Do Prehospital Antibiotics Matter?

In short, probably not, but still not completely disproven.

This randomised controlled open-label trial looked at giving 2 grams of IV ceftriaxone to patients that met SIRS criteria (save for WBC- testing unavailable to EMS) with suspected infectious illness. Patients were randomly assigned (1:1) to the intervention group or usual care group using block-randomisation with blocks of 4. This study took place across ten large regional ambulance services serving 34 secondary and tertiary care hospitals in the Netherlands over a 2 year period. They screened 3228 patients of which 2698 were eligible (pregnancy, beta-lactam or ceftriaxone allergy, suspected prosthetic joint infection, among others); 1150 in the usual care arm (IV fluids, supplemental oxygen prn), and 1548 in the intervention group (2g ceftriaxone plus usual care). 13 patients in each arm were excluded from final analysis or excluded due to withdrawn consent or being lost to follow up. The primary outcome was all-cause mortality at 28 days.

So, while they screened over 3,000 patients over 2 years (a massive undertaking!), unfortunately, only 37 (3.3%) patients in usual care and 66 (4.3%) patients in the early antibiotics group had septic shock. Perhaps you could make an argument that the intervention group was slightly sicker with 22% vs 17% having 2 or more qSOFA criteria. Despite a median time to antibiotics of 70 minutes in the ED (thus, probably close to 90+minutes faster in the intervention cohort), and with 14% having antibiotics >3hrs from presentation and 14% having none at all (suspected viral syndrome) – there was 8% mortality in both arms at 28 days and 12% at 90 days in both arms. No difference.

When you look at mortality for septic shock it was 27% (10/37) in the prehospital antibiotic cohort vs 28.8% (19/66). Again, not statistically significant. While prehospital antibiotics might make a difference in a larger cohort, its probably going to be very hard to ever do that study – this was a 2 year study looking at over 3,000 patients and they were barely able to accumulate over 100 septic shock patients.

While an American might argue “they only gave ceftriaxone, you need a real drug like Pip-tazo and vancomycin!” – slow down. The authors acknowledge that ceftriaxone may not have been appropriate because it was “a big gun” that they could all agree on and most patients were rapidly narrowed to receive, most commonly, amoxicillin–clavulanic acid with ciprofloxacin and ceftriaxone the second and third most common antibiotics given. They did not have culture reports back at time of publication, but having low mortality, and 9% of each cohort were not given antibiotics from the ED due to suspected viral illness makes me suspect that they do not have nearly the resistance problem (or concerns) that the Americans do, likely do to appropriate stewardship. Likewise, while one may be concerned about missed diagnosis due to premature closure, there was a miss rate of 1.4% in the intervention group vs 1.7% in the usual care group, also not statistically significant.

In the end, the authors provide a sensical view of the current state of prehospital antibiotics, “Studies showing that early antibiotic treatment is beneficial for reducing mortality found this positive association mainly in patients with more severe illness and a (time to antibiotic) of more than 5–6 hours… However, we currently do not advise antibiotic administration in the ambulance to patients with suspected sepsis.“

While it is certainly plausible that prehospital antibiotics may be beneficial for those with septic shock, it is a near certainty that, at least in the USA, sepsis hysteria would further ensue and the inertia of giving everyone a dose of broad spectrum antibiotics will likely occur – not to mention our continued fixation with iatrogenic salt-water drowning. The cost to the system – including other patients in the department – of responding to these prehospital alerts for those not in shock will likely be the hidden cost infrequently published or discussed by administrations.

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, 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.

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?

Cardiology, Cardiology, Critical Care, Improving Outcomes, Improving Throughput, Mythbusting, Pulmonary, Radiology, Radiology

Probing the dyspneic patient.

For undifferentiated dyspnea, how would you like to have an accurate diagnosis in 24 minutes?

I love this study.

Basically, for all dyspneic patients (not trauma related, and over age 18), 10 EP’s were given an H&P, vital signs, and an EKG, as well as access to a Chest X-Ray, Chest CT, cardiologist performed echo, and labs including an ABG.

These same 2,683 patients, in tandem, had point of care ultrasound testing (lung, IVC, echo). Here’s the catch – the ultrasonographers were only provided the H&P, vital signs, and EKG then asked to make a diagnosis. The treating provider was blinded to POCUS diagnosis.

These numbers for diagnostic accuracy of POCUS are astounding.

+LR for acute HF? 22 (-LR 0.12)

+LR for ACS? 105 !!!

+LR for pneumonia? 10.5 (-LR 0.13)

+LR for pleural effusion? 95 (-LR 0.23)

+LR for pericardial effusion? 325!!! (-LR 0.14)

+LR for COPD/asthma? 22 (-LR 0.14)

+LR for PE? 345!!!

+LR for pneumothorax? 4635!!! (-LR 0.12)

+LR for ARDS? 90

Yes, for certain things like pneumonia, the difference in p-values between tradition means and POCUS diagnosis was not significantly different, but what about volume status? I cant imagine blindly giving 30 cc/kg would benefit the patient with a plethoric IVC and pleural effusion. There is some elegance a play here.

Additionally, sure, ED diagnosis for ACS had a higher LR, but they also had a cardiologist performing and interpreting echos in the ED (a rather rare siting in a US ED I would imagine) – without much improvement in their -LR (0.53 vs 0.48). For PE, the -LR of POCUS was predictably mediocre if not outright bad (0.6), while the -LR for ED diagnosis of PE, with the benefit of chest CT, was -0.10.

Now look, I get that these EP’s were quite sono-savvy. They all had 2+ years of experience, over 80 hours of ultrasound lessons & training, with at least 150 lung and 150 ED echo’s under their belt. The diagnosis was made in 24 minutes with POCUS in comparison to 186 minutes for traditional means. And while most of us can not do a year+ ultrasound fellowship, and neither can we all be as savvy with the probe as these authors (or Matt, Mike, Jacob, Resa, Laleh, etc) – it does not mean we shouldnt try. You can still greatly increase your yield just by practicing. To boot, the cognitive offload you experience by saving yourself a few hours by (correctly!) knowing which direction you are heading with a patient is an immense boon to both your mental heath & your patients well being.

Improving Throughput, Mythbusting

More No-Value Care: pre-procedure INR for cirrhotics

You have a cirrhotic patient in front of you. They need a procedure. You reflexively order a cbc, comprehensive metabolic panel, and PT/INR because you’d like to know about their platelets/ liver enzymes / coagulation ability.

Or maybe it’s a consultant who refuses to do a procedure the patient needs until you order these tests.

And then the platelets come back at 40; or maybe the INR returns at 1.4. Now what?

Do we need to transfuse platelets or FFP? Well, this case series looked at 852 consecutive cirrhotics from Jan ’11 – March ’14 who needed an invasive procedure the decision to transfuse PLT / FFP at attending discretion. Here’s a breakdown of their patient demographics:


And the number of complications:


Now, sadly, despite discussing the World Health Organization classification for bleeding events, they did not really get into the severity of bleeding events. With that said, complications were unrelated to platelet count, INR, CHILD classes, and MELD score. Only 1 in 379 paracentesis had a bleeding event, and only 2 of 228 TIPS/ CVC/ PICC/ hemodialysis/ I&D procedures had an event.

Perhaps most importantly, while attempts to normalized PLT and INR values, PLT/FFP transfusions barely affected the corresponding abnormalities, the scheduled invasive investigations were carried out in the presence of still subnormal parameters- with no or only a few bleeding complications.

Ergo, I agree with the authors, – “we have verified clinically the futility of this recommendation.”