry of midazolam, fentanyl, hydromorphone the patient was currently receiving, push-dose phenylephrine was utilized.  Except that 50 mg rather than 50 mcg was given, and propofol was then given to treat the resultant hypertension.  Now, they also suggest fluid boluses and blood, but since it was in transport… I dont necessarily think push dose was wrong, and I’m not sure where they would have gotten blood from since they were in transit, but yes, the providers certainly could have used phenylephrine concomitantly with toning back on the sedation package.

Take on case one: Tough case. You’re in transport, so options are limited.  Good thought, room for improvement.

2) A post-laminectomy patient who was receiving a norepinephrine infusion developed Afib RVR and was treatment with diltiazem IV boluses followed by continuous infusion. The patient developed asymptomatic hypotension (again, no BP or MAP measurements given) and push dose phenylephrine was given.  Unfortunately 1000 mcg was given rather than 100mcg of phenylephrine.  All while norepinephrine was still at the bedside, waiting to be restarted & titrated.

Take on case two: Dont get ahead of yourself, you’ve likely got more time than you think. Do the basics well.  Slow is smooth and smooth is fast. 

3) A hypotensive patient with angioedema who had epinephrine doses of 100 mcg, 300 mcg, 500 mcg and 1mg all intravenously (!), rather than the intended 5-20mcg.  The authors mention that the patient did not get IM epinephrine.  Being in a situation that demands to push 4 rounds of IV epinephrine must be a sticky one; I’m sure tensions were running high in the resuscitation bay.

Take on case 3: This was probably a pants-crapping case to be involved in.  Things probably could be done in tandem (IM epi while prepping IV).  Again, slow is smooth and smooth is fast.  You also fight the way you train.  I’m sure this was a nerve-racking case to be involved in.

The authors readily admit that they cherry pick cases- and in an email to the author, these cases came from anesthesia, EM, and critical care providers – attendings, fellows, and residents.  Also, in their paper they state, “we feel the time taken to manipulate these concentrations to provide small doses of vasopressor actually take the same amount of time as admixing and initiating continuous infusion vasopressor. “

But… Could you do that in transport?  What about facilities where norepinephrine has to come from pharmacy?

I *partially* agree with the author’s call for a more thought out process, and I think that this can be a call for more appropriate training (mentally, simulations, etc) prior to implementation.  Using push-dose pressors without being able to pull up how to mix and give them is akin to saying “I heard it on a podcast” without digging into the data yourself.  Perhaps maybe premixed vials handy are not the worst idea, hey, maybe we can get a push dose pressors dispenser akin to a fast food restaurant straw dispenser!  I do not agree with completely giving up pushing the boundaries and settling for “par for the course” when there is potential to do better.  Joe Bellezzo managed to do everything wrong on his first ECMO cannulation, but it did not stop the group from refining their approach and pushing the envelop to improve the next patient’s care.

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GI, Mythbusting

Haloperidol- one anti-emetic to rule them all.

When all else has failed, and the patient does not meet admission criteria, where do patients go?  Obs, of course!  I view it as a valuable tool to augment my ED armamentarium.  Specifically, for instances like, say, gastroparesis or cyclic vomiting.

This randomized, double-blind, placebo-controlled trial was performed at two urban hospitals looking at patients with a previous diagnosis of gastroparesis comparing conventional therapy + placeo to conventional therapy + 5mg of IV haloperidol.  They looked at pain severity and nausea every 15 minutes for 1 hour.  Secondary outcomes were disposition status (hospital admission or discharge), ED length of stay, and nausea resolution at 1 hour.  Sadly, they only looked at 33 patients total over a two year study period.

While the two groups were similar in terms of the conventional therapy received, in the haloperidol group, disposition was made sooner and more patients were discharged home, with a significant reduction in pain at one hour (on a scale of 0-10, a mean improvement of 5.37 vs 1.11 in favor haloperidol), as well a reduction in nausea at one hour (scale of 0-5, improvement of 2.7 vs 0.72 in favor of haloperidol).  Fewer patients were admitted (26.7% vs 72.2%) who received haloperidol, with median length of stay shorter for haloperidol (4.8 hrs vs 9 hrs).  Surprisingly, patients in the haloperidol group experienced no adverse events, including QT prolongation and dystonic reactions.  This is probably due to small sample size.

This does not address haloperidol as sole treatment,  and at only a few dozen patients in this study, certainly does not solidify haloperidol’s use as first line.  However, it does add to the pile of data showing haloperidol as safe and efficacious in these patients.  As an aside, if your hospital is anything like mine, you can not give haloperidol IV, so I’ve trialed 5-10mg IM.  Over the last 4-5 years, I’ve become fond of IM haloperidol for refractory vomiting, and (anecdotally) I’ve used it dozens of times with high rates of success.

So yes, better analgesia, decreased nausea, fewer admissions, and decreased LoS with haloperidol.  Pretty much everything you want.  I just wish a broader study in non-specific abdominal pain with vomiting would compare haloperidol as singular treatment and compare it to standard care.

Look, there are some patients who are vomiting so profusely that they seemingly require an exorcism.  For those patients, I think adding a bit of haloperidol for symptomatic relief does not have much downside, I just wouldnt go mixing multiple QT prolonging agents at once.

So, I ask, whats downside?

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Radiology

If you build it, will they come (back)?

This is a review of 2.5 years worth of lower back pain.  Basically, every single patient with an ICD-9 code had their chart reviewed to ask the question, “If you got an MRI in the ED, are you less likely to return?”

They specifically did not look at yield, rather, just whether or not patients initially thought to have plain, old back pain came back.
The answer, contrary to those of us who think more is more, is no.   Repeat visits for those that had an MRI was 4.3%, repeat visits for those without an MRI at initial visit- 4.6%
However, it does give you some insight into who returns – they were more likely male (5.9% vs 2.8%) – further demonstrating that males are in fact the weaker sex.  They were more likely English speaking (4.9% vs 2.1%) and, speaking of which, non-English speakers were less likely to have an MRI (12.2% vs 7.4%), and self-pay patients were also less likely to have an MRI (9.8% vs 5.1%).   Its unclear if this further demonstrates a touch of bias on the provider side, if English-speaking patients speak up more about wanting diagnostics, or if non-English speakers just go to another hospital since this was a single center study.
As a secondary measure, they also looked at disposition for these patients.  Only 16% were discharged after MRI (vs 82% of those without MRI), 74% of those MRI’ed were placed in observation status (vs 11% of those not), 9% of those MRI’ed were admitted vs 3%, and 4% of those not MRI’ed left prior to completing treatment. Now, for some fancy math.
of the 797 patients who received an MRI over this time period, if only 11% were placed in obs status (rather than 74%), that is only 88 patients rather than 591 patients placed in obs status. that’s 503 patients with an unnecessarily padded bill. At $35.8013 per RVU, were talking tens of thousands of dollars billed that’s wasted.
Or, to put it another way, if you are in an area with a good payor mix, why not just obs & MRI them all?
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Improving Outcomes, Mythbusting, Radiology, Radiology

Spinal Abscess: The Baystate Review

This is a review of all spinal abscesses at Baystate (total 162), from 2005 – 2015.  They compare 88 randomly selected controls whom had similar ICD-codes less the spinal abscess plus an MRI that was negative for acute infectious process. 

Interesting take home points, much of which is consistent with prior (albeit scant) literature:

-73% of patients are over age 50.

-more likely to have their second visit (50.6% vs 29.6% of controls) – though this 50.6% of patients with a second visit is surprisingly low for me – no word on how many were sent home from the ED, and had an MRI as an outpatient that were not included in this calculation.; or maybe we’re getting better at finding the needle in the haystack?  Or maybe we’re MRI’ing everyone?

-Many received antibiotics within the month: (35.2% vs 6.8% of controls) – this signifies a huge red flag for me.  If a patient revisits the ED and recently had pyelo (or anything infectious really), and now presents with back pain, probe a bit more for the possibility of vertebral osteo or discitis. 

-percentage of patients with history of IVDA: 20.4% vs 4.6% … this number seems low, but also is somewhat in line with prior studies – thus making me wonder how many I’ve missed…

– percentage of patients with alcoholism with a spinal abscess: 19% vs 8% – the more I get interested in ID, the more I realize that alcoholism is basically a form of immunosuppression.

-percentage of spinal abscess patients with obesity 21.6% vs 2.3%; I’m surprised only 2.3% of controls were obese.  Not sure what role this plays as being a diabetic in and of itself was not associated with a higher increased risk in this study.

-fever was present 62.4% in those with a spinal abscess vs 13.6% of those without; this includes self reported fever, which I have to wonder how often we sweep this aside when the patient is afebrile in the ED.

-16% had no identifiable risk factors; a third of the patients  presented with back pain, fever, neurologic deficits vs 6%

-Other symptoms and signs related to potential spinal cord impingement were seen with similar frequencies and of similar durations among cases and controls- meaning, focal deficits seen in both groups.

-noncontiguous co-infection: 53.7% of time (pneumonia, distant osteo, endocarditis… of those with a co-infection, 20% had more than one).

-blood cultures were positive 63.4% of the time, and >75% of the time it was staph Aureus. 

-Majority of lesions were found in the L-spine at 56.2%  – which means almost half are elsewhere!

-while “admits” for spinal abscess were up from 2.5 to 8 in 10,000 admissions from 2005 to 2015, I have to believe that number is somewhat inflated as admits like chest pain, pneumonia and renal colic probably decreased, while MRI became more readily available. 

All in all, this paper is pretty much in line with others on this topic, and strengthens the signal a bit for certain key points: a good number of spinal abscesses are not in the L-spine; many patients are older than you think, and, among other things: its more than just IVDA. 

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