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.

Improving Outcomes, Improving Throughput, Neurology

Opiates beget Opiates – Headache edition.

This is a study comparing 3 EDs in my homeland of CT and their (mis)use of opiates for headaches over a 14 month period. This compared an academic tertiary care center with an approximate 110,000 annual patient volume; an urban hospital with an approximate 85,000 patient annual volume, and a community ED that sees approximately 19,000 patients annually. A total of 1,222 visits were included for final analysis.

Results? Opiates, are not good, mmmmkay?

Patients given opioids as first line treatment had a 37.7% increase in visits over the study period compared to those who were not given opioids. If you were given opioids as first line, 36.0% required rescue treatment compared to 25.1% in those who were not given opioids. Strangely, female patients were significantly more likely to have opioids ordered than male patients (38.2% vs 24.2%).

Need more reason not to give opiates? Patients not given opioids had a 30.3% reduction in length of stay.

I’m surprised these numbers are so high.  As a community EM AP, I’m embarrassed at these numbers – A shocking 58% of headaches in a community setting were given opiates as first line compared to 6.9% of those at the academic center). Then again, opiates beget opiates.  Opiates lead to repeat visits, more rescue meds, and an increased length of stay, without an improvement in patient satisfaction with opiates.  I question how often those in the community ED just gave opiates to avoid conflict.

Just.  Stop.  Giving.  Opiates.  For.  Headaches.  NOW.

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.

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?

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. 

Critical Care, Improving Outcomes, Mythbusting

Procalcitonin: Holy Grail, or Holy Sh*t ?

Procalcitonin is marketed as, “a marker of broad routine use, both for differential diagnosis of bacterial infection as well as for antibiotic stewardship.

But is it?  This study looks at 107 ICUs that had >25 sepsis cases in 2012, and had an ability to perform procalcitonin (PCT) levels on their septic patients, and essentially looked to compare the outcomes of those that had PCT ordered and those that did not.  All in all, there were about 17,000 septic patients without a PCT ordered, and about 3800 patients with a slightly lighter wallet and slightly more anemic after their admission than their comparators.

There was little difference in baseline characteristics – save for those having PCT ordered more likely hailing from the West (27.9% of PCT orders vs 12.7% of those not getting PCT ordered) and the opposite holding true for the South (55.3% without vs 49% with PCT).  PCT was slightly less ordered at teaching facilities (37.8% of septic patients without PCT orders vs 31.9% of those with a PCT ordered).  All other OR were <1.25.

There was no difference in length of stay and no differences in mortality.

There was an increase in days of antibiotic treatment for those in whom a PCT was ordered (relative risk increase 1.17), and with that an accompanying increase in Cdiff (OR 1.42) .  Of course, 1 PCT begets another (33% of the time, and about 3 days later).  Patients with serial PCT orders had higher rates of antibiotic use, higher Cdiff, and again, no mortality benefit.

Stop the madness.  Indiscriminately ordering tests that will not change management should not be done.  And they certainly should not be repeated.