Video:

 

Audio:

Or you can download audio here (right-click) or

A few points of difference between this lecture and Australasian practice:

• O2 not needed for abdo pain if sats normal.
• ECG not needed in kids
• LFT and amylase or lipase on everyone with upper abdo pain
• CT often before pt s/b surgeon
• Ischaemic gut: normal lactate does not r/o ischaemic gut
• I disagree that every abdo pain needs a blood gas.  I don’t do  a blood gas on a young person with mild to moderate abdominal pain.  If you are doing blood gases make sure they are venous and not a cruel ABG.  We can r/o DKA or Addisonian crisis from the electrolytes and a blood sugar.  All extra tests cost money.  Blood gas is not part of the ACEM lab test guidelines, there is just “consider lactate” for severe abdominal pain only

The 2013 ACEM and Royal College of Pathologist of Australia guideline on pathology testing in ED:

RCPA_ACEM_Guideline_v01__Mar-13__Final

The post Abdominal Pain. Mike Clancy. SEMEP appeared first on EM Tutorials.

Video:

Audio:

or download audio here (right click) or

A few things we do differently Down Under are that we seldom do ABGs on COPDs, and almost never on asthmatics. A VBG can tell you whether a CO2 is high, low or about normal – and if it is changing over time without repeated painful arterial stabs. More importantly we figure we can tell if a patient is tiring or failing to respond to treatment from the bedside.  Blood gases are more useful for talking to consultants at home who can’t see the patient.

We tend to use more spacers than nebulisers to reduce the spread of infection via the droplets and so patients can learn that spacers work quite well and therefore they can treat themselves at home a lot of the time.  Nebulisers are only used for severe asthma.

A final point is that a lot of acute mitral regurgitation will settle with treatment of LVF without the need for surgery, acute rupture of a papillary muscle or chordae tendoneae is relatively rare, but get a big person to have a look at these patients and make the big decisions.

References:

NZ guidelines for asthma recommending nebulisers for severe asthma only.

The post Shortness of Breath. Iain Beardsell. SEMEP appeared first on EM Tutorials.

Video:

Audio:

or download (right-click) here or

Key points (plus some extras from me)

History:

• Previous episodes
• Family history of sudden death
• Hx of cardiac disease – more likely to have a dysrhythmia
• Syncope during exercise
• Witnessed convulsion (but may occur with syncope)
• Standing vs lying (lying much more suspicious)
• Food intake
• Preceding symptoms such as feeling faint, hot, nauseated probably more likely benign
• Preceding chest pain or palpitation more likely to be cardiac or PE
• Preceding drug use – commonly GTN

Examination:

• Signs of seizure (not syncope): tongue biting, incontinence, drowsiness/confusion, neurological deficit
• Signs of TIA/CVA (not syncope): neurological deficit
• Heart murmur – especially aortic stenosis
• Brief abdo exam to rule out peritonism, including ultrasound for ?AAA if > 50 years old
• Signs of CCF – higher risk of cardiac arrhythmia
• Signs of DVT to suggest PE

Investigations:

• ECG
• Blood glucose
• BHCG in all females of child-bearing age (unless Hx hysterectomy)
• Hb if pale

Key ECGs

• WPW http://lifeinthefastlane.com/ecg-library/basics/preexcitation/

• Heart blocks / fascicular blocks – prone to complete heart block.  http://lifeinthefastlane.com/ecg-library/trifascicular-block/
• HOCM http://lifeinthefastlane.com/ecg-library/hcm/

• Brugada http://lifeinthefastlane.com/ecg-library/brugada-syndrome/

• Prolonged QT

• One not mentioned in the video: ECG suggestive of PE eg tachycardia and inferior and anterior T wave inversion

•  LVH on ECG with an aortic stenosis murmur suggests critical aortic stenosis as the cause of syncope.  High risk of sudden death.  Needs inpatient cardiology assessment with view to valve replacement

Disposition:

In our hospital for a single syncope with low risk history, normal examination and investigations as above, the patient does not get admitted or referred to outpatients clinic – the yield would be too low.

The post Syncope. Beardsell. SEMEP appeared first on EM Tutorials.

Image from http://www.pharmtox.utoronto.ca/programs/cpbt.htm

The post Toxicology for PGY1+2 appeared first on EM Tutorials.

An 8-year-old came into ED with a fractured femur from a school rugby practice. He was about to be sent to the ward with a Sagar Splint on his leg with no traction on it, no femoral nerve block and no opioid charted.

One of our nurses correctly pointed out that we are happy to provide you with your own femur fracture if that is what is required for you to develop empathy with your patients.

If you don’t know how to do any of these procedures, or are too busy, an ED senior will be happy to help out.

The post Oligoanalgesia appeared first on EM Tutorials.

A 78-year-old woman came to ED with nausea, vomiting and a headache. It seemed to have started during her recent admission to hospital with paroxysmal atrial fibrillation. To be fair to the physicians, they had tried her on decent doses of metoprolol and diltiazem and hadn’t been able to get her rate under control. They had started her on digoxin which finally slowed her down. In retrospect the dose of 125µg daily with a eGFR of 30 was probably a little generous. Always think twice before discharging a patient with a new prescription for digoxin and ondansetron!

On return to ED, her renal function was unchanged and her potassium was her digoxin level came back as 2.96 nmol/L (therapeutic range 0.6-2.0). Many references, including UpToDate and Toxinz, don’t recommend treating chronic digoxin toxicity unless the digoxin level is > 10nmol/L, they are hyperkalaemic, haemodynamically unstable or have life threatening dysrrythmias. Others such as the Toxicology Handbook (co-authored by LITFL’s Mike Cadogan) recommend treating anyone with an elevated digoxin level, renal impairment and symptoms of toxicity eg nausea and vomiting.

This woman was had been treated with several antiemetics and analgesics with little effect. She was lying in bed, looking miserable with intermittent vomiting. 2 hours after being given digoxin immune FAB (eg Digifab) was feeling much better and was sitting up in bed looking as bright as a button.

By the way here is her ECG.

Digoxin

The lateral ST depression suggests digoxin use – but not necessarily toxicity. The classical ECG findings in digoxin toxicity are heart blocks and automaticity, and bidirectional tachycardia. You can also get almost any arrythmia from digoxin. See http://lifeinthefastlane.com/ecg-library/basics/digoxin-toxicity/ for lots of good digoxin toxicity ECGs

I’m currently trying to track down a great talk from Billy Mallon several years ago in which he said “digoxin is a dinosaur looking for a tar pit” which summarised a lot of the reasons ED docs don’t like digoxin.

Another trick to digoxin is not to do another digoxin level when treating digoxin toxicity. The assay measures the bound digoxin and the antibodies binding it and the measured digoxin level doubles – causing much confusion.

The post Why I don’t like Digoxin appeared first on EM Tutorials.

Amal Mattu is Associate Professor; Program Director, Emergency Medicine Residency, University of Maryland School of Medicine, Baltimore, Maryland. He is the go-to-guy on all things ECG for emergency medicine in the USA, and speaks at all the big conferences. He also replies to emails same day! Here is what he has to say about amiodarone.

Video

If your hospital blocks the video, here is the audio:

or download audio here or here

Here is a link to the AHA 2010 guidelines Amal discussed in the talk http://circ.ahajournals.org/content/122/18_suppl_3/S729.full

The post Why Amal Mattu doesn’t like amiodarone. appeared first on EM Tutorials.

There was an emergency call to CCU.

A 70-year-old gentleman was in CCU being treated for renal failure secondary to angiography to investigate the cause of his dilated cardiomyopathy. He had extensive coronary artery disease but no revascularisation was performed. While eating dinner he went into this rhythm – with no symptoms.

He was then given amiodarone.

Then he developed this rhythm:

with a blood pressure of 40 systolic. That’s when we got called.

He was breathing, able to talk but mentating very slowly, he had distended neck veins but his chest was clear.

The CCU nurses had stopped the amiodarone and were drawing up some atropine.

We gave the atropine and put some pacing pads on him. We waiting a bit because external pacing isn’t pleasant for the patient. We drew up some midazolam and fentanyl in case we needed to pace him. His K was normal

After 2 minutes his HR was 70 and his BP 85/ with a MAP of 70 and he was looking a bit more awake. Great. (? due to atropine ? due to the amiodarone infusion being stopped)

5 minutes later his BP was 60 systolic with a HR of 72. Pacing probably isn’t going to help much (thanks Bridget). I don’t want him to give him an inotrope as that may put him back into VT. Hmmm fluid load or phenylephrine? We went with 250ml of crystaloid which seemed to do the trick.

Bottom line amiodarone is nasty. In my opinion this guy should have been electrically cardioverted (or, second best, given procainamide).

But don’t listen to me … next we have Amal Mattu, American emergency medicine ECG guru on the subject of amiodarone.

Image from http://blog.ercast.org/tag/early-repolarization/

You can download the audio here or here

The post Why I don’t like amiodarone appeared first on EM Tutorials.

Video:

Play audio:

Download audio here (right-click to save) or here

The post Sepsis – the basics. Dr Kiuber. SEMEP appeared first on EM Tutorials.

The video is here

If you want to download to listen on you bike the audio-only is here (R click to save) or

To play the audio on your computer if your hospital’s firewall won’t let you watch the video use this:

A couple of things we do differently:

1) we use a CRP rather than ESR to look for temporal arteritis because it’s cheaper and faster
2) we will usually not do an LP if we have a negative CT within 6 hours of onset of a rule out subarachnoid (reference http://emergency-medicine.jwatch.org/cgi/content/full/2011/805/1) but this is controversial.

More on subarachnoid in Life in The Fast Lane here

The post Headache. Sarah Robinson. Southampton Emergency Medicine Education Project appeared first on EM Tutorials.