Tamworth Masterclass 2012 from hneemergency on Vimeo.

hope we don't have to make an adriano zumbo croquembouche

I hope to see you all there.

This is a sample low carb meal my hospital gives diabetic patients. We are a diabetes center of excellence. No wonder we can’t control obesity and diabetes in our population

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!

USS and intubation

Haney, love your work!

Minh

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.

Minh

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.

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

High INRs

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

Low Risk

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

Moderate Risk

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

High Risk

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

Recurrent

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

Upper Ext

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)

Atrial Fib

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

Stroke

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…

Case discussion

Diagnosis

Treatment

Outcome

Rick Body

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!

Epi is bad! Epi is good! Which is it? Well, this week it's good to give epi in out-of-hospital cardiac arrest (OHCA). Seriously, I think this article is pretty compelling for the use of epinephrine in OHCA.

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