Manual vs. Mechanical CPR; which is better?

There are theoretic advantages to a mechanical chest compression device (i.e. Lucas device). They demonstrate improved blood pressure and coronary perfusion pressure compared to regular CPR. In addition, the earlier observational studies looked promising.

However, there is a theoretical downside. Paradoxically, CPR may be interrupted more when fumbling to fit the device. Or even worse, they may increase time to defibrillation.

So, which is better?

This meta-analysis gathered the available data from out-of-hospital cardiac. Survival to hospital admission was the primary outcome of interest. They also looked at any ROSC, survival to hospital discharge and favourable neurologic outcome at discharge.

The authors found 20 studies of which 5 were RCT’s. In total, there were 21,363 patients included with just over half from the trials. The observational studies and the clinical trials were pooled and analysed separately.

For survival to admission, the RCT’s showed no advantage to the mechanical devices. Whereas the lower quality observational data demonstrated a benefit in favour of mechanical CPR.

How could this be?

Confounding. 

In observational studies, patients are not randomised to a treatment allocation. As such, one group is usually “sicker” than the other. Perhaps the machine was utilised more when the paramedics thought the patient had a greater chance of survival (i.e. younger, witnessed arrest, bystander CPR, shockable rhythm)?

Researchers try to correct for this by doing some fancy statistics; propensity scores, stratified analysis, multivariate adjustment, logistic regression, etc. But these techniques are far from perfect. Furthermore, there are always the unknown and unmeasured confounders.

This may be irrelevant anyway.  The most important outcome, “favourable neurologic outcome at discharge” was no different in both the RCT’s and observational meta-analysis.

What’s the take home?

In all comers, it looks like there is no advantage to a mechanical compression device.

But there remains some “what if” questions.

What if we educated staff in how to fit the device very quickly while ensuring rapid defibrillation? What if it’s an overdose patient that needs prolonged good quality CPR? What if it's a bridge to the cath lab? What if the technology improves? What if we use the device as a cocktail shaker?

That’s a lot of what if’s…

Covering:

Bonnes JL, Brouwer MA, Navarese EP, et al. Manual Cardiopulmonary Resuscitation Versus CPR Including a Mechanical Chest Compression Device in Out-of-Hospital Cardiac Arrest: A Comprehensive Meta-analysis From Randomized and Observational Studies. Ann Emerg Med. 2016;67:349-360. [Link]

Battlefield acupuncture to treat low back pain in the ED; witchcraft in action

Acupuncture has been around for thousands of years… so it must be good.

We all dread treating the patient with low back pain. We don’t have a magic bullet that will provide a fix. It’s frustrating for the patient and provider.

As such, maybe we should engage in witchcraft! Perhaps something that “has been around for thousands of years.”

This was a “feasibility study” enrolling 30 patients with low back pain in New York City. They were randomised to either standard care alone vs. standard care plus “battlefield acupuncture.” Evidently, this is ear acupuncture that has been used by the US military… so, it must be good.

Primary outcome was the 10 point numerical rating scale (NRS) and the “get-up-and-go” test (GUGT). The GUGT is how much time it takes a patient to get out of a chair, walk three meters, turn around and sit back down again.

Results?

Abracadabra! The post-intervention NRS in the acupuncture group was better at 5.2 vs. 6.9 (p=0.04). The GUGT showed no difference.

But wait a minute…

This study was listed at www.clinicaltrials.gov. This is where original study protocols are published. All too often researchers change the goal posts mid-study or suppress negative results. (My all-time favourite example was gabapentin for off-label use.)

A search of registration number NCT02399969 shows the GUGT as the sole primary outcome. The NRS was a secondary outcome. Research misconduct anyone? One would hope the peer review process would pick up on this… it’s not hard! At the very least, the manuscript should mention why they changed their primary outcome to give them favourable results.

But there’s even more than an allegation of research misconduct.

• Acupuncture was not blinded. Not even a sham acupuncture arm. This introduces bias that favoured acupuncture.
• Placebo works; in particular for pain and nausea. Acupuncture is theatrical placebo at it’s best. All the results in the NRS can easily be explained by placebo effect. The GUGT is a more objective measure and the trend favoured standard care alone.
• A quarter of patients approached for enrolment declined to participate. Did they screen out the patients who were acupuncture non-believers?
• There’s more… but for brevity, I’ll stop now…

What are we to conclude?

Please stop the nonsense.

Acupuncture has been around for a long time. Currently we have no consistent good quality evidence to demonstrate efficacy beyond placebo effect.

No more study is needed.  

Covering:

Fox LF, Murakami M, Danesh H, et al. Battlefield acupuncture to treat low back pain in the emergency department. Am J Emerg Med. 2018;36:1045-1048. [link]

Supraglottic airway vs. endotracheal tube for out-of-hospital cardiac arrest; which is better?

This study was a large cluster-crossover clinical trial in the USA attempting to answer this research question. 27 EMS agencies were randomized in clusters to either a laryngeal tube or endotracheal tube with crossover to the alternate strategy at 3 to 5 month intervals.

Why randomize EMS agencies? Wouldn’t it be better to randomise individual patients?

Think feasibility.

Research in cardiac arrest is challenging.  The last thing paramedics want to do during a code is open a study envelope. They’ve got other things on their minds. Hence randomise EMS agencies. Of course this can introduce bias and statistical inefficiency. But such is compromise in research.

The primary outcome was 72-hour survival. They did report the much more important outcome of favourable neurologic status (mRS<3) at discharge from hospital.

Results?

3000 patients were enrolled. About half were unwitnessed and/or had no bystander CPR. 80% had non-shockable rhythms. It’s no surprise overall outcomes were terrible. It is also challenging to demonstrate a difference in treatment strategies when the vast majority were going to die regardless of intervention. But such is life… and death.

Rates of initial airway success were 90% with the laryngeal tube but a pretty dismal 50% with the endotracheal tube. Yikes!

72-hour survival was 18% with the laryngeal tube and 15% with the endotracheal tube. Rates of favourable neurologic outcome was 7% vs. 5% favouring the laryngeal tube.

What are we to think?

Unfortunately, this study did have some problems. It had poor rates of first pass success with intubation. The pragmatic study design and cluster randomisation introduced noise. They only studied one type of supraglottic airway… i.e. not the LMA.

But in the end, there probably is no compelling reason to push for endotracheal intubation in the field. This may distract from other meaningful interventions such as good quality CPR and rapid defibrillation.

It’s unclear how much of this is externally valid to a well-resourced Emergency Department. A dedicated airway doctor and lots of hands might change our outlook.  Nevertheless, this study does push our focus away from the endotracheal tube in cardiac arrest.

 

Covering:

Wang, HE, Schmicker RH, Daya MR, et al. Effect of a Strategy of Initial Laryngeal Tube Insertion vs. Endotracheal Intubation on 72-Hour Survival in Adults with Out-of-Hospital Cardiac Arrest. JAMA 2018;320(8):769-778. [link to abstract]

Give honey for button battery ingestion? The tale of two anesthetised pigs…

Believe it or not, UpToDate recommends honey as first aid for button battery ingestions.

Perhaps we should look at the evidence.

We know button batteries can cause nasty and sometimes lethal caustic oesophageal injury.

This study was a cadaver and live American Yorkshire piglet model looking at potential pH neutralizing agents prior to definitive endoscopy.

In vitro, they tested the final tissue pH of cadaver oesophagus after installation of various products. They included different kinds of honey, Carafate, apple juice, orange juice, Powerade, Gatorade, maple syrup, simulated saliva and 0.9% sodium chloride control.

In the lab, the honey and Carafate seemed to work the best and underwent further study.

Bring on the live pigs!

9 anaesthetised pigs had a button battery placed in their oesophagus for an hour. (Poor creatures.) Serial irrigations of study solution occurred every ten minutes starting at the five-minute mark.

2 pigs got honey, 3 got Carafate, and 4 got saline control.

On day 7, the unfortunate piglets were euthanized and histology obtained.

Results?

Honey was the big winner! They had much less depth of injury. Half  of the saline piglets had delayed oesophageal rupture.

This little piggy went to market… to get honey! Give honey for button battery ingestion.

Really??!!?

This recommendation is based on TWO anesthetised pigs that got honey.

This is extremely low-quality evidence.

One should only change practice based on such low-quality evidence if the treatment or therapy was considered to be extremely low risk.

Perhaps honey is extremely low risk. But are we certain?

Would care get delayed in finding and administering honey? Does honey impair endoscopy? What about aspiration or honey induced mediastinitis? Will kids get nasal-oesophageal tubes to administer honey? Would we tend to delay endoscopy because they "got the honey?” 

Perhaps risk may be minimal… But changing practice based on two honey glazed pigs??

(ok… I’d give the honey too… I can’t believe I just said that…)

Covering:

Anfang RR, Jatana KR, Linn RL, et al. pH-Neutralizing Esophageal Irritations as a Novel Mitigation Strategy for Button Battery Injury. Laryngoscope 2018 Jun 11. doi: 10.1002/lary.27312. [Link to article]

Clinical Trial of Fluid Infusion Rates for Pediatric DKA

Dr Annoying Bowtie, RACP

Emergency physicians often get criticised for overhydrating children with DKA. “Too much fluids will cause their heads to explode,” as spoken from an annoying bow tie.

But there has never been good quality evidence to prove fluid administration causes cerebral edema. In fact, a study by Glaser etal. in 2001 showed no association between fluids and bad outcomes.

But as there is no definitive RCT, the debate still rages!

Hopefully this clinical trial will put matters to rest.

After 17 years, Dr Nicole Glaser is back! Now teamed up with the PECARN mega-group, they randomised 1255 children with 1389 DKA episodes to one of 4 treatment arms (please see original paper for further details)

• Fast administration of 0.9% normal saline
• Fast administration of 0.45% normal saline
• Slow administration of 0.9% normal saline
• Slow administration of 0.45% normal saline

(Just to give an idea of what is fast vs. slow, a 50 kg child would get an infusion started of 300ml/hour vs. 140ml/hour.)

The primary outcome was a decline in mental status (measured by GCS) during treatment. Secondary outcomes included clinically apparent brain injury during treatment and some measures of memory.

Results?

No difference. Neither the rate of administration nor the sodium chloride content of the IV fluids resulted in bad outcomes. 

So the debate is over?

Unfortunately, no.

98% of the children recruited in this study started out at GCS 14-15.  We know it is the sickest cohort of DKA that develop bad complications. This study was never going to show a difference. The clear majority were going to get better with any reasonable management... regardless of fluid protocols.

What about the child with a pH of 6.9 and GCS 6? Does the rate of fluid administration matter?

Hmmmmmm....

Unfortunately, an adequately powered RCT of severe DKA will never happen. It is simply not feasible. 

Alas, the annoying bow ties will continue...


Covering

Kupperman N, Ghetti S, Schunk J, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med 2018;378:2275-87. [link to original full text article]

Change the guidelines! An RCT of Epinephrine in Out-of-Hospital Cardiac Arrest; the PARAMEDIC2 Trial

Should we still be giving adrenalin in cardiac arrest?

Despite decades of tradition and guidelines, there has never been any good evidence showing adrenalin improves meaningful outcomes.

The PARAMEDIC2 trial was a very well conducted RCT of 8014 patients in the UK with out-of-hospital cardiac arrest. Patients were properly randomised to getting either adrenalin 1mg q3-5 minutes or matching placebo.

Primary outcome in this study was rate of survival at 30 days. But we all know the real outcome of interest is hospital discharge with a favourable neurologic outcome.

Results?

The adrenalin group had more patients with ROSC, transport to hospital and ICU resources. Rate of survival at 30 days was marginally better at 3.2% vs. 2.4%. (NNT 112)

Yes, the rates of survival were abysmal.  But remember the patients included in the study did not respond to initial resuscitative efforts (CPR and defibrillation). They were only enrolled when they got down the pathway requiring adrenalin.

But the real outcome of interest; neurologically intact survival?

No difference.

In the end, adrenalin increases resource utilization and increases survival of the neurologically devastated.

Sounds pretty bad to me. Sounds pretty bad to the consumer groups too.

Will this change the guidelines?

Old habits die hard. But there will never be a trial more definitive than this one. It would have been unethical to start this trial if the authorities (in the UK at least) were not prepared to change practice.

But adrenalin may be worse. Ask yourself; does giving a worthless treatment distract the focus from more important resuscitative efforts? This study didn't address this question but I think I know the answer.

Yes, change the guidelines!

Covering:

Perkins GD, Deakin CD, Quinn T, et al. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. N Engl J Med 2018 Jul 18. doi:10.1056/NEJMoa1806842 [full text]

Paper critiqued at Emergency Tasmania 2018. Special thanks to Dr Mark Reeves, FANZCA and audience for feedback.

Fake News: Intraosseous vascular access is associated with lower survival and neurologic recovery among patients with out-of-hospital cardiac arrest

Prior observational studies have challenged the widely held belief that IO access is just as good as IV. This paper further explored the association between IO access and poor outcomes compared to IV.

The authors performed a secondary analysis of a large trial of patients with out-of-hospital cardiac arrest. They were able to identify patients that got IV vs. IO as their means of access.

They excluded patients who had any failed attempts at either route of vascular access or who had both performed.

The primary outcome was favourable neurologic outcome on hospital discharge (mRS <3 i.e. patients could at least walk without assistance).

Results?

13,155 were included in the analysis. 5% had IO access and 95% had IV (obviously patients were not randomised to this intervention)

For all outcomes, the IV access was far superior. 7.6% of patients with IV access had favourable neurologic outcome vs. 1.5% with IO.

This is astounding! A huge difference… let’s throw away the IO’s!!!

But there is no way this is true.

No amount of fancy statistics can make up for systematic bias and residual confounding that is present in this cohort study. There is clearly a reason why paramedics went directly to IO rather than IV. The IO group was obviously a “sicker” cohort to start with and had worse outcomes.

Not all cardiac arrest is the same. We know those with witnessed arrest, bystander CPR and shockable rhythms do better. There are also many other factors that influence outcomes.

Capturing all potential confounders in a resuscitation is problematic. When under duress, data is hard to measure accurately. In addition, there are always the unknown confounders that go unmeasured and unadjusted. No statistics can truly fix bad or absent data.

Futhermore, what was the magic medicine they used to account for this five fold increase in favorable outcomes? No drugs have really been shown to work in ALS. 

In the same context of “fake news” sometimes bad evidence is worse that no evidence at all. This study has the very unfortunate possibility to mislead and cause harm. At best, it is hypothesis generating for future prospective study.

For now, reject the fake news and keep drilling your IO’s. 

 

Paper critiqued at Emergency Tasmania 2018. Special thanks to Dr Mark Reeves, FANZCA and audience for feedback.

Covering:

Kawano T, Grunau B, Scheuemeyer FX, et al. Intraosseous Vascular Access is Associated with Lower Survival and Neurologic Recover Among Patients with Out-of-Hospital Cardiac Arrest. Ann Emerg Med. 2018;71:588-596.

Association of Preprocedural Fasting with Outcomes of Emergency Department Sedation in Children

Many guidelines still call for patients to be properly fasted prior to ED procedural sedation. Although this is steeped in consensus and tradition, is this really beneficial?

No.

This was a planned secondary analysis of a multicentre prospective cohort study of 6183 children who received parenteral procedural sedation in one of 6 Canadian ED’s.

They compared fasted and non-fasted children with the occurrence of pulmonary aspiration, adverse events, serious adverse events and vomiting.

Results?

Most children were very healthy at baseline. 80% of the procedures were for orthopaedic reductions and laceration repairs. Two thirds of children got ketamine alone. (This is obviously a different cohort from those patients that get treated in the operating theatre.)

How many children were not properly fasted?

About 50% for solids and 5% for liquids.

In the end, there was no association between fasting and any bad outcomes. This is concordant with all of the previous studies on this subject.

Naysayers can complain about the limitations of this study; not huge enough to make definitive claims about safety, ketamine is airway protective, conducted in tertiary centres, and it was not randomised.

The excellent accompanying editorial by Steve Green (Dr Ketamine) shreds these arguments with further evidence. In addition, he emphasises many of the potential harms of fasting.

Even before this study was published, the American Collegeof Emergency Physicians (ACEP) 2014 clinical policy recommended not to delay procedures solely on fasting time.  

Outside the USA, I would imagine most of us have quietly changed our practice anyway and don’t consider fasting to be a mandatory requirement. Perhaps is time to formally change our policies.  

Covering: 

Bhatt M, Johnson DW, Taljaard M, et al. Association of Preprocedural Fasting with Outcomes of Emergency Department Sedation in Children. JAMA Peiatr. 2018. 172(7):678-685. 

Bougie vs Endotracheal Tube with Stylet for ED Intubations: an RCT

“…use of a bougie compared with an endotracheal tube + stylet resulted in significantly higher first-attempt intubation success among patients undergoing emergency endotracheal intubation.”

Should we all go bougie first?

As is often the case, the devil is in the details…

This was a single centre clinical trial randomised 757 adult patients to the two arms (bougie vs. stylet) using mostly a C-MAC Macintosh blade.

The primary outcome was first-attempt success in patients with at least one difficult airway characteristics (obesity, short neck, cervical spine immobilisation etc.)

They had a ridiculously high 96% first attempt success rate with the bougie but only an 82% with the stylet. (To put this in perspective, the first attempt success rate in the ANZEDAR registry was 84%)

Before you jump on the gum elastic bougie train, consider a few things.

This study was conducted in an ED where the tradition was to use a bougie first. They would have obviously been more comfortable with this technique and the stylet was new to them.

The vast majority of the intubations were done by less experienced PGY 2 - 4 emergency residents and fellows. Emergency medicine faculty only performed 3% of the procedures.

The incidence of hypoxemia (13% vs. 14%) did not differ between the groups. This is a more relevant patient oriented outcome. This study did not report any patient harms from the lower first-attempt success of the stylet (but to be fair, was not powered for safety).

In the end, I don’t think this study will be overly practice changing. Most clinicians will stick with what they know best. But a 96% first pass success rate is extremely high and hard to ignore.

Covering:

Driver, BE, Prekker ME, Klein LR, et al. Effect of Use of a Bougie vs Endotracheal Tube adn Stylet of First-Attempt Intbuation Success Among Patients with Difficult Airways Undergoing Intubation; A Randomized Clinical Trial. JAMA. 2018;319(21):2179-2189.

Early application of continuous femoral nerve block for neck of femur fractures: an RCT

Many patients with neck of femur fractures get some form of a nerve block in the Emergency Department. This is most often a single injection and wears off in several hours. Would a continuous block via infusion be better?

This UK single centre trial randomised patients to standard care vs. a continuous infusion of 0.2% ropivacaine at 5ml/hour for 48 hours. The medication was delivered by perineural catheter placed by experienced anaesthesia doctors.

Included patients had to be >70 years old, without cognitive impairment, live at home and independently mobilise. Yikes! This obviously limited the number of eligible patients and made this study less feasible to undertake.

The two primary outcomes were the Cumulated Ambulation Score and Dynamic Pain Score score over three days. Whatever those are...

111 patients with fractures underwent analysis.

It is no surprise no difference was found. (Other than a secondary outcome of improved pain at rest) With these small numbers, the researchers had low statistical power and could only hope to find a big difference. In addition, there were several issues that may have drawn the conclusion to the null hypothesis.

Many questions remain; did they use the right dose, did they do the correct block, were the primary outcome scores appropriate & relevant, etc.

In the end, the jury is still out. Despite the negative conclusion, the research question really remains unanswered. If there was a longer delay to theatre, one would hope a continuous infusion would be better than standard care… but who knows, there still is clinical equipois

 

Covering:

Rowlands M, van de Walt G, Bradley J, et al. Femoral Nerve Block Intervention in Neck of Femur Fracture (FINOF): a randomised controlled trial. MJ Open 2018;8:e019650. doi: 10.1136/bmjopen-2017-019650

Aromatherapy for nausea? Inhaled isopropyl alcohol vs oral ondansetron for nausea in the ED; an RCT

A patient with nausea presents to your ED...

A busy triage nurse to hands a patient an isopropyl alcohol pad and says, “sniff on this.” 

Nausea magically disappears.

Believe it or not, this is not a new concept. The use of aromatherapy to reduce post-operative nausea & vomiting has been studied for decades. But it has only just just recently popped its head (nose?) into the ED.

This was a very well conducted RCT that enrolled 122 young adults with a chief complaint of nausea & vomiting >3 on a numerical rating scale. They excluded patients who had already got IV cannulation and prior antiemetic therapy.

They were randomised to one of three arms:

• Inhaled isopropyl alcohol alone (with oral placebo)
• Ondansetron alone (with inhaled saline placebo)
• Both inhaled isopropyl alcohol and ondansetron

They were told to sniff on the isopropyl alcohol pad as much as they like and could get a new/fresh one about every 10 minutes.

The primary outcome was reduction in nausea as measured on a visual analog scale (VAS) at 30 minutes.

Results?

Both arms using isopropyl alcohol had reductions in nausea by about 30mm. The ondansetron alone arm only had reduction by 9mm. This was statistically significant and the authors made the expected conclusions.

Despite elegant methods, this study did have some important limitations.

• It is difficult to blind alcohol. (but you can get blind with alcohol… sorry). This could have introduced bias.
• Persistence and duration of effect is difficult to gage. What about the repeat customer who states, “you’re not going to try to get me to sniff on that alcohol pad again?”
• These were low risk patients who didn’t need IV’s.
• Small studies reporting large treatment effect are often disproven

In the discussion, the authors state the mechanism of action remains unclear but could be “related to olfactory distraction.” Perhaps a nausea voodoo dance would have met with the same effect? Who knows…

What should we conclude?

Inhaled isopropyl alcohol might help some low risk patients in the ED with nausea. It is very unlikely to cause harm. But I still like the idea of a voodoo macarena.

Covering:

April MD, Oliver JJ, Davis WT, et al. Aromatherapy Versus Oral Ondansetron for Antiemetic Therapy Among Adult Emergency Department Patients: A Randomized Controlled Trial. Ann Emerg Med 2018 Feb 17. pii: S0196-0644(18)30029-5. doi: 10.1016/j.annemergmed.2018.01.016. [Epub ahead of print]

  

Unsuspected Critical Illness Among ED Patients Presenting for Acute Alcohol Intoxication

During my ED training, I was taught the maxim; nobody is ever "just drunk." Of course, this was meant to emphasize caution in recklessly labelling patients as such. Some may have subdurals, infections or other bad illness.

These authors attempted to quantify the proportion of patients who were thought to be just drunk but who ended up requiring critical care resources. In addition, they sought to find clinical features that might be associated with the need for these resources.

Enter Minneapolis, Minnesota. (Evidently, a lot of people resort to drinking here.) Their ED has a “dedicated intoxication unit” where these presumed low risk patients are grouped.

Over five years, they put over 35,000 patients through this area. One patient was readmitted 227 times!

Of these low risk patients, what proportion of them ended up requiring critical care resources?

1%

Abnormal vital signs, hypoglycaemia and parenteral sedation were associated with this outcome. This has face validity i.e. makes sense.

However, this study had substantial limitations.

It was a retrospective review of EHR data which we know to be rather unreliable. It also rested on subjectivity in the definition of their study population and other assumptions.

At best the 1% estimate is a ballpark figure.

But the accuracy doesn’t matter. The overall message has not changed; a small proportion of patients who you suspect to be “just drunk” will really have something bad. Pay attention to vital signs and overall be cautious.

Where have I heard this before?

Covering:

Klein LR, Cole JB, Driver BE, et al. Unsuspected CriticalIllness Among Emergency Department Patients Presenting for Acute AlcoholIntoxication. Ann Emerg Med 2018;71:279-288.

Haloperidol for cannabinoid hyperemesis syndrome; why not…

It seems “Vitamin H” is pretty good for lots of things.

Add it to the list for cannabinoid hyperemesis syndrome (CHS)!

Ok, this “study” if far from high science (forgive the pun). It’s a retrospective chart review reporting a case series of 4 with lots of limitations.

All included patients were thought to have CHS. Perhaps they were diagnosed in the hot shower? They seemed to all have refractory vomiting until they were given haloperidol 5mg IV.

The authors provide some physiologic reasons why this might be efficacious and appropriately temper their conclusion by stating their success “warrants further investigation.”

In summary, this study is arguably a level of evidence just above anecdote. But who cares… did I say I love vitamin H?

Covering:

Witsil JC, Mycyk MB. Haloperidol, A Novel Treatment for Cannabinoid Hyperemesis Syndrome. Am J Therap. 2017;24:e64-7.

Intralipid emulsion treatment as an antidote in lipophilic drug intoxications- Worst paper of the decade?

This case series from Turkey published in the American Journal of Emergency Medicine is a fabulous example of intoxicated peer review (perhaps they needed the intralipid?)

It is awful from the first sentence.

Intravenous lipid emulsion (ILE) is a lifesaving treatment of lipophilic drug intoxications.

Of course, this is not referenced.  

There is no definitive high-quality evidence demonstrating a reduction in mortality from intralipid. There best evidence is mostly case series. (Although I did find an RCT of 34 cats poisoned by permethrin!)

So, getting past the first sentence is problematic… but I’ll continue.

The authors report a case series of 10 patients admitted to their ED who had allegedly taken overdoses of mostly amitriptyline but also some metoprolol, nifedipine, quetiapine, lamotrigine, sertraline, fluoxetine, alprazolam and of course Bonsai.

Bonsai?

This term is not explained in the manuscript. Gut if you google Bonsai, you get some beautiful images of small trees. If you dig a bit further, you come to discover it is a popular synthetic cannabinoid in Turkey. Who would have known?

Another tangent… back to the paper.

The authors describe each patient in some detail, but don’t really mention if any standard treatment was given. It looks like only one of the patients with TCA overdose ever got sodium bicarbonate except one who (I think) died.

She did not answer cardiopulmonary resuscitation, and she was admitted as exitus.

What should we conclude?

In the end they gave intralipid to 10 patients who may or may not have needed it. They may or may not have derived benefit or harm from this therapy. We’re not sure…

The authors conclude

According to these results, it was found that ILE treatment is a lifesaving agent in lipophilic drug intoxications and can be used in unconscious patients who have cardiac and/or neurologic symptoms, but no history of a specific drug ingestion.

I conclude the authors and the peer reviewers were probably on the bonsai… and I’m not talking small trees.

Covering:

Cevik SE, Tasyurek T, Guneysel O. Intralipid emulsion treatment as an antidote in lipophilic drug intoxications. Am J Emerg Med 2014;32:1103-1108.

Predatory journals recruit fake editor

We live in an age of digital scams. Not a day goes past when we aren’t tempted by emails or other messages from nefarious individuals attempting to extract money. Why should academic journals be any different?

A couple of decades ago, it was challenging to manage an academic journal; snail mail, printing costs, office rental, advertisers etc. The digital age and the open-access movement have made it such that anyone with some decent IT skills can create an official looking scientific journal in their attic.

The opening of this study does a great job of summing up the current state of play.

Thousands of academic journals do not aspire to quality. They exist primarily to extract fees from authors. These 'predatory' journals exhibit questionable marketing schemes, follow lax or non-existent peer-review procedures and fail to provide scientific rigour or transparency.

Crucial to the quality of an academic journal is its editors. They should have a strong research background, been involved with peer review and ultimately qualified for the job.

These researchers from Poland concocted a sting to see if a “dismally inadequate” scientist would be invited to be an editor. They created the profile of “Anna O. Szust.” (Oszust is the Polish word for “a fraud.”)

Her CV and application was sent to 360 journals. They were sent to one of three directories; the JCR (journals with an official impact factor), the DOAJ (Director of Open Access Journals), and finally to a group thought to be predatory journals (from Beall’s list).

Results?

None of the JCR journals accepted the application. By comparison, 40 predatory and 8 DOAJ journals appointed her as editor. There were some hilarious and sometimes disturbing responses from the journals. I strongly encourage people to read the original manuscript at this link

What should we take away from this?

• There are over 10,000 predatory journals on the planet that do not exist for the advancement of scientific knowledge. They are fraudulent and have been created to make money.
• Be VERY sceptical of papers published in predatory journals. They were likely accepted not on their merit & methodologic rigor but rather their ability to pay a fee.
• If you are a researcher looking to publish a study, do your homework. Ensure that the journals you engage are known to be reputable.

Covering:

Sorokowski P, Kulczycki E, Sorokowska A, Pisanski K. Predatroy Journals recruit fake editor. Nature 2017;543(7646):481-483. doi: 10.1038/543481a

  

Severe Hyperkalemia: The ECG can risk stratify for short term adverse events?

This may seem rather obvious, but these researchers found little formal evidence to support this notion. As such, they performed this decent but small study.

From their laboratory database, they were able to pull the records of all adult patients over a few years that had a potassium of >6.5 mEq/L. They included patients that had ECG’s done within one hour of the blood test and had no treatment for hyperkalemia.

Two blinded emergency specialists reviewed the ECG’s to record the rate, rhythm, peaked T’s, PR intervals and QRS duration.  

They defined short term adverse events as symptomatic bradycardia, VT, VF, CPR and/or death within 6 hours of the ECG. Relative risk was calculated to determine the association between the ECG changes and adverse events.

Results?

They found 28 short term adverse events in 188 patients with severe hyperkalemia. Most of these adverse events (22) were bradycardia. There were 4 deaths, and 2 episodes each of VT & CPR.

An increased likelihood for adverse events were found for:

• Bradycardia RR 12.29 
• QRS prolongation RR 4.47 
• Junctional rhythm RR 7.46

There was no statistically significant correlation between isolated peaked T’s and short term adverse events. But all adverse events were preceded by ECG abnormalities.

So, it looks like bradycardia is the most powerful predictor?

Not so fast. (Get it… not so fast…)

In this study, bradycardia was both a predictor and outcome variable. Therefore, it comes as no surprise that bradycardia is associated with bradycardia. I’m not sure what to do with this…

The biggest limitation of this study was the small numbers of meaningful adverse events. As such there are wide confidence intervals. No study is really “definitive” and this research would officially be far from this standard.

Nevertheless, what are we to conclude?

An ugly ECG in the setting of severe hyperkalemia is a bad thing. But don't go bananas about isolated peaked T’s (in the short term.)

Ok… this is not earth shattering, but does help fill in the research gap.

Covering:

Durfey N, Lehnhof B, Bergeson A, et al. Severe Hyperkalemia: Can the Electrocardiogram Stratify for Short-term Adverse Events? West J Emerg Med. 2017;18(5)963-71.

Noninvasive Cardiac Testing vs. Clinical Evaluation Alone in Acute Chest Pain: Less is more

These researchers from St. Louis wanted to see if “nothing” was a good diagnostic strategy for the evaluation of low risk acute chest pain.

Ok… not really nothing. But they hypothesised that non-invasive testing (i.e. CTCA, treadmill, stress echo, SPECT) would provide no benefit beyond the typical evaluation using history, physical examination, ECG and troponins.

To try to answer this research question, they got their hands on de-identified data from the Boston led ROMICAT II study. This was a 1000 patient RCT looking at CTCA vs. standard practice in the evaluation of chest pain performed in 9 ED’s in the USA. This robust prospectively collected data was subsequently analysed by these new researchers using a different angle.

They found that 118 (12%) of the 1000 patients did not undergo non-invasive stress testing and they had better outcomes than those who got testing. Specifically, they had shorter lengths of stay, less downstream testing, less radiation exposure and less cost with no change in clinical outcomes.

Apparently there no advantage to performing these non-invasive tests. Less is more.

I love this message.

We never get congratulated for the tests we do not order. Perhaps now is the time for a cultural shift that emphasises the potential harms of these non-specific tests; radiation, cost, time, and most of all overdiagnosis. Let’s clap our hands together for doing nothing!

But unfortunately, my evidence-based bones just can’t completely embrace the conclusions of this study.

This subanalysis was not an RCT. It was up to the physician judgement as to who got non-invasive testing in the usual care arm. It is very likely that the cohort of patients that got nothing were at less risk for bad outcomes. (To be fair, they did try an adjusted analysis, but these are always fraught with problems.)

What are we to think?

It is likely true that over zealous non-invasive testing in low risk patients with chest pain is potentially harmful. A targeted approach for higher risk patients is probably better.

In the end, this study has raised a decent hypothesis for prospectively testing in a proper RCT. If you are a patient with chest pain, perhaps nothing can be a real cool hand.

Covering:

Reinhardt SW, Lin CJ, Novak E, et al. Non-invasive Cardiac Testing vs Clinical Evaluation Alone in Acute Chest Pain. JAMA Intern Med. 2018;178(2):212-19.