If we are going to change education and get beyond all of the boring Power Point presentations…if we are going to change the way we teach our kids…if we are going to finally realize that a lot of how we teach doesn’t work that well…then we need to be creative and shake things up a bit.
Comedian John Cleese tells us what we need to know about being creative. Although this isn’t specifically focused on medical education, it’s an interesting perspective on creativity.
Want to change the face of education? Want to get the creative juices flowing? Get started by watching this video.
I couldn’t resist adding a short snippet from Monty Python’s Flying Circus. Enjoy.
Nun zu ein paar Fakten bzw. interessanten Daten:
1) Der Biomarker der Wahl bei der Abklärung von akuten Thoraxschmerzen ist zwischenzeitlich das kardiale Troponin (cTnT oder cTnI). Die Bestimmung von CK bzw. CK-MB hat keinen Nutzen und wird deshalb nicht empfohlen. Es sollte aus diversesten Gründen überhaupt nicht mehr bestimmt werden (einzige Indikation könnte sein der Patient mit Niereninsuffizienz bzw. der Patient mit subakuten Infarkt mit erhöhtem Troponin und V.a. Reinfarkt). Wer mehr zu diesem Thema wissen möchte, kann bei Saenger et al. nachlesen: "Requiem for a heavy-weight"
2) Nun zum eigentlichen Thema. Gibt es eine Möglichkeit, die Patienten at risk sicher zu identifizieren? Sie kennen ja vielleicht den TIMI-Risk Score, oder den GRACE Risk score, die zumal schon unterstützen. Spannend finde ich eine aktuelle Publikation zum ERLANGER HEARTS 3 Score (hat nichts mit der schönen mittelfränkischen Stadt um die Ecke zu tun). In der Publikation von Fesmire wird der Vorteil dieses Scores diskutiert und gleichzeitig ein Online Calculator angeboten
3) Nachdem wir uns ja mit diesem Thema beschäftigen, hänge ich noch eine aktuelle Studie von der Basler Gruppe dran. Tobias und Kollegen haben einen Algorithmus entwickelt, der anhand der absoluten Werte von cTnThs und den Veränderungen der Werte nach 1h eine Aussage zulässt, welcher Patient einen INfarkt hat und wer nicht. Dies wird die weitere Abklärung von betroffenen Patienten beschleunigen. Ein begleitendes Editorial führt sehr gut auf die entsprechenden Überlegungen bei Chest Pain Patienten ein.
ABER Vorsicht: Diese Untersuchung ist zwar ein Meilenstein nach vorne, aber muss erst noch in anderer Settings validiert werden. Wir verwenden nach wie vor das 3 Stunden-Protokoll, wie es in den Leitlinien empfohlen wird.
Hier noch die zentrale Abbildung der Arbeit von T. Reichlin et al.:
Hi folks.Tonight’s episode is on ECMO retrievals with Dr Anne Creaton, Flight Physician and Retrieval Medicine Specialist with Adult Retrieval Victoria, based in Melbourne.
We discuss the history behind Adult Retrieval Victoria and ECMO retrievals, the logistics involved and the indications for this level of support for interhospital transfers.
We conclude with a shout out to an exciting new retrieval medicine course that Anne and her colleagues are providing.
Check it out at Medicine on Location.
Now on to the Podcast
Right Click and Choose Save-as to Download the Podcast.
Filed under: Aeromedical retrieval, Emergency medicine and critical care, Interviews of interesting people, prehospital and retrieval medicine podcast Tagged: anne, creaton, ECMO, itunes, retrieval
This is the discussion for "Snapshot: 64 Year Old Male–Chest Pain".
First, let's talk about the patient presentation.What is concerning is the substernal chest pain, radiating to the shoulder and neck area. While this occurred about 30 minutes after exercise, it did not occur during exercise, so that is somewhat atypical. Still, enough red flags in the history to be very concerned.
Here is another look at the 12 lead:
It is a regular sinus rhythm, at a rate of 65. The PRI is on the long side of normal at 200 ms, and the QRS is slightly wide at just over 100 ms. The axis is normal, and there does not appear to be anything causing secondary ST changes.
The question is, do we see signs of ischemia on this ECG?
This is not an obvious ECG, so as we would expect, many of you said yes, and many said no. Is this a normal ECG? We don't have an old ECG for comparison, but I would say this ECG is not normal.
Let's break it down. What jumps out at me most on this ECG are the morphologies in leads I and aVL:
There is almost 1 mm of flat ST depression in lead I, and a very notable T wave inversion in aVL.
While the T waves look large in leads III and aVF relative to the size of the QRS, there appears to be no ST elevation at this time.
Dr. Stephen Smith, of the famed Dr. Smith's ECG Blog, has written numerous times that depression and/or T wave inversions in aVL will often precede ST elevation in the inferior leads in IWMI.
Also see this recent case by Dr. Amal Mattu for another case on this subject.
Are there any other findings on this ECG that might support these concerns?
There is about 1 mm of ST elevation in V1. Could there be RV involvement?
At the very least, I would be very concerned about a developing IWMI. The patient's discomfort is diminished, but not resolved. His complaints of "indigestion" are common with IWMI, and diaphoresis is another red flag.
Having said that, would I activate the cath lab based on this ECG? I have to say I would probably not activate based on this ECG alone.
I think this ECG is very concerning, but not yet diagnostic. I would certainly acquire serial ECGs and scrutinize the inferior leads for any subtle signs of change.
Dynamic changes would be a clincher. I would also treat with ASA and NTG, and would divert to PCI center if any changes in the ECG evolved.
This being a "Snapshot" case, we do not have follow up on this patient, or repeat ECGs.
We run into this in the field often. The spectrum of ACS is far and wide, and we are often presented with borderline ECGs.
I think the best course is to treat based on what is best for the patient, and do serial ECGs!
Thanks for all of the insightful comments on this case!
Any additional thoughts?
The most striking thing about this article, however, remains the gruesome number of false positives generated by each of these head CT decision rules. While, obviously, the intent is to capture all the cases requiring neurosurgical intervention, the New Orleans Criteria could not rule out potential need for neurosurgical intervention in 1,180 out of 1,582. When the theoretical purpose of these rules is to prevent "scanning everyone", we're not getting much bang for our buck. The Canadian Head CT Rule was better - but still indicated a need for scan in 656 out of 1,582.
While the article focuses mostly on the need for neurosurgical intervention in GCS 15 patients, it's interesting to see their "secondary outcomes" which did not need "intervention". Only 34 total patients in their cohort required intervention - while they found 133 skull fractures, 41 subdurals, 45 epidurals, 69 subarachnoids/hemorrhagic contusions, and 1 case of pneumocephalus. The Canadian rule would have missed 11 of the 218 "clinically significant" findings, for a sensitivity of 95%. The article does not specific precisely which types of findings were missed, but, clearly, many of those may be argued to be not significant. Unfortunately, deriving a better rule based on a more liberal definition of "clinical significance" is likely to result in more missed interventions - but it's still probably worth trying.
"Prediction Value of the Canadian CT Head Rule and the New Orleans Criteria for Positive Head CT Scan and Acute Neurosurgical Procedures in Minor Head Trauma: A Multicenter External Validation Study"
There’s a reason that the greatest speakers of truth in our society are still the comics and the poets. As a member of the medical profession I would like to imagine that in our own way we aspire to offer truth to our patients. Sadly, we often fall short of this high aspiration. For example, I will be discussing the practical implications of the IST3 trial in an upcoming post, but first I have to calm down.
To the IST3 collaborative I only want to say, I understand, sometimes being able to say what you really mean is hard, and when the emperor has no clothes it’s even harder. So this EM Notecard is for you, I’ve tried to sum up the findings of your work as concisely as I can. You should know I have found the act of distilling several thousand words of important sounding medical speak into a few lines of verse profoundly cathartic. I can only hope is has a similar therapeutic effect for you.
For everyone else, I have bundled up the latest postings on the subject. If you click on the card above it will link you to the EM Notecards in verse Pinterest board with a link to the IST3 study for your perusal. I also suggest the wonderful summary by Ryan Radecki of EMlitofNote, the post by Amit Maini over at EDTCC, and David Newman’s discussion on SMARTEM as well as his alway erudite blog post on the subject. Then come back here for a second helping of thoughtfulness on this amazing study.
Filed under: Notecards in Verse
I've put together a short Prezi on Ultrasound guided vascular access, which you can find here.
The anatomy portion is currently devoid of images as there is probably a bit of an issue with just cropping images from Fank Netter's beautiful compliation. I'll put in images of my own, unless any of you out there have some non-copyrighted originals that you would be prepared to allow me to use; with full credit of course.
The "How to" section is a series of You Tube videos that I found useful. I'm kind of surprised there aren't more. (Come on Ultrasound Podcast!!). Some of the videos wouldn't embed so I've provided the URLs.
Anyone who wants to, can use this Prezi for talks at their own institutions.
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In an effort to help you all out when visiting the blog, I have added a bunch of new links to the right that will send you to pages where my posts are linked by category. For example, click Cardiology and you’ll see all my Cardiology related posts in isolation. Also, please check out the links page, where I have linked to a few of my favorite blogs and educational websites.
Let me know if this helps, and as always thanks for reading!
Dr Haney Mallemat of Baltimore produces yet another short but incredibly helfpul screencast video on how bedside USS can assist in emergency tracheal intubation. Check it out! Got no Endtidal CO2 monitor, got no video laryngoscope? Well grab your bedside USS and avoid those awkward, uncomfortable moments immediate post intubation when you and your colleagues dont know if the tubes in the right hole or not!
Haney, love your work!
Filed under: airway, Emergency anaesthesia, Emergency medicine and critical care, Online critical airway training Tagged: haney-mallemat, intubation, ultrasound
Master Jim DuCanto is back, demonstrating a Glidescope/Bougie assistend tracheal intubation. He is testing the Pocket Bougie by Bomimed
Note his improvised crankshaft maneuver to disimpact bougie tip from anterior tracheal wall, allowing easier passage.
Note the right arytenoid cartilage arresting passage of the railroaded ETT, requiring anticlockwise rotation of the ETT.
and here is another video of him using the Pocket Bougie with a standard Macintosh laryngoscope
Its an excellent demonstration of proper bougie assisted tracheal intubation, even if there is no bougie prepass.
Filed under: airway, Emergency anaesthesia, Online critical airway training Tagged: airway, bougie, glidescope, intubation
From American College of Chest Physicians
Chest 2012;141:7S-47S (Executive Summary)
For outpatient treatment, start 10 mg daily for the first 2 days followed by INR measurements
Give 1 day of LMWH or UFH before initiation, if treating VTE
If the patient is on VKAs, avoid NSAIDs and certain ABX (table 8 from full guidelines)
Avoid anti-plt agents unless clinical condition warrants
Normal goal is 2-3, including antiphospholipid
No need to taper when d/cing
Heparin – 80/18 for VTE, 70/15 for cardiac or stroke patients
For outpatients with VTE treated with SC UFH, they suggest weight-adjusted dosing (first dose 333 units/kg, then 250 units/kg) without monitoring rather than fixed or weight-adjusted dosing with monitoring
4.5-10, no bleeding: no vitamin K necessary
> 10, no bleeding: Oral Vitamin K
If anticoagulant related major bleeding: 4-factor PCC and Vitamin K Slow IV Injection
See Michelle Lin’s Paucis Verbis on the same
Critically Ill Patients
Recommend against routine screening
Use LMWH or LDUH in all patients unless contra-indicated
For travelers at risk of VTE, use graded compression stockings; do not prescribe aspirin or anticoagulants
Diagnosis of DVT
moderate sens d-dimer, high sens d-dimer, or CUS of proximal veins only. D-dimers are preferred
If d-dimer is positive, get Compression Ultrasound (CUS) of proximal veins
Use High sens d-dimer, CUS of prox, or CUS of whole leg
Can stop if high-sens D-dimer is negative
If no d-dimer or d-dimer postive, need a second CUS 1 week later if only prox CUS done
If whole leg CUS is negative, you are done
Prox CUS or Whole Leg CUS
If prox CUS and d-dimer negative as well, done
If d-dimer positive or only prox CUS, get 1 week f/u CUS
If whole leg CUS is negative, you are done
In patients with past DVT, recommend high-sens d-dimer, if positive get Prox CUS and 1 week Prox CUS
If negative, get just one Prox CUS
If the old CUS is not available, confirm with venography if positive CUS
Go right to Doppler CUS for upper extremity dvt suspicion
Treatment of DVT
Start with IV or SQ UFH, LMWH, or fondaparinux (Latter two preferred)
If high pretest, start heparin immediately; If moderate, start heparin only if diagnostic tests are expected to be > 4 hours delayed
Isolated distal DVT-serial CUS rather than treatment unless severe symptoms or risk factors for extension (see full text)
Ambulate DVTs, no bed rest
In patients with hypotension (SBP) < 90 and PE, give systemic thrombolytics (through peripheral, rather than PA cath)
Chads 0 – nothing
Chads 1/2 – VKA/oral anti-coag; Dabi is preferred
If a-fib > 48 hours; give 3 weeks of VKA/dabi before cardioversion. Or get TEE with LMWH. Follow with 1 month of Vka/oral anti-coag
If a-fib < 48 hours; Start LMWH and then VKA for 4 weeks
If hemodynamically unstable, treat with anticoagulation ASAP preferably before cardioversion and then continue for 4 weeks
Treat a-flutter like a-fib for all of the above
If hemorrhagic, can start heparin between days 2-4, LMWH preferred
What is EMCrit Drinking?
A White IPA–Boulevard # 2
Here we go with what I hope will become a regular feature of the St. Emlyn’s blog – a cardiology case of the month. This is something I’ve been running for short while in my department, so it makes great sense to start sharing the cases with a wider audience, in the interests of #FOAM.
I certainly can’t promise to live up to the genius of Amal Mattu or Steve Smith, but still I hope you’ll find this a worthwhile feature! They’re the scribbles of a busy academic emergency physician so please bear with me if there are one or two typos. The details will be based on real cases from my experience but, in the interests of confidentiality and after speaking with our data protection experts, key details will always be amended to ensure that no patients are identifiable. On to case 1…
A 45 year old man is brought to hospital by paramedics after being found by passers by sat on the roadside. The paramedics can’t obtain a coherent history and score his GCS as 13/15 (E3V4 M6). They perform an ECG and transport him to hospital.
On arrival the patient is agitated and non-compliant, has a blood pressure of 90/40, a GCS of 13 and 2mm equal and reactive pupils. You elicit generalised abdominal tenderness with guarding. The patient denies chest pain. The ECG is below…
Here we have a patient with a diagnostic ECG for inferoposterior STEMI. There can be little doubt about that. We have up to 5mm ST elevation in leads III and aVF with deep reciprocal ST depression laterally and anterior ST depression with tall R waves suggesting posterior STEMI. The challenge in this case is the clinical presentation. The patient has no chest pain and there are things that we wouldn’t expect with a straightforward STEMI.
On the one hand, we know that time is muscle and we don’t want to delay revascularisation, whether that be by thrombolysis or PCI. However, these treatments come with significant risks of causing major haemorrhage and that’s not something to be taken lightly when the presentation is not straightforward. We have to consider other pathology that we might be missing, including the possibility that the STEMI could even be secondary to another disease process with associated physiological stress.
Indeed, plaque rupture is often secondary to an ‘acute risk factor’ causing surges in blood pressure. Perhaps that helps to explain why AMI is more common on a Monday! Due to their shape and typical position in the coronary circulation, coronary plaques may have to withstand pressures that are up to 7 times normal arterial wall stress. Add in to the mix the fact that unstable plaques will have eaten away at their own fibrous caps leaving only the single cell layer of endothelium between the lipid-rich, procoagulant core and the circulating blood, and you can see why surges in blood pressure might lead to plaque rupture.
We also have to consider ‘STEMI mimics’ that could give us a false positive ECG. A number of conditions can do this, and it’s worth considering these in this patient. We may, for example, want a blood gas and a BM to exclude DKA.
So, what shall we do on a practical level for the patient in this case? First, we need to explain that GCS. Before we can do that, it’s just not safe to administer powerful antiplatelets or thrombolytics. We could, for example, be seeing a subarachnoid haemorrhage complicated by STEMI here. So I think we need a cranial CT as a standard of care. That much is probably a given.
What about the abdomen? There’s significant abdominal tenderness and guarding. The question is whether we need to be sufficiently worried about that to delay treatment of the STEMI. What are the primary diagnoses we need to consider? For sure, we need to exclude a AAA. Thrombolysing a patient with a leaking AAA probably isn’t going to go very well. Fortunately, in the era of ED ultrasound it’s relatively straightforward to all but exclude that diagnosis if we can visualise the whole aorta and document a diameter of <3cm throughout. Let’s take it that we’ve done that, and a FAST scan too. What else do we need to worry about?
Mesenteric ischaemia has to be in there. A normal lactate reassures us but probably doesn’t completely exclude it. Going against that, a textbook case of mesenteric ischaemia will present with a paucity of abdominal findings, while the guarding is quite significant here. We also need to consider conditions that could bleed – and a perforated viscus could certainly do that. Ultimately, there’s a very good argument for a CT abdomen.
Finally, we should consider the possibility of aortic dissection. The clinical probability is relatively low, so (taking a Bayesian approach) we could consider excluding the diagnosis on the basis of a CXR and bilateral blood pressures. Given that we’re scanning the abdomen and head, there’s also an argument for completing a CT aortogram while we’re at it.
Hope you enjoyed the case. This is the first, hopefully of many, so all feedback is very gratefully received.
Before we answer the question, let’s talk about how to approach these and break them down.
First, let’s look at the question type. This is a type 2 question. Type 1 questions are simple, straightforward questions. ”What is the recommended door to balloon time in a patient presenting to the ED for STEMI?” Simple question, simple answer. Type two questions require a mental leap. They propose a scenario, require you to come up with a diagnosis, and then ask a question about how to either treat or diagnose that condition without giving you the name of the condition. So for this question, I clearly want you to think the patient has a AAA.
This brings me to the question itself. The exam writers put information in there for a reason, and information is sometimes excluded for a reason. So let’s go back to my question:
“A 65 year old make with a history of hypertension and a 50 pack year history of smoking presents s/p syncope and abdominal pain. On exam, his HR is 110/min, BP 82/40, RR 16, and Pox 98% on RA. You note abdominal tenderness in the midline, and a palpable pulsitile abdominal mass on exam. What is your next step in the management of this patient?”
He has a history of HTN and smoking, two major risk factors for AAA. He passed out, complains of abdominal pain, and has a palpable pulsitile mass on exam. This is their way of telling you he has a AAA without just saying “A patient comes in with a AAA.”
So now you made the diagnosis. The question then, based on the answers provided, is what is the best way to make that diagnosis in this patient. Again, look at the question above. Your patient is hypotensive (with a history of HTN), and tachycardic. The answer is easy if you rephrase the question as a Type 1 question:
“What is the best way to diagnose AAA in an unstable patient?” He is unstable, so CT and MRI are out, and when was the last time you ever did standard arteriography to diagnose AAA? The answer, of course is bedside US (Choice D).
Another strategy I find helpful when studying is to think about how the question could be worded differently and how that would change the answer, or if different answers were provided. What if the patient was stable, and US was not a choice? What if instead of angiography, one of the answers was “Establish 2 large bore IV’s, volume resuscitate, type and cross for blood and early surgical consultation?” Think about different ways the question could be phrased. AAA is a must know for EP’s, so you know you’ll see it.
My personal opinion is that the majority of tattoos make people look trashy. No, you don’t look “edgy”, you look low brow. Not to say that everyone who gets one IS low brow, but it cheapens your appearance. Especially if you are super pale, fat, and or schlubby with skinny little arms. It also depends on where it is, what it is, and the size. In general, isolated small ones of things like roses or other flowers on the ankle look OK, while “Tramp Stamps” and “sleeves” make you looks like a slut, poseur, IVDA patient trying to cover up needle marks, or a hoodlum. I don’t get these stupid-assed reality shows that glorify the tattoo business. It appears that many of the people that work there are either drug addicts, recovering addicts, or ex-cons. Also, just think how it will look when you are 85 years old and all shriveled up? Personally, if I were an ED director, I would not hire a doctor with a tattoo visible in work clothes.
Anyway, enough of my personal opinions. There is another reason to be wary of tattoos. Infection. Traditionally, infections come from nonsterile needles or from artists who don’t wear gloves. Hepatitis and AIDS are of course the most worrisome things you can get from a tattoo. However, now there is a new source of nastiness. The ink. A recent outbreak of a bacteria, Mycobacterium chelonae, a relative of tuberculosis, in people who got tattoos from a parlor in New York, was found to originate from an unopened bottle of ink. In the past, ink has caused infections because it was diluted with nonsterile water, but this was in untouched samples. Not much you can do about avoiding that – except not getting a tattoo!
Another ripper ultrasound case this week! I was doing a Sunday – my favourite day! No lab, no Xray department, no Admin folk doing QI stuff etc….. Just straight clinical work. Of course it is tourist season – so the average age of Broome goes up about 30 years!
Elderly chap presented with 24 hours of vomiting. He had had a bit of diarrhea the week prior, but then went on a rough boat ride and developed a tender lump over his umbilicus. Being a stoic fellow he didn’t present until the vomiting was bilious and he was all out of buckets!
On exam he looked pretty crook with a distended belly and a firm, red, warm lump ~ 5 cm above his umbi.
Medical school diagnosis really – SBO secondary to incarcerated umbi hernia. But, here is the trick. This chap had a list of comorbidities a page long, was on another page of meds and was not the sort of person I would usually opt to anaesthetise. Having said that – not a good candidate for a 12 hour plane ride either!
So what to do?
A quick call to the surgeon – he wants to have a look. There are 2 operations we could do here:
(1) A small hernia repair – if the gut is viable and no bowel resection is required.
(2) Laparotomy with small bowel resection of dead gut, possible ileostomy etc – this is major stuff for Broome, especially with a man with this many chronic problems.
So how do we decide what to do? Traditionally I think we would have gone in and hoped for the best, with a plan to evacuate ASAP if it turns out to be a major resection.
BUT bring back the US machine with the surgeon at the bedside…
So – off to theatre and a modest incision, nice healthy bowel returned to the peritoneal cavity and a mesh in. Of course we used the US to do a few TAP blocks at the end of the case – no opiates if we can get away with it.
Over all – a very satisfying case, a happy patient and a lot less stress for all concerned.
WHat do you think – how would you play this one?
... finde ich einen aktuellen Artikel von Hulleman und das begleitende Editorial höchst interessant:
Hulleman präsentiert Daten aus Holland und stellt dar, wie sich die Inzidenz von "out of hospital cardiac arrest" (OHCA) mit Kammerflimmern bzw. einem nicht-Kammerflimmern-Erstrhythmus entwickelt hat. Die Ergebnisse sind erstaunlich: Die Abnahme eines Schockbaren Rhythmus bei OHCA konnte im Verlauf gezeigt werden und wird auf die Errungenschaft des AICD zurückgeführt. Gleichzeitig nimmt die Inzidenz von nicht-schockbaren Rhythmen als Erstrhythmus eines OHCA signifikant zu. Hierzu gibt es natürlich 1001 verschiedene Erklärungen. Dies können Sie im Originalartikel als auch im Editorial detailliert nachlesen. Auch die zur Prävention eingesetzte medikamentöse Therapie (z.B. Betablocker) könnten hier einen Beitrag geben.
Im begleitenden Editorial wird sehr detailliert auf die verschiedenen Aspekte der Prävention und der Therapie des plötzlichen Herztodes eingegangen. Wirklich lesenswert. Zumindest mir wurde in einigen Aspekten die Augen geöffnet.
Extrem spannend bearbeitetes Thema. Any comments?
World Sepsis Day is on Thursday the 13th of September.
Here is a link to a game to help you learn about sepsis
On World sepsis day follow the conversation on twitter
Twitterchat – an international conversation via Twitter in relation to sepsis.
We will host an international Twitterchat and ask the audience 3 questions
related to sepsis, this will generate a conversation across Twitter. This is a
fantastic opportunity to discuss topics related to sepsis treatment and
management, connect with people interested in similar topics and discuss
strategies to overcome challenges. We will be using the #WSD12, please join in.