Tuesday, 29 September 2015

Are you going to order a serum lactate?

The A&E orders the most serum lactate tests in our hospital. Most of it are probably justified as we are the first point of contact for patients with sepsis and trauma in the hospital. However, there are occasions when that order for serum lactate is actually puzzling and one wonders how that impacts diagnosis or management.
To use the test efficiently, I suppose we all need to understand lactate physiology at a deeper level, and the current controversy surrounding it.
Here, folks at St. Emlyn’s have done up a good post on lactate physiology. It is recommended read. Click here: Lactate = LactHATE
Those who want to read a proper journal article on this subject should read Daniel de Bakker’s writing here. (Free access)
Those who just want a quick update can refer to St. Emlyn’s infographic here:

Tuesday, 22 September 2015

Webucation 22/9/15

This edition of webucation includes lots of orthopaedics with a smattering of cardiology and a fine trick for central lines. As always, credit to original content creators.
The last link is a good indicator of where risk stratification in ED is going. It will not be long where presentation troponins and 2 ECGs are all that is required once a good history is taken in low risk chest pain. Watch this space.

Tuesday, 15 September 2015

Does this patient have a seizure or syncope?

There are many components to this topic, and the knowledge is variable from junior to senior physicians. So, I put together this Q&A style post to consolidate all the web resources, my collection, and hopefully educate someone. Enjoy :)


 A universally challenging problem facing emergency physicians; this Lancet article sums up the topic very well, in fair detail. (See this reference).

It really boils down to a good history - here is where the eyewitnesses and paramedics are really helpful (sometimes). And no... urinary incontinence doesn't quite help (See this reference). This questionnaire may be useful:

Syncope scoring

Or this flowchart combining history, physical and eye-witness account:

Syncope clinical features

Convulsions are often seen in syncope as well (convulsive syncope), and are more common than you think (70-90%), but the duration is usually brief.

Seizure is more likely if:
  • Tonic-clonic movements are usually prolonged and their onset coincides with loss of consciousness
  • Hemilateral clonic movement
  • Clear automatisms such as chewing or lip smacking or frothing at the mouth (partial seizure)
  • Tongue biting (especially laterally)
  • Blue face
  • Prior to the event: aura (such as unusual smell)
  • Post-ictal confusion
Syncope is more likely if:
  • Tonic-clonic movements are always of short duration (<15 sec) and they start after the loss of consciousness
  • Prior to the event: Nausea, vomiting, feeling of cold, sweating (neurally-mediated)
  • short duration


Nope, serum prolactin is almost completely hopeless. (See this reference - report form the American Academy of Neurology)

 What the article recommends:
  • Serum prolactin assay does NOT distinguish epileptic seizures from syncope (in both conditions, serum prolactin are elevated). Level of Evidence B
  • Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children. Level of Evidence B


 A misconception is that transient LOC are commonly due to a TIA. The fact is, to have LOC in TIA/stroke, there must be either bilateral carotid artery disease or posterior circulation disease, in which there must be other accompanying neurological signs and symptoms! (e.g. cerebellar signs)

(See this reference - TIA definition) - What it says:

Syncope: A transient self-limited loss of consciousness, usually leading to falling. The onset is relatively rapid, and the subsequent recovery is spontaneous, complete and relatively prompt. The underlying mechanism is a transient global cerebral hypoperfusion.

Transient ischemic attacks are different in that they represent focal cerebral or retinal hypoperfusion. In general, syncope is brief loss of consciousness without focal neurologic signs or symptoms, whereas transient ischemic attacks are brief focal neurologic signs and symptoms without loss of consciousness.

 European Society for Cardiology syncope guidelines say this:

TIA related to a carotid artery does not cause T-LOC. When almost all cerebral arteries are occluded, transient obstruction of the remaining vessel subtending a large portion of the brain may extremely rarely affect consciousness only in the standing position. Moreover, focal neurological signs are much more prevalent.

TIA of the vertebrobasilar system can cause LOC, but there are always focal signs, usually limb weakness, gait and limb ataxia, ocu-lomotor palsies, and oropharyngeal dysfunction. For all practical purposes a TIA concerns a focal deficit without LOC, and syncope the opposite.


This is a common mis-understanding. Somehow, many doctors think that patients with syncope mandates a CT brain. In fact, European Society for Cardiology guidelines and ACEP guidelines DO NOT recommend routine CT / MRI for syncope. Image only if a seizure is suspected to be the more likely cause.

ALIEM goes on to advise when a CT brain is advised:

Clinicians might consider obtaining a Head CT as part of the syncope evaluation for the following findings:
  • Trauma above the clavicle 
  • Persistent neurologic deficit or complaint 
  • Age >65 
  • Sudden onset headache 
  • Patients on warfarin (coumadin)


 The most well known tools are the San Francisco Syncope Rule and the Boston Syncope Rule.

  Syncope risk stratification

 This is from ALIEM post on Management of Syncope, it is a good read. What do they say?

Bottomline: "Educated clinician judgment based on EBM guidelines (European Society for Cardiology and ACEP) seems to be the best strategy for management. Syncope prediction rules can certainly aid this process, but they do not yet fit for use alone for risk stratification in any population."

I generally agree with that, and don't use any form of risk stratification tool for syncope. If you do use the SFSR for example, use it as an adjunct to clinical judgement. So what then? See below...  


In my opinion, I like what Dr Smith's ECG blog has laid out, and more recently on emDocs as well. What they say also follow fairly closely what ACEP guidelines recommend. In fact, all you really need is HISTORY, PHYSICAL and a good read of the ECG! (Dr Smith's post is longer than mine, and contain very valuable info, references to this topic). After that, it is about a GOOD CLINICAL ASSESSMENT and investigating for what you think the likely causes are.

Only last month in Aug 2015, ESC published a consensus syncope risk stratification in the emergency department. (See this reference). A very simple conceptual flow chart:

  ED syncope model

 A short 6 page article well worth your time and to think about.  

Web References

Monday, 31 August 2015

Gaining traction

Here's another of Prof Larry Mellick's great videos. Self explanatory with great x-rays and commentary. Love the ketamine adjustment!

For more of his videos, go here.

Sunday, 23 August 2015

Smells like team spirit

In times of crises, certain traits are desirable and some, admirable. One of those is situational awareness. What is most desired is knowing your limits and calling for help.

A competent registrar notified me of an impeding airway disaster:

  • Semi conscious patient in respiratory distress
  • Oro-pharyngeal tumour (undergoing chemo)
  • Bleeding acutely from unknown site in oropharynx or lower
  • Shocked clinically
  • The best description I can give to those who understand is "peri-arrest".
Here's the really good news though:
  • A RSI checklist had been commenced prior to my arrival
  • The airway team had been called
  • Nursing staff were ensuring all the items on afore-mentioned checklist were prepped
  • Tranexamic acid given
  • Cric kit was opened and location marked (as best we could due to oedema)
The inevitable happened and the soon GCS deteriorated as did BP. Subsequently, this followed:
  • Ketamine 
  • Unmatched blood as soon as we got it
  • Peripheral pressors 
  • Paralysis and attempt by Anesthetist
  • Continuous suctioning of blood with no view of cords
  • Bougie assisted intubation with no desats and good CO2 trace
  • Good post intubation care
The whole hospital team successfully oxygenated and ventilated this patient. I did practically nothing. Which is why I am elated. This was a triumph for systemic preparation & team sport...

... but it all started with a keen-eyed doctor with the sense to know they couldn't do it all by themselves. 


Monday, 10 August 2015

ACL exam - all you need to know.

Dr Nabil Ebraheim makes some fine videos and this is no exception. It demonstrates the Lachman and Pivot shift tests and explains the pathology, relevant investigations and follow up as well. I'm a biased ACL tear sufferer but this is a common injury and it pays to know the sensitive and specific tests.

Sunday, 26 July 2015

Webucation 26/7/15

Web musings from around the globe this round include pointers on trauma, paeds, cardio and a good rundown on the ever challenging asthmatic.
The last link is a notion supported by our group as well. It is essential to know the basics of trauma resuscitation and how teams work in that arena. It just shouldn't be termed "Advanced" in this day and age.