October 2017

Author: Becky Maxwell / Codes: / Published: 01/10/2017


The content you’re about to read or listen to is at least two years old, which means evidence and guidelines may have changed since it was originally published. This content item won’t be edited but there will be a newer version published if warranted. Check the new publications and curriculum map for updates


  • Dr Andy Neill and Dr Dave McCreary

Codes: HAP3, CC5

Paper number 1

Title: The HII Score – A Novel Tool to Assess Impairment from Alcohol in Emergency Department Patients

Author: Hack JB. Academic Emergency Medicine. July 2017.


Depending on where your department is located I would bet you either look after a lot of drunk patients, or an awful lot of drunk patients. They are difficult to assess and as such we have all missed or had delayed diagnosis of injuries in this population as we try to get the balance between over investigation and pragmatic emergency medicine practice. In addition, different patients handle their booze differently, some can have a blood alcohol of 0.25 (5 times the legal limit to drive) and look like theyve just had a quick pint as they complete the times crossword, others will be ‘on their arse’. In the UK, we rarely even measure blood or breath alcohol levels, favouring clinical judgement of sobriety, whereas here in Australia we measure it on everyone – though we’ll still make decisions based on clinical performance and ability. This paper looks at a novel objective score that can be performed and repeated at the bedside and give us a better idea of a patients real level of inebriation.


  • Retrospective chart review over 24 months of patients assessed in ED for alcohol impairment or whose ED course ultimately included a period of observation for resolution of alcohol induced impairment.
  • Patients were categorised as low frequency (1 visit), moderate frequency (2-5 visits) or high frequency (6 visits) over study period.
  • Exclusion: co-intoxication with other substances, seizure activities, hypoglycaemia, or pre-existing conditions that would affect the assessment
  • Intervention: Scores of 0-4 given for 5 tasks: speech quality and mentation, gross motor skills, eye movement, coordination with target pursuit, and fine motor skills. They got 0 if performed perfectly and 4 if they were unable to comply.
  • Comparison: Ethanol levels by breathalyser or serum level were performed at discretion of treating team. Usual nursing assessment – informally structured and varied between nursing staff.


  • 7526 visits from 2837 unique patients after exclusions
  • Initial measured alcohol correlated poorly with both the HII score and the usual nursing assessment (and tended to be even less correlated in the more frequent attenders)
  • HII score correlated well with the usual nursing assessment for alcohol intoxication.
  • Serial HII scores declined predictably over time (1/16 point per hour), which also corresponded well to nursing assessment.

Bottom Line

This score is another example of giving objective measurement to clinical gestalt but we think it could be an easy and useful method of formal assessment of the alcohol intoxicated patient. We particularly like the concept that there is a predictable improvement in the score over time. This could be of great use in the patients that we dont want to be biochemically sober – because they will be even less accessible if they are in acute withdrawal or at risk of seizing.


  • Dr Charlotte Davies and Dr Chris Allen

Codes: HAP8, CC5, CC1, CAP7

This segment discusses the initial management of chest pain syndromes, and aims to steer us away from giving everyone multiple antiplatelets. Important points:

  1. Re-load with aspirin? We don’t know, and don’t have much evidence. We could only find one paper
  2. Don’t give fondaparinux in STEMIs
  3. Carefully risk assess all your patients and decide best course of treatment

Cocaine Associated Chest Pain

Cocaine causes a sympathomimetic response, with increase in heart rate and blood pressure. It can cause acute thrombosis of the coronary artery – this is probably due to more than an increase in platelet count and activation.

Make sure you rule out aortic dissection as well, and “crack lung,” – hypoxemia, hemoptysis, respiratory failure, and diffuse pulmonary infiltrates. Also, think about MI if patient presents with dyspnoea or diaphoresis.

Troponin is still very useful, and about two thirds of MI events occurred within 3 hours of cocaine ingestion. ECGs are abnormal in 56 – 84% of patients, although this may be early repolarisation misinterpreted.

Treat as per normal ACS, but make sure you give early benzodiazepines. GTN might still help. Beta blockers are probably safe.



  • Dr Nikki Abela and Dr Arjun Rao

Recognising Paediatric Sepsis

Paediatric Emergency Physician Arjun Rao talks to Nikki Abela about pearls and pitfalls of recognizing paediatric sepsis after his talk at the Dont Forget the Bubbles Conference (DFTB17) in Brisbane last month.

In this recording Arj talks about the sensitivities of tests we use to recognize this illness. If you want to read more, this paper and this paper are good places to start.

If you are interested in how history and examination features affect post-test probability, then you should read this.

For another take on recognising paediatric sepsis, you should read Edward Snelsons blog on our RCEMLearning website.

New in EM


  • Dr Andy Neill and Dr Dave McCreary

Codes: CC5, CAP25, HAP5, HAP23

Paper number 2

Title: Predicting Short-Term Risk of Arrhythmia among Patients with Syncope: The Canadian Syncope Arrhythmia Risk Score

Author: Vankatesh Thiruganasambandamoorthy. Academic Emergency Medicine. August 2017.


Syncope accounts for 1-3% of ED visits (really? I’ve definitely had days where it feels like closer to 30%) and up to 3% of hospital admissions from the ED. It’s common, and on the surface it’s a pretty straightforward assessment process. But there are pitfalls and serious underlying conditions that we are considering during that process. The Canadian’s love a good prediction tool, and they’re recently turned their sights on syncope and trying to give us an objective tool to identify patients at risk of nastiness at 30 days from discharge. This paper is a furthering of that work to refine the tool to identify patients at risk of death or arrhythmia requiring intervention at 30-days – so those who would benefit from ECG monitoring.


  • Prospective, multi-centre cohort study
  • Population: Patients 16 years with syncope presenting within 24 hours of the event
  • Exclusion: Prolonged LOC >5 minutes, change from baseline mental status, witnessed seizure, or LOC following head injury.
  • Trained ED staff identified patients for inclusion and a raft of data variables was collected both at the time and through chart review. ECGs were all assessed by a cardiologist and abnormalities reviewed by a second cardiologist.
  • Primary outcome: Composite of death (due to arrhythmia or unknown cause), arrhythmia, or procedural interventions to treat arrhythmia within 30 days.
  • Apply fancy statistical analysis, allow to simmer, and serve up a tasty decision tool.


  • 5,010 patients analysed
  • 106 patients (2.1%; 95% CI 1.7-2.5) met primary outcome
    • 45 (0.9%) of these occurred outside the hospital
    • 22 (0.45) patients died (15 from unknown cause), 13 of these were outside of the hospital
  • Final 8 independent predictors:
    • Vasovagal predisposition (warm crowded place, prolonged standing, fear, emotion, pain)
      • -1 point
    • History of heart disease (coronary, valvular, myopathy, CCF, non-sinus rhythm)
      • +1 point
    • Any SBP <90 or >180 mmHg in the ED
      • +1 point
    • ED Dx of vasovagal syncope or cardiogenic syncope
      • -1 point for vasovagal
      • +2 points for cardiogenic
    • Elevated trop (>99%ile)
      • +1 point
    • QRS Duration >130ms
      • +2 points
    • QTc >480ms
      • +1 point
    • Scoring 0 had sensitivity of 97.1% and specificity 53.45 for primary outcome

Bottom Line

Bad outcomes from syncope evaluated in the ED are rare but do happen. Like all of these decision aids, this is just putting an objective number to what most of us already do with clinical gestalt. But this sort of score would be easy to use to provide an objective risk assessment and aid decisions re admission or discharge, and on whom to arrange outpatient ambulatory ECG measurement.


The San Francisco Syncope Rule has 96% sensitivity and 62% specificity for “death, myocardial infarction, arrhythmia, PE, stroke, SAH, significant haemorrhage, or any other condition causing a return to ED and hospitalisation for related event”.


  • Dr Craig Davidson

Codes: HAP27, CC1, CC2, CAP37, CAP21, CAP17

Spontaneous Vertebral Artery Dissection

– Main Source = Medscape


  • Neck pain or occipital headache + vague posterior circulation neurology- think VAD. Was there an neck injury that would increase your suspicion further?
  • CTA likely diagnostic investigation in UK.

Why is it important?

Increasingly recognised as a cause of stroke in the under 45s[1] largely due to imaging advances over recent years.


In the USA, the combined incidence of both vertebral artery dissection (VAD) and carotid artery dissection (CAD) is estimated to be 2.6 per 100,000.

CAD 3.5x more common than VAD. 3:1 Female to male ratio. Ave Age = 40 .


Generally, if you get through the initial event then recurrence is very (very) rare.

In the acute phase extracranial VAD does better than intracranial VAD with approximately double the risk of major morbidity or death. Assoc 10% mortality[2].


  • Generally caused by trivial neck injury for which patients do not usually present.
  • An acute dissection can heal spontaneously, cause a stenosis, cause emboli or develop into an aneurysm with compressive effects +/- rupture.
  • Usually occurs in (extracranial) the tortuous segment III of the vertebral artery. Can extend into segment IV (intracranial).
  • Implicated trivial neck injury examples: Spinal manipulation, Yoga, painting the ceiling, nose blowing.
  • Also associated with migraine, OCP, hypertension and female sex.


  • Headache or neck ache with neurology +/- minor neck injury.
  • Patient usually present with the onset of neurological symptoms which can be significantly delayed, days to weeks.
  • Classically this is lateral medullary syndrome but can include cranial nerve defects, facial pain and numbness, unilateral hearing loss, disequilibrium and vertigo.
  • Physical signs include: ataxia, nystagmus, Horner’s Syndrome and cranial nerve abnormalities.
  • Not all signs are unilateral as may involve tracts in the brainstem before or after decussation.


  • Usually start off with plain CT as ?stroke patient. Rules out haemorrhage. Usually identifies SAH.
  • CTA or MRA recommended over US by ASA, AHA and ACCF in 2011[3].


  • Early involvement of Stroke Teams, discussion with Radiology +/- Neuroradiology.
  • Thrombolysis not contraindicated.
  • Anticoagulation usually recommended although CADISS trial in 2015 showed no advantage over antiplatelet agents[4].

[1] Jaffre A, Ruidavets JB, Calviere L, Viguier A, Ferrieres J, Larrue V. Risk factor profile by etiological subtype of ischemic stroke in the young. Clin Neurol Neurosurg. 2014 May. 120:78-83.

[2] Saeed AB, Shuaib A, Al-Sulaiti G, Emery D. Vertebral artery dissection: warning symptoms, clinical features and prognosis in 26 patients. Can J Neurol Sci. 2000 Nov. 27(4):292-6.

[3] [Guideline] Brott TG, Halperin JL, Abbara S, et al, for the ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology… Vasc Med. 2011 Feb. 16 (1):35-77.

[4] The CADISS trial investigators. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 April; Volume 14, (4):361367.


Dr Nikki Abela and Dr Damian Roland

Codes: CC20

Damian Roland (of rolobotrambles.com) spares some time after his DFTB17 talk to tell us about what inspired him to get involved in academic emergency medicine.

If you are an aspiring academic, then you really should visit the PERUKI website the home of the PEM research collaborative.

If you havent already, don’t forget to also read up about RCEM partnership with the James Lind Alliance (JLA), which has conducted a Reseach Priority Setting Partnership with the aim of including patients, carers and clinicians in a process to establish the top research priorities in emergency medicine.

Don’t Forget the Bubbles have also announced that they will be holding their next conference in Melbourne next year so save the date (26-29th August 2018) if you’re interested. If you wanted to go to DFTB17 and missed it, the team are releasing the talks every week here.


  • Dr Chris Connolly and Dr Rebecca Maxwell

Codes: CAP30, CC5

Great set of guidance can be found on the RCEM clinicians page on their website and we’ve stumbled across this gem on the Mental Capacity Act

Published February 2017

In 2014 there was a house of Lords review into clinician understanding of the mental capacity act and it was found we have some deficits, RCEM has created this guidance with a view to informing us further, with a focus on the ED patient.

The mental capacity act (as is) was released 2005. At its core the act tries to provide balance and clarity. To stop those caring for patients without capacity from being too restrictive and recognising individuals rights to make decisions, be they good or bad, but mainlining their right to be free from harm if they lack capacity

So which of our patients could be affected?

  • Those who refuse treatment
  • Those who may have temporary capacity failure through drink or drugs
  • Those who may permanently lack capacity such as advanced dementia
  • Those whose capacity is being influenced by a mental health illness, be it acute or chronic.
  • Also must be considered in all absconders

The Mental Capacity Act does NOT apply to kids. It does however apply to those who are 16-18.

Key principles

1: We must presume our patient has capacity

2: Individuals have the right to be supported in order to make decisions

3: Patients have the right to choose to make what we think is a bad decision

4: Decisions made for a person under this act must be done in their best interests


  • Dr Andy Neill and Dr Dave McCreary

Codes: CMP2, HMP2

Paper number 3:

Title: Consciousness induced during cardiopulmonary resuscitation: An observational study

Author: Olaussen, Jan 2017, Resuscitation


– There was the fascinating study a few years ago – the AWARE study that looked into the out of body experience where survivors picture themselves rising above their body and watching their resuscitation. They actually studied this and put pictures on shelves that would be out of sight when supine but easily seen if you were able to float above your bed during resus and then asked the survivors if they saw them. Most people didn’t remember anything and the two patients who had the floating experience both had it in areas where they didn’t have the shelf with the picture but for one of them they were able to identify quite a few verifiable details about his resuscitation despite being in VF.

Anyhow… People may be more awake than we think even when they’re dead…

I think most of us have been involved with a cardiac arrest case where the patient kept moving their arms causing all kinds of disruptions while we check the pulse and the monitor to confirm that yes they’re still in VF and now that we’ve stopped CPR they’ve stopped moving. We turn on the LUCAS again and they start moving their arms. In the couple of cases I’ve been involved with they’ve both been the younger acute STEMI patients who have gone on to do quite well.


– retrospective review of the victorian cardiac arrest registry (this is Steve Bernard’s baby so it’s fairly high quality data set)

– the main weakness here of course is that they have no systematic means of documenting consciousness and could only identify it if someone happened to write it down

– they actually had a primary outcome of survival to hospital discharge – in other words is movement during CPR a good prognostic factor and something that suggests we should keep going or go for ECPR


– out of 17000 cardiac arrest patients they found 112 (0.7%) relevant patients with possible CPR consciousness

– these people fulfilled all the other good prognostic features (down time, age, rhythm, witness, bystander…)

– 20% of them were described as being combative (can’t blame them)

– 44% survival to discharge here.

– they did look at meds given and found that if patients with CPR induced consciousness got sedation (typically midazolam) then they did substantially worse than those who didn’t. They note in their discussion that this might be due to depressed vasomotor tone and that several regions have developed SOPs that involve a slug of Ketamine if consciousness occurs during CPR.

– only a small number had mechanical CPR (though it’s my very limited experience that you see this more with mechanical CPR)

Bottom Line

– consciousness (or at least purposeful movements) during CPR is a thing albeit quite rare

– if it does happen it’s probably a good prognostic sign

– it can make CPR difficult and sedation is probably needed and benzos might be a bad way to do it

– Kudos to our buddies Justin and Casey on their lit review podcast for highlighting this paper

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