Saturday, 29 June 2019

Buddy taping vs. Plaster for Neck of 5th Metacarpal (Boxer’s) Fractures


I love saving time in the ED. Much of this can come from avoiding procedures that don’t provide benefit to the patient.

Should we dump plaster casting for Boxer’s fractures?

This was an RCT from Queensland, Australia. Evidently, they do a lot of punching in Queensland.

They included patients between 18-70 years old, simple closed fractures without rotation and an angulation of less than 70 degrees. Yes, you read that correctly, they tolerated up to 70 degrees.

126 patients were randomised to buddy taping or plaster cast immobilisation.

The primary outcome was hand function at 12 weeks using the quickDASHquestionnaire. They also looked at pain, satisfaction, return to work or sport, and quality of life.

As expected with this cohort of patients, there were quite a few lost to follow up and 97 patients underwent intention to treat analysis.

Results?

At twelve weeks, both groups were the same on the quickDASH questionnaire. Those randomised to buddy taping returned to work earlier than those in the plaster group. Other measures were also similar. Ultimate fracture angle at follow up was similar at about 30 degrees.

The authors conclude, “we advocate a minimal intervention such as buddy taping for uncomplicated boxer’s fractures.”

However, there were several limitations to this study. It was not blinded which could have introduced bias. The study design should have really been a non-inferiority trial.

But there may have been a bigger issue.

The quality of the conclusion is only as good as the validity of the primary outcome measure. I’m not convinced that the quickDASH questionnaire is robust enough to reliably measure the big picture. In addition, capture of data may not have been the most discerning; thus pushing the conclusions towards the null hypothesis.

In the end, our referring doctors (ortho, plastics, or hand specialists) are going to dictate their preferences to us. Given the overall quality of the evidence, I don’t have a problem doing what they like.

My local hand specialists have asked us to continue with plaster immobilisation. They feel you can get a better reduction using the Jahss technique, have less initial pain, less narcotic use and possibly require less operative reduction. Of course, this is an eminence-based recommendation. If I moved to Queensland, I will probably be buddy taping... and watching my back. 


Covering:

Pellatt R, Fomin I, Pienaar C, et al. Is Buddy Taping as Effective as Plaster Immobilization for Adults With an Uncomplicated Neck of Fifth Metacarpal Fracture? A Randomized Controlled Trial. Ann Emergency Med. 2019; 74:22-97. [link to article]

Early vs. Delayed Cardioversion in Recent onset of Atrial Fibrillation


We know from prior studies that acute atrial fibrillation will frequently spontaneously revert. So, when patients arrive to the ED, which is better? Immediate cardioversion or a “wait-and-see" approach.

To attempt to answer this question, these Dutch investigators conducted a multicentre randomised noninferiority trial. They enrolled stable patients with recent onset (less than 36 hours) to early cardioversion vs. wait-and-see.

The wait-and-see approach involved giving rate control medications and eventual cardioversion if the AF was not resolved by 48 hours.  

The primary endpoint was the presence of sinus rhythm at 4 weeks. However, there were other important secondary measures they captured such as rate of spontaneous resolution, resource utilisation, recurrence of AF, safety etc.

Results?

By 4 weeks both groups were about the same and within their prespecified non-inferiority margin. Sinus rhythm was present in 91% of the delayed group vs. 94%.

So, it doesn’t matter?

Perhaps it does… In the delayed group, the rate of spontaneous resolution was 70%! This begs the question, why do we bother with such an early aggressive approach to AF when it very often spontaneously resolves.  Can we limit the potential harms of antiarrhythmic medications and procedural sedations and let nature take its course?

These findings are consistent with prior researchDoyle B et al. Heck, I may not ever get published in the NEJM but at least I have been referenced! 

What do I do?

This is the time for shared decision making. Pull up a chair and have a chat to the patient.  It also depends on how symptomatic the patient is, their prior experiences, rates of recurrence, and dare I say, a busy department.

Quick… don’t just do something, stand there!


Covering:

Pluymaekers N, Crazy Dutch Name, Dudink J, Luermans J, et al. Early or Delayed Cardioversion in Recent-Onset of Atrial Fibrillation. N Engl J Med 2019;380:1499-1508. [link to article]


Thrombolysis guided by perfusion imaging up to 9 hours after onset of stroke: how fragile can we be?


The biggest, baddest controversy in Emergency Medicine just got worse.

Yes, it’s stroke lysis.

This multicentre RCT enrolled adult patients in whom alteplase or placebo could be given between 4.5 to 9 hours after onset of stroke or on awakening with stroke symptoms. A prerequisite for inclusion was a perfusion deficit (area of ischemic but not infarcted brain) on CT or MRI.

The primary outcome was a score of 0-1 on a modified Rankin scale (mRS) adjusted for age and baseline severity of stroke. Of course, they looked at many secondary outcomes including the classic ordinal shift analysis and some safety measures.

They estimated a sample size of 400 patients would be needed in order to have 80% to detect a difference of 15% in the primary outcome.

Recruitment was slow going. They only enrolled 225 patients over 8 years in in 28 centres! That’s about one patient per centre per year! Yikes. No wonder they called it quits early. They claimed the WAKE-UP trial published in May 2018 caused them to lose clinical equipoise and they terminated early. I think they probably had enough anyway…

Results?

40 (35%) patients in the alteplase group were mRS 0-1 vs. 33 (29.5%) in the placebo group (adjusted risk ratio, 1.44 95% confidence interval 1.01 to 2.06; P=0.04). Symptomatic ICH was 6% vs. 1%.

Thrombolysis is a winner!??!!

Unfortunately, it is not so clear.

There was no statistical difference in the primary outcome when they used their originally proposed logistic regression modelling rather than a different method introduced during recruitment. The unadjusted analysis; no difference. There was no difference in the ordinal shift analysis (which ironically was touted as the saviour of IST-3). But most of all, the results are just plain fragile.

Fragile?

The fragility index was less than one. Put another way, if one less patient in the alteplase group did not meet the primary outcome, the trial would have been negative. This seems far from a definitive trial.

The authors claim that “further trials of thrombolysis in this time window are required.” This seems rather contradictory when they claim to have stopped their trial due to lack of clinical equipoise.

What to think?

If I was calling the shots, I would not extend my window. But at the same time, others may interpret this study differently. 

However, much of this might be a storm in a teacup. The vast majority of patients in this window derive neither harm nor benefit from thrombolysis (NNT 17 if you believe the results). In addition, clot retrieval is all the rage now.  


Covering:

Ma H, Campbell BCV, Parsons MW, et al. Thrombolysis Guided by Perfusion Imaging up to 9 Hours after Onset of Stroke. N Eng J Med 2019;380:1795-803.[link to article]





Wednesday, 24 April 2019

Changing target temperature from 33 to 36 in the ICU management of OHCA: a before and after study


I’ve always been skeptical of the original studies claiming efficacy of therapeutic hypothermia for out-of-hospital cardiac arrest (OHCA).

Image result for the alfred hospital
Two small studies published in 2002 demonstrated a profound treatment effect that caused most of the world to change practice.

Anytime you see a small RCT claiming results that are too good to be true, you need to think that the results are exactly that. Medical reversal is common and much of what is published in the medical literature turns out to be wrong.

Along came Nielsen’s study of Targeted Temperature Management (TTM) in 2013 and most of us reversed back to normothermia. However, several studies have indicated that it is difficult to keep patients at this warmer temperature and there are concerns about fever & possible worse outcomes.
   
The Alfred Hospital in Melbourne conducted a retrospective before and after study after they changed their targeted temperature from 33 to 36 degrees. They describe their experience and try to compare outcomes.

Over a 30-month period they had 76 patients with OHCA due to ventricular fibrillation. There were 24 in the before group and 52 in the after.

After the TTM change, less patients got active cooling (100% vs. 70%), less time was spent at the target temperature (87% vs. 50%) and fever rates went up from zero to 19%.

The authors compare the before and after outcomes and state there was a trend towards better outcomes with the before group.

Fortunately, the conclusion in the manuscript is appropriately measured:

After the change from a TTM target of 33 to 36 we report low compliance with target temperature, higher rates of fever, and a trend towards clinical worsening in patient outcomes. Hospitals adopting the 36 target temperature need to be aware that this target may not be easy to achieve and requires adequate sedation and muscle relaxant to avoid fever.

I would go a step further.

A small retrospective before and after study can be rather problematic. With such small numbers it is very likely the groups were different; akin to comparing apples to oranges. No amount of adjustment for confounding factors will fix this.

So, I don’t think we should be taking anything away from the trend toward benefit. Much better-quality evidence from the TTM trial shows there is none.

There are also some potential harms noted in this study. They note patients in the 33 degree arm were intubated a full day longer, experienced more shivering, bleeding requiring transfusion and pneumonia.

What’s the take home message?

Overall this was a small study in a single centre that is poor quality evidence to inform practice. It demonstrates it is more difficult to keep patients at a higher target temperature. Whether this has any impact on real patient outcomes is not known but I think unlikely.


Covering:

Bray J, Stub D, Bloom JE, et al. Changing target temperature from 33 to 36 degrees in the ICU management of out-of-hospital cardiac arrest: A before and after study. Resus 2017;113:39-43. [link to article]




Coronary Angiography after Cardiac Arrest without STEMI


Well regarded guidelines recommend immediate coronary angiography in patients who present with STEMI and cardiac arrest. But what about those that don’t have STEMI? Should they also go to the cath lab?

This RCT conducted in 19 centres in the Netherlands attempted to answer this question.

These researchers randomised 552 patients to immediate vs. delayed angiography.

The inclusion criteria were comatose survivors of out-of-hospital cardiac arrest (OHCA) that had shockable rhythms and return of spontaneous circulation. Patients were excluded if they had STEMI in the ED, shock, or an obvious non-cardiac cause of arrest.

The study was powered to detect a whopping 40% difference between the groups. Of course, it is quite ambitious to think immediate angiography would be so efficacious. Therefore, the study had an “adaptive design” that allowed for an increase in sample size if they detected a trend towards benefit during an interim analysis of the first 400 patients. (Kinda sounds like cheating… but I get it)

Results?

Those Dutch know how to conduct a study (must be something in the Heineken).

Adherence to protocol was fantastic. Median time to angiography was about 45 minutes in the immediate group and about 5 days in the delayed.

Acute thrombotic occlusion of a coronary vessel was found in a small minority of patients. Only 3.4% in the immediate and vs. 7.6% in the delayed. As such PCI and CABG was performed less than a third of the time.

I think you know where this is going… this was a negative study.

At 90 days 64% of the immediate group and 67% of the delayed group were alive.
So what should we conclude?

I think it is safe to say that we should not send all patients with OHCA without STEMI to the cath lab.

But one of the major challenges with evidence-based medicine is extrapolating the results of a study to the individual patient in front of us. 

What about the patient with some degree of hemodynamic or electrical instability? Or what about lots of dynamic ST and T wave changes on the ECG (of course this could also come from intracranial catastrophe)? What if they just smell like a coronary occlusion?

In summary, don’t send all patients to the cath lab. But I think we should still consider it on an individual basis. Now back to my Grolsch...


Covering:

Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med 2019;380:1397-1407. [link to article]


Effect of a Resuscitation Strategy Using Capillary Refill Time vs. Lactate in Patients with Septic Shock: The ANDROMEDA-SHOCK Trial


Related image


Can capillary refill time (CRT) replace serum lactate as a resuscitation target in septic shock?

Leave it to the South Americans to try to figure this one out… ¡Vamonos Amigos!

This was an RCT conducted in 28 ICU’s in Chile, Argentina, Uruguay, Ecuador and Colombia. (¿Valididad externa?)

424 adult patients were randomised to a resuscitation protocol aimed at either normalising CRT vs. normalising or decreasing lactate levels.

The study was powered to detect an absolute reduction of 28-day mortality by 15%. Of course, this is crazy… nothing would be expected to work this well. As such, this study was always at a high risk of a type II error (i.e. not finding a difference when one truly exists). ¿Vamonos?

Out of interest, the CRT involved training and standardisation as follows

...CRT was measured by applying firm pressure to the ventral surface of the right index finger distal phalanx with a glass microscope slide. The pressure increased until the skin was blank and then maintained for 10 seconds. The time for return of the normal skin color was registered with a chronometer, and refill time greater than 3 seconds was defined as abnormal.

Once again, the primary outcome was all cause mortality at 28 days. There were lots of prespecified secondary outcome measures.

¿Resultados?

By day 28, a total of 35% in the CRT group vs 43 % in the lactate group had died (hazard ratio, 0.75 [95% IC, 0.55 to 1.02]; P=.06; risk difference, -8.5% [95% CI, -18.2% to 1.2%]

P value was 0.06. Therefore, a negative study…

This highlights the silly dichotomous nature that we attribute to P values. Less than 0.05 means “something important” whereas above 0.05 means nothing… totalmente loco amigo.

0.05 has always been a single arbitrary cut-off of probability. It tells us nothing about the effect size, whether a study was powered correctly or whether the outcomes are clinically important. It doesn’t tell us about bias, confounding, reverse causality or if the correct statistical analysis was used. The reverence we hold to P values must stop!

In the end, this study produces quite a bit of noise in favour of capillary refill time as a target for resuscitation. But perhaps it highlights the lack of utility of lactate. To be fair, we would never use a single marker in isolation. So perhaps this is all a bit silly… almost as silly as the title, ANDROMEDA-SHOCK trial.

¡OlĂ©!


Covering

Hernandez G, Ospina-Tascon G Damiani LP, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients with Septic Shock: The ANDROMEDA-SHOCK Randomized Clinical Trial. JAMA. 2019;321:654-64. [link to article]

Tuesday, 23 April 2019

Bag-Mask Ventilation during Tracheal Intubation of Critically Ill Adults: A tack in the coffin of RSI


Related image


“Rapid sequence induction” is intended to decrease pulmonary aspiration during endotracheal intubation. Classily it requires a period of apnoea during which time we wait for the paralytic agent to take effect. No breaths are given for fear of insufflating the stomach and increasing the risk of aspiration.

But what if this period of apnoea is worse that the theoretical risk of aspiration? Herein lies a decent research question.

But spoiler… this was not fully addressed with this study.

This RCT in 7 ICU’s in the USA randomised 401 adult patients to BVM or no ventilation between induction and laryngoscopy. They excluded patients at high risk for aspiration (i.e. ongoing emesis, bowel obstruction, haematemesis etc.)

The primary outcome was lowest oxygen saturation. They also looked at many secondary outcomes and rates of pulmonary aspiration.

Results?

Those that got BVM had lower rates of hypoxemia. Rates of severe hypoxemia (sats less than 80%) were 11% in the BVM group but 23% in the no-ventilation group. This is hardly surprising but ultimately is not a patient-oriented outcome.

As expected, the incidence of pulmonary aspiration was quite low. It was noted in 5 (2.5%) patients in the BVM group vs. 8 (4%) in the apnoea group. With such small numbers, obviously this is not statistically significant.

The authors state the following:

Given the low incidence of operator-reported aspiration during tracheal intubation of critically ill adults, determining whether bag-mask ventilation increases the relative risk of aspiration by 50% would require a trial enrolling approximately 4000 patients.

Yikes! 

I don’t think we’ll see this trial anytime soon.

There were a number of limitations in this trial. It was performed only in ICU’s, high risk patients were excluded, no blinding, the gold standard for aspiration is problematic, etc.

Do we have an answer? Is RSI dead?

Not really. But perhaps this is a tack (but not a nail) in the coffin of RSI.

Ultimately, I think we can use our common sense and cater to the individual patient. Those that are hypoxic are probably fine to have some BVM. Hold off on those where oxygenation is ok and/or high risk for aspiration.


Covering:

Casey JD, Janz DR, Russell DW, et al. Bag-Mask Ventilation during Tracheal Intubation of Critically Ill Adults. N Engl J Med 2019;380:811-21. [link to article]



Tuesday, 26 February 2019

Does POCUS improve outcomes in ED patients with undifferentiated hypotension? Hocus pocus; how the SHoC-ED trial got it so wrong.


This study recruited a convenience sample of patients from six ED’s with undifferentiated hypotension. They were randomised to early point-of-care ultrasound (POCUS) vs standard care without POCUS.

The primary outcome measure was a 10% reduction in mortality. Secondary outcomes included length of stay, rates of CT scanning, use of inotropes, fluid administration, etc.

In the end, they could not find any difference. POCUS doesn’t work for undifferentiated hypotension!?

So how did this study get it so wrong?

Two primary reasons.

First, their primary outcome measure was wrong. It is preposterous to expect this diagnostic test would result in a 10% reduction in mortality. But I won’t belabour this point…

Second, and much more important, they excluded patients who stood the most to benefit from ultrasound. This merits further explanation.

“… they excluded patients who stood the most to benefit from ultrasound.”

They excluded patients who were pregnant as they thought it would be unethical to miss an early diagnosis of ruptured ectopic. They also excluded patients with trauma or suspected ruptured AAA for similar reasons.

They only included only an extraordinarily selected group of non-consecutive patients. Only 273 patients were enrolled from 6 ED’s over 4 years! That’s just over one patient per month per ED. Obviously most patients with hypotension were not included.

Even in “undifferentiated hypotension” there are still varying degrees of working diagnosis and clinical suspicion.

If I was a doctor considering enrolling a patient with undifferentiated hypotension in this study, would I be comfortable if my working diagnosis included patients at risk for pericardial tamponade, tension pneumothorax, or massive pulmonary embolism? Would I enrol them if I really wanted a good look at their lungs or IVC?

Put simply; would I enrol them if I really thought the early ultrasound was needed?

Of course not.

One only needs to look at their recruitment to see this ring true. About half had sepsis. Only about 4% had a diagnosis where early ultrasound could have had made a substantial benefit.

To say that I am annoyed by this study is an understatement. It is misleading and may result in substantial harm when it is bound to be misinterpreted. This study is hocus pocus!

I believe early POCUS for undifferentiated hypotension has face validity. It is one of the first things I do as it narrows the differential diagnosis and potentially guides treatment. It is quick and non-invasive. On occasion, it picks up a “can’t miss” diagnosis and saves lives. Misleading studies are not going to change this.


Covering:

Atkinson PR, Milne J, Diegelmann L, et al. Does Point-of-Care Ultrasound Improve Clinical Outcomes in Emergency Department Patients with Undifferentiated Hypotension? An International Randomized Controlled Trial From the SHoC-ED Investigators. Ann Emerg Med 2018;72:478-489. [link to abstract]

Monday, 25 February 2019

Effect of Cricoid Pressure Compared with a Sham Procedure in the RSI of Anaesthesia: Old habits are dying hard


The use of cricoid pressure to prevent aspiration during intubation was never based on high quality evidence. Recently, it has been dying a slow death with many ED doctors abandoning this practice. But there still is controversy, and our anaesthetics counterparts are having trouble letting go.

Pulmonary aspiration during endotracheal intubation is exceedingly uncommon. The study of rare events requires enrolment of lots of patients to have the statistical power to come to an answer. As such it has not been feasible to get high quality RCT’s to inform practice.

These authors tried… but we are still not totally clear.

This was a double blind RCT non-inferiority trial conducted in 10 academic centres in France. 

Patients undergoing RSI in the operating theatre (not the ED) were randomised to proper cricoid vs. sham cricoid (hand was put in place, but no pressure applied).

The primary endpoint was aspiration and they also looked at several secondary outcomes.

They considered sham to be “non-inferior” if the incidence of aspiration was not more than 50% higher (i.e. relative risk of 1.5).

Results?

After enrolling 3472 patients they only had 10 cases of aspiration in the cricoid group vs. 9 in the sham. This gives a relative risk of 0.9.

Sham wins!?!

Not officially…

With such tiny numbers of aspiration, it is no surprise that the confidence intervals are rather wide. The 95% confidence interval was 0.33-2.38. This is greater than the non-inferiority margin of 1.5 and as such this is officially a negative study… i.e. they failed to demonstrate the non-inferiority of the sham procedure in preventing pulmonary aspiration.

From a purist EBM standpoint this may be a negative study, but many interpret this as another nail in the coffin for cricoid pressure. Outcomes were rare regardless. A look at the secondary outcomes shows worse laryngoscopic view and greater time to intubate with cricoid. There was really nothing to suggest any benefit from cricoid pressure.


If someone happened to “invent” cricoid pressure today, we would never take it up. But tradition, culture and "eminence-based" medicine is hard to kill.


Unfortunately, this study has the possibility of being misleading. Years from now, I imagine it will be casually mentioned as evidence in favour of cricoid pressure. This is precisely why it is good to dissect these papers, take the pressure off (pun intended) and to find the hidden truth.



Covering:

Birenbaum A, Hajage D, Roche S, et al. Effect of Cricoid Pressure Compared with a Sham-Procedure in the Rapid Sequence Induction of Anesthesia. The IRIS Randomized Clinical Trial. Jama Surg 2019;154:9-17. [link to article]




Saturday, 23 February 2019

ED Discharge of Patients with Pulmonary Embolism; Marketing Rivaroxaban

Do PE patients discharged from the ED on rivaroxaban have a shorter length stay than those admitted to hospital?

Yes, you read the question correctly…

This was essentially the aim of a recent study published in Academic Emergency Medicine.

This RCT conducted at 35 hospitals (yes 35… but they planned on 57!) enrolled 114 subjects randomised to early discharge on rivaroxaban vs. “standard of care” (generally admission to hospital). Primary outcome was length of stay.

It turns out the early discharge had a much shorter length of stay at 4.8 hours vs 33 hours for standard care.

Huh?

Why would anyone conduct an RCT to answer such an obvious research question (Notwithstanding, it is considered unethical to conduct an RCT without clinical equipoise… oh well…)

Answer?

Marketing.

All 11 of the authors disclosed conflict of interest in taking money from Janssen. Guess what drug they make…

Two of the authors were employed by the drug company and declared that they were involved in the study concept, design, analysis, interpretation and revision of the manuscript.

One other important aspect may have slipped your attention.

Was this a “seeding trial?”

Huh?

As per Sax HC & Rennie D, Seeding Trials: Just Say “No” (Ann Intern Med. 2008;149:279-280)

Why would a drug company go to the expense and bother of conducting a trial involving hundreds of practitioners- each recruiting a few patients- when a study based at a few large medical centres could accomplish the same scientific purposes much more efficiently? The main point of a seeding trial is not to get high-quality scientific information: It is to change the prescribing habits of large numbers of physicians. A secondary purpose is to transform physicians into advocates for the sponsor’s drug. The company flatters a physician by selecting him because he is “an opinion leader” and incorporates him in the research team with the title of “investigator.” Then, it pays him good money: a consulting fee to advise the company of the drug’s use and another fee for each patient he enrols. The physician becomes invested in the drug’s future and praises its good features to patients and colleagues. Unwittingly, the physician joins the sponsor’s marketing team. Why do companies pursue this expensive tactic? Because it works.

Without internal company documents, we’ll never know the true reason for this study. But I highly doubt it was to advance great research.


Covering:

Peacock WF, Coleman CI, Diercks DB. et al. Emergency Department Discharge of Pulmonary Embolism Patients. Acad Emerg Med 2018;25:995-1003. [full text link]






Thursday, 21 February 2019

Ketamine for severe ethanol withdrawal?


Ketamine seems to be good for everything; procedural sedation, induction of anaesthesia, pain management, depression and now severe alcohol withdrawal?

These authors from the heavily drunk city of Pittsburgh point out that there is a good reason why ketamine might work. Ethanol, like ketamine is also an NMDA receptor antagonist. I didn’t know that…

We have traditionally only targeted the GABA receptor. But perhaps there could be some benefit with also hitting the neglected NMDA.

This was a chart review comparing outcomes in 29 patients before and 34 patients after a guideline for ketamine infusion was instituted in their ICU. The infusion was at 0.15-0.3mg/kg/hour continuously until the delirium resolved. This is about 10-20mg/hr in an a 70kg adult… not very much.

Results?

Ketamine worked great!

Mean ICU days were almost halved. There were shorter mean hospital days, less benzodiazepine use and the rate of intubations plummeted (see table below for more details).

But before we get too enthusiastic, we need to remind ourselves this is very low-quality evidence.

There were no methods to their chart review, and they did not appear to use prespecified outcome measures. Retrospective data can be of poor quality etc.

But the biggest issue is the retrospective nature of this study. The small before and after groups could have been rather different to start with… like comparing apples to oranges. Therefore, the observed differences may have had nothing to do with ketamine.

Some would say the evidence of ketamine in severe alcohol withdrawal is as weak as vitamins for sepsis!

Ahhhhhhggggg…

In the end, what would I do?

I could easily be proven wrong, but I might consider this low dose ketamine infusion if I had a suitable patient with severe ethanol withdrawal… and I would also give them some vitamins.



Covering:

Pizon AF, Lynch MJ, Benedict NJ, et al. Adjunct Ketamine Use in the Management of Severe Ethanol Withdrawal. Crit Care Med 2018;46(8):e768-e771. [Free full text link]