SMACCDUB: Bayes 2016 – A Diagnostic Odyssey

At the last SMACC outing in Dublin I gave this talk about Bayes’ theorem in medicine.  The challenge was to try and show how we can use this elegant idea in our day-to-day work.

Today the audio version has been released on the SMACC podcast for all to hear.  It is a somewhat technical talk and there are a few concepts which I did illustrate with graphics – so I have uploaded a video version of the slides for you to see as you listen to the chatter.


If you are running, driving, walking in a hospital corridor and cannot afford to watch as you listen then you can hear the “Audio Only” version over on the Intensive Care Network.

Clinical Case 136: the Diagnosis and Discussion

Last week I posted Clinical Case 136: A Maternity Mystery

If you have not had a read – then please go back and ponder the scenario before reading the rest of this post.

If you have been following along on the comments or social media then you will know that this is a tragic case.

Kelli became increasingly hypertensive, tachycardia, tachypnoeic and hypoxic over the initial hours after giving birth.

She suffered a cardiorespiratory collapse about 6 hours postpartum and died after a prolonged resuscitation.

The clinical picture in the peri-arrest period and after intubation was that of severe type 1 respiratory failure secondary to cardiogenic pulmonary oedema.  This did not respond to non-invasive ventilation or vasopressors, catecholamine support or diuresis.

The diagnosis was not clear until autopsy.  Though it was suspected after a careful review of the chart and all the data that we usually do not have time to contemplate in the heat of the Resus.

Tom and Leah were both right in the comments after the initial post.  Kelli had an undiagnosed adrenal phaeochromocytoma.

Case courtesy of Dr Prashant Mudgal,

Case courtesy of Dr Prashant Mudgal, From the case rID: 11765

This is an impossible diagnosis to make in the labour ward or in the ensuing resuscitation.  Only with the benefit of retrospect can one see how it all fits together.  My reason for sharing this case is not to see how smart you all are, or to scare you with horrific & undiagnosable demons.  I believe that this case contains a number of very important lessons.  It illustrates how we can do better as clinicians working in teams with shared ideas and respect for one another’s strengths and weaknesses.  The case also demonstrates the folly of “risk management” when it comes to our practice.  Obstetric practice is especially demonstrative of our inability to predict risk with alarming regularity and disastrous consequences.

This is an incredibly rare scenario.  It is estimated to occur in 1 in 54,000 pregnancies.  It is basically clinically indistinguishable from pre-eclampsia in the second half of pregnancy.  Hypertension and other symptoms are more distinctive in the earlier stages of gestation.  Without a strong clinical suspicion it would be very difficult to arrive at this diagnosis unless it is discovered incidentally on imaging or it the vasoactive symptoms are witnessed but a trained eye.  Unfortunately the symptoms are transient and sometimes subtle.

It is estimated that there is about a 50% maternal and foetal mortality if undiagnosed during pregnancy with most succumbing in the peri-partum period.

If you want to read more about the presentation and diagnosis of Pheochromocytoma in Pregnancy then have a read through this summary in European Journ Endocrinology, 2012 by Lender et al.  If you know about it – then you may think about it.  However, I suspect most of us have a vague recall of this diagnosis from undergrad physiology and pathology exam papers.  It is rare to see in practice.

So lets go back and review the case – with the optically flawless retrospectoscope.

If we review the only historical features that are prominent in the notes we get the following list:

  1. Panic-attacks
  2. Palpitations
  3. Epistaxis – review of the ED notes showed a BP of 180/100 during this episode
  4. Intermittent severe headaches, self-resolving
  • There were no specific mentions of symptoms such as profuse sweating or flushing – although these are usually symptoms we need to ask about in order to unmask.
  • Weight change, frequent urination, vague abdominal pains and constipation are so prevalent in pregnancy that they become useless to help in this scenario.

With the wisdom of hindsight – all the holes line up! The symptoms are reasonably classical if one managed to arrange all the pieces of the puzzle in the right order.  Alas, there is always a but…

Each of the symptoms that might have been used to triangulate this esoteric diagnosis had been “referred and reviewed”.  The Cardiologist saw the tachycardia, the Psychiatrist – the anxiety and the Neurologist had screened the headaches… it is a perfect storm of explanationitis.

I certainly do not believe that any single specialist would have been in a better position to clinch the diagnosis than another.  This is the nature of specialism – or “single-organ doctors” as Dr Leeuwenburg sometimes calls them.  There is a tendency to investigate symptoms and exclude causes that originate in the organ to which that doctor is devoted.  Thinking outside the box (or heart, cranium or psyche..) doesn’t come naturally.  This is really the lot of the generalist.  In retrospect I think that Kelli would probably have been most likely to be diagnosed if she had seen a crusty old General Physician or very enthusiastic, experienced GP.  For me this is one of the most important lessons to learn from this case:

  • Generalists are masters of the bigger picture.  We should absolutely take specialist advice and appreciate it.  However, we need to be aware of the biases and limitations that specialism brings to the table.  It is our role to bring all the pieces together either in the ED or clinic.  We are the ones with knowledge of the patient’s environment and family dynamics.  We understand the symptoms within the context of a life.  So we need to be circumspect when we incorporate our partialist colleagues’ advice into our care.

Then there is of course imaging…

Review of the chart revealed an incidental finding of a 4.5 cm right adrenal mass on the 19 week anatomy scan done by the local sonographer.  This was noted and a plan to investigate with CT in the post-partum was discussed with the reporting radiologist.  This report was summarised as “normal foetal anatomy & growth. Incidental adrenal mass on the right.”

[Ed: I did not include this in the initial case notes as the information was not available on the day.]

I can completely understand how a busy clinician in an antenatal clinic can see this report and, in the absence of any clinical suspicion, put it to one side until after the baby is out.  Ultrasounds in pregnancy throw up all sorts of oddities – maternal and foetal.  Most are purely incidental and require no action.  Indeed ignoring them can be perfectly anxiolytic for expectant mothers-to-be.

The next big lesson that I have taken away from this case is about being “empirically aggressive” with treatment in the face of an enigmatic, malignant processes.  This is essentially the core tenant of RESUSCITATION: empirical treatment in the absence of a diagnosis.  Playing the odds that doing something will have a benefit over doing nothing.

That may seem like an obvious concept.  Most of us are perfectly happy to perform CPR or a jaw thrust without knowing what is “going on”.  However there are many shades of grey.  This case demonstrates perfectly the paralysis that can arise when we think we know what is happening and are wrong, or when we are perplexed and frozen by diagnostic indecision.  Certainly, after dissecting this case backwards I am sure that the wrong moves were made as a result of early closure and fixation biases.  The clinical evolution just did not fit pre-eclampsia, and yet that was the pathway followed.

So my take away lesson is this: always keep an open mind and be prepared to abandon your “beliefs” in favour of aggressive treatment based on empirical data – even if it doesn’t seem to make sense.  The degree of “aggression” should match the virulence of the clinical picture.  I have spent many days, hours and moments in my career fixing physiology whilst remaining in the “diagnostic dark” as a result of being a long way from a surgeon, CT, MRI or fancy biochemical test.  This is not ideal medicine, but it works.  We keep the patient alive until the clouds clear and the way forward becomes clear.

In the case presented the resuscitation was aimed purely at Obstetric issues, specifically treating eclampsia… however the picture was clinically identical to a sympathetic, crashing pulmonary oedema.  In retrospect, it was of course an acute, decompensated cardiomyopathy in the face of a massive adrenergic crisis – maybe precipitated by the labour, anti-emetics or the physical process of pushing.  My “automatic” treatment of this situation is to attempt to kill afterload and preload simultaneously with GTN and PEEP…  who knows, it may have helped.

Thanks to all of you who have read and commented upon this case.

Hope these lessons come in handy for you one day.




Clinical Case 136: Maternity Mystery

Another case from the archives this week.  This is a really tough case… things are not what they seem.  Although this is an Obstetric case it does contain a lot of valuable lessons for all critical care practitioners.    I will describe the case and leave it hanging for you all to ponder and comment upon… will be back in a few days to close it out and discuss the diagnosis.

Here we go:-

Kelli is a 27 yo woman who is G2P1.  She is currently 39 weeks and has been having irregular contractions all day but is now in early labour.  It is 9 PM.  As the GP-Anaesthetist you have been called in as she has requested an epidural for her labour analgesia

Her antenatal records are relatively normal and she has had a full set of routine antenatal care with bloods and ultrasounds as per protocol.  Her BP, urinalysis, fetal growth and weight had all been tracking normally and there were no symptoms of pre-eclampsia.

Bloods done in clinic last week including FBC, LFTs and electrolytes are all completely normal.

The only information on past medical history are:

  • Anxiety disorder with panic attacks early in the pregnancy.  She was seen by a local Psychiatrist who felt she was a good candidate for cognitive therapy (not SSRI) given her pregnancy and she had 6 sessions with  clinical psychologist.  She had a good outcome and was coping well with infrequent panic episodes without any interval anxiety.
  • Palpitations 1 year prior.  She had experienced this in the post-partum period with her first child.  She had a Holter monitor which showed brief episodes of sinus tachy.  She was reviewed by the visiting Cardiologist who felt this was benign, possibly anxiety related.  Reassured.
  • A few ED presentations for epistaxis which have required a nasal pack on one occasion – none recently.
  • Headaches ? migraines vs. tension / daily headaches.  Have been infrequent in the last year.  Previously had disabling headaches about once every few months.  Never really diagnosed. Saw a Neurologist 2 years ago – empirical nasal Sumatriptan trialled with some resolution.

OK, so back to the labour ward.  On arrival the midwife informs you (the GP anaesthetist) that Kelli is now 5 cm dilated with good, frequent contractions in spontaneous labour.  She is moderately hypertensive 130/90 but in quite bit of distress with contractions.

She consents to epidural and it is inserted with no complications.  After an initial bolus her BP settles to 120/85 and she gets good pain relief after 20 minutes.  However…

… as you are about to leave you note that she seems “a bit twitchy”.  Something doesn’t seem right.  Despite the epidural wearing in you decide to check her reflexes.  Her knee and ankle jerks are quite brisk.  On testing she has 2 – 3 beats of clonus.  Hmmm…

The BP is now 110/65 and she is looking quite relaxed.  She denies any headache, visual symptoms, or abdominal pain to go along with PET.

The midwife inserts an IDC as part of the epidural protocol and you check the initial CSU on a dipstick – there are 4+ protein and a trace of red cells.  Rechecking the chart shows no prior proteinuria.

Confused by the findings you call your colleague who is covering the labour ward and outline what you have seen.  They agree to come in and review Kelli for possible PET and maybe the need for prophylactic MgSO4 to prevent an eclamptic seizure.  By 10 PM Kelli is “cracking on and a repeat exam shows her to be 8 – 9 cm dilated.  The plan is to push ahead and get this baby out as soon as possible.   You head home.

At midnight you give the midwife a call: “how is Kelli going?”

Good news: “she has just had a little boy and both are well.  Thanks for coming in, that epidural really worked great.  Are you happy if we pull it out now?”

“Sure, pull it,” you reply.  “Goodnight.”

At 1 AM your Obstetric colleague phone you back with a question…

Kelli has developed a headache now.  It is bi-temporal and not really postural.  Do you think you might have caused a dural tap with the epidural?

Her BP is now 145/95 with a pulse of 100.  She has had a small postpartum haemorrhage of 700 mls, however this has stopped with a dose of oxytocin and uterine massage.

The headache doesn’t really sound like a dural tap leak; it is too soon – besides you were very certain that you didn’t trash the dura on insertion.  “Maybe it is part of the evolving PET picture?” you postulate with your mate…  Together you decide that she should probably get loaded with MgSO4.

OK I will leave this case here.  Sorry if you are not Obstetrically inclined.  This is a tough case.

What is going on?

Hit me on the comments if you have any ideas.

If you get it right you may save the day.


October 2016 Journal Club with First10EM

Welcome back to the podcast for October’s Articles of the Month

Another month of interesting reading with Dr Justin Morgenstern.  Check out the First10EM blog for full written version.

Here’s the podcast:


Below are the written summaries and the links to the original papers:

Coming soon: Daily home D-Dimer testing
Prandoni P, Lensing AW, Prins MH et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. N Engl J Med. 375(16):1524-1531. 2016.
This paper will definitely be the most talked about of the month. It has the potential to be the most misunderstood paper of the month as well, and cause problems between emergency physicians and our specialist colleagues, but hopefully we can get ahead of it and understand the data for what it really shows. The paper’s misleading conclusion is “pulmonary embolism was identified in nearly one of every six patients hospitalized for a first episode of syncope.” Pulmonary embolism can definitely cause syncope, and there may even be a few patients with no other symptoms, but this data does not support working up PE in otherwise asymptomatic syncope patients.
Bottom line: You will hear about this. You will be asked to order CTs. Don’t. Use your clinical judgement and continue to assess patients for PE like you have been. Your patients will be better off for it.
Read more: R.E.B.E.L.EM, EM Nerd, St. Emlyn’s, EM Lit of Note


That’s not a knife… that’s a knife (I’m always alright when I’m with you, Dundee)
Pracy JP, Brennan L, Cook TM. Surgical intervention during a Can’t intubate Can’t Oxygenate (CICO) Event: Emergency Front-of-neck Airway (FONA)? British journal of anaesthesia. 2016. PMID: 27646054
This statement from the UK Difficult Airway Society gives a clear recommendation, based on the evidence, on how to deal with a can’t intubate can’t oxygenate scenario: you should immediately proceed to a surgical cricothyroidotomy. Specifically, they recommend the scalpel-bougie technique. They have removed all needle or catheter based approaches from their algorithms, because in real life settings, these techniques fail at a very high rate.
Bottom line: Anyone who manages airway should be prepared to cut the front of the neck. I don’t work a shift without a scalpel in my pocket.

I’ve included the NAP4 trial in these reviews before, but just as a review:
Cook TM, Woodall N, Harper J, Benger J, . Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency departments. British journal of anaesthesia. 106(5):632-42. 2011. PMID: 21447489
This was a massive undertaking. Based on a network of reporters from local institutions, all major airway complications in the United Kingdom over the course of a year were recorded. With regards to surgical airways, there were 75 incidents in that year. Needle cricothyroidotomy failed about 60% of the time, whereas surgical cricothyroidotomy was 100% successful.
Bottom line: It’s not an RCT but it’s as good as we have: you don’t use a needle for an emergency cricothyroidotomy, you use a scalpel.

Jet ventilation: complications
Duggan LV, Ballantyne Scott B, Law JA, Morris IR, Murphy MF, Griesdale DE. Transtracheal jet ventilation in the ‘can’t intubate can’t oxygenate’ emergency: a systematic review. British journal of anaesthesia. 117 Suppl 1:i28-i38. 2016. PMID: 27566790
My concern about relying on needle based anterior neck airway approaches in can’t intubate can’t oxygenate situations is that, especially when under pressure and your hands are shaking, I think they will be slower and less reliable. This study describes another major problem with relying on transtracheal jet ventilation: barotrauma. This is a systematic review, looking at both published and unpublished literature, that found 44 papers describing transtracheal jet ventilation. There is a very high failure rate in the literature. In the papers describing transtracheal jet ventilation for the can’t intubate, can’t oxygenate situation, device failure occurred 42% of the time, barotrauma 32% of the time, and the total number of procedures with one or more complications was 51%. When a patient is dying in front of me and every second counts, I definitely want something more reliable than a coin flip. Scalpel, finger, bougie cricothyrotomy is the way to go. (Unfortunately none of these papers give us much insight on what to do for young children.)
Bottom line: Jet ventilation is a procedure with a high failure and high complication rate
Read (or listen) more: Scott Weingart had the lead author (Laura Duggan) on EMCrit to discuss this paper.

Good suction – a key to preventing cricothyroidotomies
Kei J, Mebust DP. Comparing the Effectiveness of a Novel Suction Set-up Using an Adult Endotracheal Tube Connected to a Meconium Aspirator vs. a Traditional Yankauer Suction Instrument. The Journal of emergency medicine. 2016. PMID: 27751699
OK, one last airway paper. Blood and vomit don’t mix well with airway management. There is nothing that can ruin a shift faster than a routine intubation disappearing behind a curtain of blood and vomit. And of course, the standard Yankauer suction immediately clogs on the chunks. Scott Weingart has suggested attaching a meconium aspirator to the back of your endotracheal tube to turn it into a large bore suction device that can also be used to secure the airway. These authors decided to test that set-up. This isn’t a clinical trial. They were just testing how well a Yankauer suction worked as compared to an 8.0 endotracheal tube with a meconium aspirator when sucking fluids out of a pitcher. However, they did use real blood (pig’s), as well as blended hamburger, french fries, and soda for realism. The meconium setup was faster when suctioning water and blood (although the differences weren’t huge). Both devices clogged when trying to suction hamburger, but the meconium device managed to remove 90 mL whereas the Yankauer removed 0 mL.
Bottom line: Clearly this isn’t the kind of research that should lead to wholesale clinical practice changes, but it is a good technique that I would like to have in my arsenal when managing a difficult airway.

The pediatric assessment triangle
Horeczko T, Enriquez B, McGrath NE, Gausche-Hill M, Lewis RJ. The Pediatric Assessment Triangle: accuracy of its application by nurses in the triage of children. Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association. 39(2):182-9. 2013. PMID: 22831826
This prospective observational trial looked at the outcomes of 528 children for whom the triage nurse had performed an assessment using the pediatric assessment triangle (PAT) at a large academic pediatric emergency department. Two pediatricians, blinded to that triage assessment, retrospectively reviewed the chart to determine the final diagnosis (of stable versus unstable). The biggest weakness of this data is that although 1002 charts were selected for review, only 528 contained adequate data for inclusion. The PAT did a good job screening for instability (97.3% sensitive 95%CI 64.6-98.8%), although like most screening tools it does overcall (specificity of 22.9% with 95%CI 17.0-30.0%). The triangle was reasonable for identifying respiratory distress (LR+ 4, 95% CI 3.1-4.8), respiratory failure (LR+ 12, 95% CI 4.0-37), shock (LR+ 4.2, 95% CI 3.1-5.6), central nervous system/metabolic disorder (LR+ 7, 95% CI 4.3-11), and cardiopulmonary failure (LR+ 49, 95% CI 20-120). Perfect identification of the final assessment is not the role of a triage tool, like the PAT. The PAT tool performed well here, but perhaps a more appropriate measure would have been something like the number of children who become unstable within the first hour who were missed by the PAT?
Bottom line: The pediatric assessment triangle is an excellent triage tool, but you still have to follow it with a complete medical assessment.
The pediatric assessment tool was also featured in the most recent First10EM post: the crashing infant.

Hey doc, this patient has a wide complex tachycardia. OK, give me a minute to find my callipers
Pava LF, Perafán P, Badiel M. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart rhythm. 7(7):922-6. 2010. PMID: 20215043
This is an interesting study looking at a way to distinguish between SVT and ventricular tachycardia in patients with wide complex tachycardias. Looking at 218 ECGs of VTach (obtained during electrophysiologic studies done for a variety of reasons) 2 cardiologists measured something called the “R-wave peak time” in lead II. Using a cutoff of 50 msec, it was 93% sensitive and 99% specific, with a positive likelihood ratio of 51 and a negative likelihood ratio of 0.06. Those are excellent numbers (although we might want more than 93% sensitivity for VTach. I am not sure how accurate most of us are when measuring 50 msec on an ECG. The biggest problem is that this is a derivation study, and I am not aware of any validation studies. An R-wave peak time of 50 msec in lead II is incredibly specific, and you could imagine that the authors might have measured other variables as well, resulting in p-hacking that would undermine the validity of this study. If validated, this looks far more promising, both in terms of accuracy and ease of use, than any other V tach tool. However, I am still not sure where the value of these tools is for emergency physicians. If the patient has a wide complex tachycardia, I still think the safest and best approach is propofol followed by electricity. These algorithms are more important for cardiologists deciding on long term management.
Bottom line: R-wave peak time is interesting, but I wouldn’t use it in the emergency department based only on this study.

You just can’t beat good old ASA
Johnston SC, Amarenco P, Albers GW. Ticagrelor versus Aspirin in Acute Stroke or Transient Ischemic Attack. The New England journal of medicine. 375(1):35-43. 2016. PMID: 27160892
Although not strictly emergency medicine, we are often asked to start long term treatment on patients. Also, we have already seen a huge rise in ticagrelor use for MI despite a lack of convincing evidence of superiority, so staying on top of the literature seems like a good idea. This is a large, international, double-blind, randomized, controlled trial comparing ticagrelor (180mg loading dose then 90mg BID) to aspirin (300mg loading dose then 100mg daily) in 13,199 patients with low risk stroke (NIHSS score <6) or high risk TIA (ABCD2 score >3) for 90 days. The primary outcome was a composite of stroke (ischemic or hemorrhagic), myocardial infarction, or death. It was the same in both the groups (6.7% vs 7.5%, p=0.07).
Bottom line: Stick with aspirin in your CVA and TIA patients.

Another old, but excellent medication: nitroglycerin
Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of Nitroglycerin by Bolus Prevents ICU Admission in Patients with Acute Hypertensive Heart Failure. The American Journal of Emergency Medicine. 2016.
One of the most satisfying emergencies to manage is flash pulmonary edema, because the patients dramatically improve when put on CPAP and given nitroglycerin. This is a chart review of all adult patients who were given IV nitroglycerin for acute heart failure (according to the diagnostic coding) at a single large academic emergency department. They compared the outcomes of patients given a bolus of nitroglycerin to those who received an infusion and those who received both. The boluses they used here are much larger than most of us are using. They push 2 mg of nitroglycerin at at time. On the other hand, the infusion rate is lower than I would use, with a starting dose of 20 mcg/min and a maximum rate of 35 mcg/min. They report that patients receiving bolus therapy alone were less likely to need ICU admission than either the infusion alone or a bolus plus infusion (48% versus 69% vs 83%.) I wouldn’t get too hung up on the differences, though, as the groups were not randomized, and there is evidence that the infusion groups were sicker than the bolus alone group (higher resp rate and more total nitro given). Really, I include this to point out the value and safety of nitro boluses. One patient received 10 boluses (20mg of nitro total) without harm. Even with 2 mg IV boluses, the incidence of hypotension (whether clinically significant or not) was only 2%.
Bottom line: Acute hypertensive pulmonary edema needs nitro. Early boluses are a good idea.

McDonald RJ, McDonald JS, Carter RE. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology. 273(3):714-25. 2014. PMID: 25203000
I can’t resist a good myth. I have been holding off of including papers on this topic for a while, however, because this is a decision we can’t make on our own, and I don’t like provoking fights with our colleagues. This is a large chart review looking at patients undergoing CT, and comparing those who received contrast material to those who didn’t. This is a relatively good topic for a chart review, as creatinine, dialysis, death, and CT scans are all objective events that are likely to be clearly recorded in the chart. They only included patients who had a Cr measured in the 25 hours before a CT and also in the period of 24-72 hours after the scan. They also excluded patients already on dialysis and those who were given multiple contrast doses. Ultimately they ended up with 21,346 patients who they matched 1:1 based on a propensity score so they had 2 groups: contrast and no contrast. Overall, the rate of acute kidney injury was 5%. The rate was the same whether you received contrast or not (4.8% versus 5.1%, p=0.38). The incidence of emergent dialysis was the same in both groups, and extremely low (0.2% vs 0.3%). The 30 day mortality rates were also similar, at 8.0% and 8.2%. Although the propensity matching done here means the results could be flawed, it highlights the important issue that led us to think contrast is dangerous: older and sicker patients tend to need contrast CTs, and they are at a high risk of developing acute renal failure in the first few days of their illness, whether or not they get the contrast. The contrast is just an easy scapegoat. This trial is not enough to demand changes in policy from radiology, but I think it fits with the bulk of the literature. I will attempt to do a deeper dive on the topic in the future.
Bottom line: Contrast may not be the kidney killer we have all been taught.

Wichmann JL, Katzberg RW, Litwin SE. Contrast-Induced Nephropathy. Circulation. 132(20):1931-6. 2015. PMID: 26572669
A review on the same topic that concludes: “The risk of AKI from CM, especially when administered intravenously for the purpose of noninvasive imaging, has been exaggerated by previous, noncontrolled studies. More recent evidence from controlled studies suggests that the risk is likely nonexistent in patients with normal renal function. There may be a risk in patients with renal insufficiency; however, even in this patient population, the risk of contrast-induced AKI is probably much lower than is widely accepted.”

I seem to have a thing for Roller Coaster Studies
Mitchell MA, Wartinger DD. Validation of a Functional Pyelocalyceal Renal Model for the Evaluation of Renal Calculi Passage While Riding a Roller Coaster. The Journal of the American Osteopathic Association. 116(10):647-52. 2016.
I had to throw this one in, because it contained some excellent quotes, such as “we thank Walt Disney World Resort’s Magic Kingdom theme park for allowing us to conduct this research on the park’s premises” and “seat assignment on the roller coaster was random and determined as a function of place in the waiting line.” Aside from the great quotes, I’m not sure the paper means much. They made a silicone model of a urinary collecting system containing 3 real kidney stones, and report that the stones had moved in location after the roller coaster was finished. This is clearly not ready for time prime, and I can’t imagine that people with back pain from renal colic are going to be excited to be getting on rickety old roller coasters. I will stick to suggesting sex for now.
Bottom line: Sometimes I just include papers for fun


Commins SP, Jerath MR, Cox K, Erickson LD, Platts-Mills T. Delayed anaphylaxis to alpha-gal, an oligosaccharide in mammalian meat. Allergology international. 65(1):16-20. 2016. PMID: 26666477 [free full text]
This story is fascinating, and I actually found it through an excellent Radiolab podcast rather than through the thousands of abstracts sent to me each week. If you asked me if adults could suddenly develop a new anaphylactic reaction to red meat (you know, the same stuff that makes up our muscles), I would have said you were crazy. In fact, until a few years ago, almost all allergists would have too. But there were a slew of patients reporting exactly that. Their doctors though they were wrong. But then a new cancer drug also started causing a lot of allergic reactions, and the allergist looking into it discovered that the cause was galactose-alpha-1,3-galactose – which also happens to occur in red meat. But why were people suddenly developing an allergy to this almost universal antigen later in life? In turns out that these meat allergies were only being reported in certain communities, and by searching through maps, the allergist was ultimately able to find one that overlapped: the distribution of the lone-star tick (the same tick that carries Rocky Mountain Spotted Fever). It turned out that the tick bites were sensitizing patients to this sugar found in all red meat, and that was resulting in seemingly impossible allergies.
Bottom line: First, if you love red meat as much as I do, don’t go hiking anywhere you might find this tick. I mean really, this is scary stuff. And second, it is never a good idea to call patients with unexplained symptoms crazy. Unexplained symptoms will sometimes be explained in the future.
The Radiolab podcast is excellent and worth a listen. You can also read about this in the New Yorker.

Clinical Case 135: Tackling Trauma in the Bush

This vodcast is a version of the talk I gave last week at the ACEM Annual Scientific meeting in Perth.

We were asked to present a “challenging case” – I decided to present a trauma case that I think represents the maturation of my trauma practice.

The case is pretty straightforward.  However, there are a few concepts thrown in that you may not have heard before.  Airway management, massive transfusion, head injury… it is a tough case.

Let me know what you think or if you have any comments.