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(adapted from a  St Emylyns blog post on corridoor medicine)

1.  Be Strategic

  • It is easy to get sucked into the care of individual patients when the department gets busy... you can quickly fall into the trap of losing oversight of the unit. When it gets busy, take a step back and assess the entire department, not jus the patient you are looking after.
  • Make an assessment of the current situation. How risky is it? Is this a temporary situation or is the overcrowding likely to persist.
  • On the busiest shifts the senior doctor should be responsible for  very few patients. Busy days require strong leadership and that is not possible when the most senior doctor is task focussed.

2. Talk: Communicate up, down and sideways.

  • Talk to other managers directly (access manager/ exec on call etc) and tell them what you want them to do. Give them actions.
  • Talk down to your team (the multiprofessional team) empathise, understand and explain what the situation is and how they can help.
  • Talk to your in patient colleagues. Again tell them how they can help. Be as specific as you can.
  • Get your shop floor management team together regularly (hourly) to discuss what can and cannot be done.
  • Walk the shop floor. Talk to all the staff. Gather information.

3. Be positive

  • Your attitude, your behaviour and your words will be heard by all. If you adopt a passive, pathetic or hopeless position then so will your staff. Great shop floor leadership sometimes means putting on a persona that can support and motivate others, no matter what you feel inside.
  • Challenge (gently) others figures who publicly catastrophise the situation. Ask them what they can do to support the team.

4. Allocate a waiting room doctor.

  • If ambulances are waiting to offload then allocate a competent doc to speak to all patients and waiting crews. Task them to make an assessment of who gets the next bed. Tell them to alert you if they have concerns.
  • Task them to make a rapid assessment of priority and then to report back to you and the triage nurse.

5. Report the overcrowding

  • Unless the overcrowding issues are shared across an organisation nothing will happen.  Whilst it can often seem pointless to fill in incident reports about overcrowding (it happens so often) it is a mechanism for making the executive notice.
  • Report individual patient harms

6.  Use non traditional space

  • If you are told that there is nowhere to see patients be pragmatic, think about what urgent clinical assessments can be made in different areas and prioritise. Try and ensure your patient’s dignity and confidentiality.
  • In a crisis any space can and may be used. See patients wherever they can be safely reviewed.

7. Be honest with patients.

  • Apologise for the delays.
  • Apologise for the circumstances they find themselves in (no-one wants to be on a corridor for 4 hours)
  • Tell them about delays when they first arrive and (where appropriate) suggest alternative health care providers.

8. Look after your staff

  • We all want to deliver great care, but that cannot be done in an overcrowded ED. 
  • Inability to deliver care to the level that we would wish is probably the biggest stressor for our teams.
  • Recognise this. Thank them, be nice, look after them.
9. The senior nurse is your best friend.
  • Touch base frequently & Review department status.
  • Decide on action plans. Consider escalation to executive on- call when things are unsafe.
  • The inevitable reponse if things go wrong will that they needed to be informed at or before the time.

10. Look after yourself

  • As a senior clinician you’re expected to be able to suck up all the pain, the risk, the danger and yet still lead with a positive attitude that supports everyone else.
  • This is tough and I know of many casualties.
    • If you think you need help ask for it before it’s too late.

  1. Position the limb using the uninjured arm or prop up with a wedge or a pillow
  2. Extra cotton padding on bony prominences and slightly beyond the planned length of the cast
  3. Water temperature  - warm shorter working time, cold longer working time
  4. Landmarks – determine where the bandage starts and where it ends
  5. Wrap around a joint to ensure the edges of the cotton/plaster do not cut into the joint crease
  6. Plaster application - grip the plaster roll by the plastic core to avoid slipping.  As you wrap around the limb, ensure the plaster roll remains in contact with the cast as it is being formed to avoid stretching and overtightening
  7. Smoothen the plaster with water using a circular motion in same direction of bandage.  Smoothening the plaster will avoid creating an onion-skin effect between the plaster layers
  8. Mould plaster to the natural shape of the limb using the palms of the hands until an oval-shaped cross section is achieved.  Never use finger tips as they will create pressure points.




This  post is a response to a number of case reviews  in recent years and noticing an association between badness and collapse...

In these scenarios syncope wasn't necessarily the presenting problem but rather a feature on history that perhaps should have led to a higher degree of concern. Often it can be difficult to determine the specific cause and the goal of our management is to exclude immediately life threatening pathology and observe the patient for  asuitable period to establish safety. The jury is still out on the significance of the very common pre-syncope or near syncope variant.

Below is an approach to patients for whom the triage comments suggest syncope.

Definition: Brief loss of consciousness with loss of postural tone and complete spontaneous recovery without medical intervention.


Approach to Assessment

  1. Confirm  syncope, and not seizure occurred:  (note: Syncope often results in  a short episode of tonic-clonic activity that mimics seizure)
  2. If the patient has Abdominal Pain, Chest Pain, Dyspnea, Hypoxemia, Headache or Hypotension, then these should be considered the primary presenting problem (not syncope).  
  3. Once Syncope is confirmed as the primary presenting problem obtain a detailed history to construct a list of possible causes:



Bleeding:  Ruptured AAA, GI bleed, ruptured ectopic pregnancy, other spontaneous bleed such as mesenteric aneurysms.

Check:  Vital signs, Abdo/Pelvic / Aortic ultrasound, Orthostatic BP, Haemoglobin,


Stroke: (very uncommon cause of syncope, must be TIA, as syncope implies reversibility: Subarachnoid haemorrhage (severe headache at moment of syncope), TIA  (must be either vertebra-basilar or hemispheric in patient with previous stroke of other hemisphere)  

Check:  History, Neurological examination


Obstructive: Pulmonary Embolism (Dyspnea?), Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade.  

Check:  Vital signs, SOB, Chest Pain, Ultrasound



Independent Predictors of Adverse Outcomes:

Note: Derived from three large studies –  OESIL, EGSYS, and SARASIN

An excellent review of these can be found here.


Abnormal ECG: (looking for cardiac syncope)

San Francisco Syncope Rule) as any new changes when compared to the last ECG or presence of non-sinus rhythm. If no previous ECG was available, ECG was classified as abnormal if any abnormality was present.  


Worrying abnormal ECG Findings:

  • Long QT (at least 480-500ms)
  • Brugada morphology
  • RV dysplasia
  • WPW
  • HOCM
  • Non-sinus rhythm
  • SVT or VT (obviously, and this makes for an abnormal vital sign anyway)
  • 2nd or 3rd degree AV blocks or sinus pause of at least 2 seconds
  • Right bundle branch block (BBB) with hemi block (bifascicular block)
  • Left BBB
  • Evidence of acute ischemia (may be subtle)
  • Pathologic Q-waves
  • LVH or RV


Abnormal but less worrisome:

  • Frequent or repetitive PACs
  • Isolated Right BBB or intraventricular conduction delay
  • PVCs

Not generally considered abnormal:

  • Isolated PAC
  • First Degree AV Block
  • Sinus bradycardia at a rate of 35-45
  • Nonspecific ST-T abnormalities (even if different from a previous ECG).


Positive Predictors of Adverse Outcomes:

  1. Age greater than 65
  2. History of Cardiovascular disease   (Especially  heart failure or structural cardiac disease)
  3. Syncope without a prodrome, no precipitating factors
  4. Haemoglobin less than 10
  5. Syncope with Exertion
  6. Syncope while supine
  7. Palpitations preceding syncope

Negative predictors of adverse outcome: 

  1. Pacemaker
  2. Pre-syncope or "near-syncope"
  3. Hypotension
  4. SOB or Hypoxemia 



Vasovagal Syncope (Neurocardiogenic syncope or Reflex Syncope) is the most common cause of cardiac syncope, even in patients with cardiac disease:  In this entity, there is BOTH a bradycardic and/or a vasodepressor response.  

if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope more dangerous cardiac causes are unlikely.  


Premonitory symptoms  (Nausea, pallor, diaphoresis, flushing), or triggers (Valsalva, Pain, Emotion, Prolonged Standing, Dehydration) are very useful in making the diagnosis.


Vasovagal syncope is generally benign.  


Patients with syncope as the primary presenting problem require exclusion of  bleeding, stroke and  obstructive pathology.


Predictors of other significant pathology are: 

  • Age greater than 65
  • History of cardiovascular disease, especially Heart Failure, or structural heart disease (especially valvular disease)
  • No prodrome
  • Syncope with exertion, preceded by palpitations, or
  • Haemoglobin less than 10g/dL
  • Family history of unexplained sudden death, especially if at age < 40
  • Abnormal ECG


Standard Assessment should include: 

  • Orthostatic BP and HR
  • Heart auscultation (aortic stenosis)
  • ECG


Consider in some patients:

  • Ultrasound of aorta, of heart
  • Abd free fluid (FAST exam)
  • Hb
  • Urine Pregnancy Test in women of child bearing age
  • Troponin
  • D dimer

Admission and/or Further Assessment is required if:

Serious symptoms often mandate admission and/or further workup: chest pain, SOB, Abdominal Pain, Severe Headache, or Hypotension

Worrisome physical findings suggesting a serious etiology

Admit for observation patients with presence of 1-2 or more high risk factor (in case of pre-syncope or near syncope, which is much lower risk than full syncope, more than one high risk factor is usually required)



Mendu ML et al.  Yield of Diagnostic Tests in Evaluating Syncopal Episodes in Older Patients
Arch Intern Med 2009 Jul 27; 169:1299-1305.   

BackgroundSyncopal episodes are common among older adults; etiologies range from benign to life-threatening. We determined the frequency, yield, and costs of tests obtained to evaluate older persons with syncope. We also calculated the cost per test yield and determined whether the San Francisco Syncope Rule (SFSR) improved test yield.
Review of 2,106 consecutive patients 65 years and older admitted following a syncopal episode.
Electrocardiograms (99%), telemetry (95%), cardiac enzymes (95%), and head computed tomography (CT) (63%) were the most frequently obtained tests. Cardiac enzymes, CTs, echocardiograms, carotid ultrasounds, and electroencephalography all affected diagnosis or management.

Postural blood pressure, performed in only 38% of episodes, had the highest yield with respect to affecting diagnosis (18-26%) or management (25-30%) and determining etiology of the syncopal episode (15-21%).


The cost per test affecting diagnosis or management was highest for electroencephalography ($32,973), CT ($24,881), and cardiac enzymes ($22,397) and lowest for postural blood pressure ($17-$20). The yields and costs for cardiac tests were better among patients meeting, than not meeting the San Francisco Syncope Rule (SFSR) e.g.  the cost per cardiac enzymes affecting diagnosis or management was $10,331 in those meeting, versus $111,518 in those not meeting, the SFSR.

ConclusionsMany unnecessary tests are obtained to evaluate syncope. Selecting tests based on history and examination and prioritizing less expensive and higher yield tests would ensure a more informed and cost-effective approach to evaluating older patients with syncope.

Adapted from: Stephen Smith’s ECG Blog April 8, 2015



When you can't intubate or can't ventilate, the 3 things that can save a life are a scalpel, a bougie and your non-dominant index finger.... this awesome video shows us how it's REALLY done, thanks to the fabulous EMCrit Blog.  A must watch!!



The ED team manages aggressive and agitated patients multiple times on a daily basis.

For many this involves verbal deescalation and implementation of strategies ranging from provision of a cup of tea to listening to long and detailed tales of woe.

At times further step are required to ensure the safety of the patient, other patients and staff.

At this point a code grey is required..

Once the team arrives a quick huddle should result in a plan of action..

This may involve a decision to apply physical restraint but it should always involve some form of medication plan tailored to the level of agitaion and the likelihood of gaining cooperation.

There is a lot of training happening around deescalation and use of physical restraints. One thing that can sometimes be left behind is ensuring everyone is on the same page with regards to medication.

Below is the detail from our new ED code grey guideline. We should all be following this and ensuring the other members of the code grey team are aware of the plan.

   Oral Medication


Oral medication may be offered in parallel with efforts to engage the patient deescalate using verbal and non-verbal techniques.

Options include:

Diazepam 5 to 20 mg orally, repeated every 2 to 6 hours, titrated to clinical response, up to a maximum of 120 mg in 24 hours


lorazepam 1 to 2 mg orally, repeated every 2 to 6 hours, titrated to clinical response, up to a maximum of 10 mg in 24 hours

If the desired effect is not achievable with diazepam or lorazepam alone, or the other indications for using antipsychotic drugs apply

A suitable dose of the patient’s current antipsychotic medication

OR (if the patient is not currently taking antipsychotic medication)

olanzapine 5 to 10 mg orally, repeated every 2 to 4 hours, titrated to clinical response, up to a maximum of 30 mg in 24 hours, or 15 to 20 mg as a single initial loading dose on the first day


risperidone 0.5 to 1 mg orally, repeated every 2 to 4 hours, titrated to clinical response, up to a maximum of 6 mg in 24 hours. Risperidone may cause orthostatic hypotension and extrapyramidal adverse effects, particularly if doses exceed 4 to 6 mg


chlorpromazine 50 to 200 mg orally, repeated every 2 hours, titrated to clinical response, up to a maximum of 800 mg in 24 hours. Avoid using chlorpromazine in older patients. Chlorpromazine may cause orthostatic hypotension


haloperidol 0.5 to 2 mg orally, repeated every 2 hours, titrated to clinical response, up to a maximum of 10 mg in 24 hours. Haloperidol may cause significant extrapyramidal adverse effects, including acute dystonia, particularly if doses exceed 3 to 4 mg in a patient who has not previously been exposed to antipsychotic drugs.



If oral medication offered this is best administered by the team member with greatest rapport.



Parenteral Medication


The Intramuscular Route is preferred for initial sedation of the agitated patient.

If intramuscular medication is considered appropriate the first medication to be given should be a benzodiazepine.

Use:  midazolam 5 to 10 mg IM.



Droperidol or olanzapine should be considered in patients who are tolerant of benzodiazepines or if there is a failure of midazolam.

Use:  droperidol 5 to 10 mg IM


olanzapine 10 mg IM

NB: If droperidol is unavailable, haloperidol may be substituted using the same dose as for droperidol, but haloperidol is less effective than the recommended drugs.





Adverse Drug Effects:

If significant extrapyramidal adverse effects (particularly acute dystonia) emerge due to antipsychotic drugs, they may be relieved by the administration of an anticholinergic drug.

benztropine 1 to 2 mg orally, IV or IM


Sedation End-points:

Aim for the patient to be drowsy but rousable.


Physical restraint should be continued until clinical response is apparent. Intravenous access may then be established. Apparent failure to respond after intramuscular administration should be determined cautiously before giving additional doses. It is preferable to titrate sedative drugs intravenously however the risk of staff performing intravenous access must be weighed against any benefit and in the event of a combative or very agitated patient the intramuscular route is strongly recommended.

The Richmond Agitation Sedation Scale (RASS) below is a Validated Tool for the assessment of patient sedation and agitation in the clinical setting.

 The idea is to rapidly achieve a score of 0 to -2 (or -3 at most). Short acting agents are best to beginb with but then considewr a long acting agent (such as Olanzapine) to maintain the effect  beyond the first hour.

NB Please also refer to the following Northern Health Polices and Guidelines available on PROMPT:

Level 1 Policy - Safe/ Effective Clinical Care

Level 2 Policy and Procedure - Security

Level 2 Policy and Procedure - Physical Restraint

Level 3 Guideline  - Aggression Management

Level 3 Guideline  - Code Grey – Unarmed Threat / Aggression

Level 3 Guideline -  Weapons and Dangerous Articles including Firearms – Detection and Management

Level 3 Guideline - OH&S - Employee Health & Wellbeing – Peer Support Program and Critical Incident Debriefing


RICHMOND AGITATION SCALE                        







Overtly combative, violent, immediate danger to self/ others


Very agitated

Pulls or removes catheters, tubes, uncooperative aggressive or verbally threatening



Frequent non-purposeful movement,, pacing, staring



Anxious but movements not aggressive


Alert and Calm

Doctor or nurse



Not fully alert but sustained awakening to voice


Light Sedation

Briefly awakens with eye contact or voice


Moderate sedation

Movement or eye opening to voice but no eye contact


Deep sedation

No response to voice but movement or eye opening to physical stimulation



No response to voice or physical stimulation



Richmond Agitation Scale Procedure:

1)      Observe Patient

2)      If not alert, say patient’s name and ask patient to open eyes and look at speaker

-1 if awakens with sustained eye contact to voice

-2 if awakens with eye contact to voice <10s

-3 if moves or opens eyes to voice but no eye contact

3)      If no response to voice, use physical stimulus (flex arm by wrist, shake shoulder) -

-4 if any movement to physical stimulation

-5 if no response to physical stimulation



Target RASS                        0 to -3








Almost every Emergency Department in the country has opened some form of observational medicine unit in the past 15 years. They may be called many things – Emergency Assessment Unit, Emergency Observation Unit, Clinical Decision Units or our flamboyant choice - Short Stay Unit (SSU). This just expanded from 14 to 21 beds which makes it a pretty big unit which beckons consideration of the drivers of this change and the aims of such a move.

Ultimately it comes back to the patient – Patients don’t like being in Emergency Departments for periods of more than 4 hours and for good reason. Not only is it uncomfortable and noisy but evidence shows clearly that long stays in an ED are associated with worse outcomes.

Patients are not necessarily better off on the ward either. Ward processes and culture dictate that admissions often run into days whilst extensive testing and consultations are considered. This is expensive and not always in the patients best interest.

Observation Medicine Units fill the gap and deliver intensive short term assessment, observation or therapy to optimize early treatment and discharge whilst maintaining or improving outcomes.

The Northern SSU is where we practise observation medicine. (Dr Steven Pincus of Royal Melbourne ED fame labels this sub-acute emergency medicine).

The aim of this model of care is to:

  • Reduce inappropriate inpatient admissions.
  • Provide timely assessment and treatment thus allowing discharge in the shortest clinically appropriate time
  • Standardize care using evidence-based pathways.
  • Facilitate care provision by a multidisciplinary team
  • Reducing ED representation rates
  • Increase capacity to manage surges in ED patient volume
  • Improve cost efficiency

Optimising Observation medicine has been a priority for the Victorian Health System since 2007. This has resulted in rapid development of this subspecialty of Emergency medicine and resulted in improvements in patient flow and outcomes and the patient experience.

There are 20 SSU pathways (expanding to 25) based around specific problems but an admission may be considered for any stable patient requiring:

  • Repeat or serial diagnostic testing
  • Treatment not readily provided in the ED
  • Stable undifferentiated patients requiring lengthy evaluation or serial review where the need for intervention is not clear.
  • Rapid and comprehensive multidisciplinary assessment
  • Treatment and observation of conditions expected to resolve or stabilise within 12-24/24
  • Early specialist or subspecialist review 


Making it happen:

SSU pathways should be commenced as soon as possible in the patient’s ED journey.

This may occur anywhere from triage on and requires approval from the SSU Physician.

Most diagnostic categories do not require results of pathology or radiology tests to be available prior to admission however tests should be requested and required sampling performed prior to transfer.

All SSU patients must have a signed Medication chart and SSU Pathway completed prior to transfer. ED electronic Medical Records should be submitted as soon as they are complete.

It should be clarified with the SSU Physician whether follow-on care will be completed by the POD Medical Officer or needs to be handed over to a SSU Medical Officer. If handover is to occur the ED Medical Officer must verbally handover the patient to the SSU medical officer.

The treating doctors’ name must be entered on the SSU pathway and on the SSU staff base and cubicle whiteboards to allow immediate identification of the treating doctor by SSU clinicians.

 Then what:

If you have handed the patient over your job is to find another one but if not you will need to chase necessary results and check in with other team members to keep tabs on your patient’s progress.

 The art and science of Observation Medicine:

The skill in optimizing the benefit of observation medicine is recognizing the patient who will require emergency assessment and care beyond that 4 hour window but with a low (<20%) probability of needing a multi-day stay.

They must be stable and whilst they may need a high level investigation such as contrast CT or MRI they must have a low requirement for nursing care.

When it all goes smoothly it’s like any great short break - the destination is reached quickly, the service welcoming and everyone leaves in a happier state than when they arrived.



From now on, EDventures will host the famous James Hayes ED Clinical Resources.  James will continue his email updates for those who prefer this avenue, otherwise his resource is now available via registration on the EDventures website.  To register, simply click on "Register Here" on the top left hand column.

You may choose to subscribe for automatic email notifications when a new post appears on any EDventures page and clicking on your username and choosing "subscribe to page updates" at the top right hand of the screen.  Subscribe to the James Hayes Resource page today.




The trauma symposium provided a great forum for discussion of a topic close the heart of most involved in emergency care. We were privileged to have Professor Russell Gruen as a guest speaker who brilliantly articulated just how far we have come and where we are going with Trauma Care.

Shu Ooi presented our latest audit figures and led an interesting discussion around some local cases:

 Case discussion:

1)      MVA with chest pain.

Discussion: Management of multirib # (+small pneumothorax) locally is very reasonable.

2)      Elderly HLC patient with fall. (altered conscious state)

Surgical opinion was that these patients should routinely get (in addition to CTB/ CTCx) plain TL spine imaging even if no tenderness.  Studies show poor correlation between exam findings and injury location.

50% of trauma in trauma centres are these low impact falls in the elderly which often results in severe injury


Shaun Baxter presented some of the differences he noted moving from Alfred to TNH in terms of approaches to trauma. He highlighted the variability of radiologist reporting and interpretation by ED staff. Absence of a pathology trauma panel and potential use of protocols from the trauma centre setting were also discussed.

Surgical fellow Dr Andrew McLeod presented also presented a number of interesting cases which rounded off a great learning experience:

1)  Third Trimester MVA – Tender abdo, Borderline haemodynamics

 If you are concerned enough about the patient’s examination then do the CT scan.

Foetal risk of childhood cancer (all gestational ages) increases by absolute risk of <1% at 50 gy (a CT chest/ abdo/ pelvis) ie number needed to harm between 100 to 200.

This patient also had abdominal pain and arguably if CTG accessible before CT (in this case CT was faster) the non-reassuring CTG would’ve been enough to take pt to theatre.

CT showed placental abruption but also 2 rib #. Good short term outcome

2) 25YO M Penetrating trauma suspected arterial injury to leg (based on blood loss ++

Think about using massive transfusion Protocol

CT angio reported as normal

Lesson is to view the pictures

Do not to close a purulent wound.


3)    Young M - Penetrating trauma (multiple self-inflicted)

Peri arrest hypotension, then arrests in ED after L) ICC insertion (blood ++)

Discussed roles of emergency thoracotomy and ED laparotomy and damage control surgery/ packing.


The final presentation by Professor Gruen described the move away from damage control surgery and use of excessive fluids. Earlier use of physiologic fluids (blood products) to minimise inflammation (and subsequent ARDS, SIRS, coagulopathy etc.) is now recommended.

Selective angiographic embolization is increasingly recognised as the optimal strategy to control bleeding.

Recent studies (Brohi et al) reveal a subgroup of patients are already coagulopathic by the time of arrival from trauma alone. The CRASH 2 trial was discussed but however with approx. 1% pts studied from countries with developed trauma systems questions remain re external validity.  

The PATCH trial from Monash/Alfred where prehospital use of tranexamic acid is underway. A recent genomic study showed that 60% pts have a prothrombotic (hypofibrinolytic) trauma response and only 20% have a coagulopathic (hyperfibrinolytic) response raises concerns that tranexamic acid may lead to DVT/ PE in the prothrombotic population. Other mechanisms and effects are also poorly understood.

Future directions were discussed:

Personalised Medicine in Trauma (esp. Therapeutics)

Use of technologies derived from organ donation research to make organs more resistant to hypoxia

Use of topical dressings and packs with haemostatic properties

A link to the slides from his talk can be found here.

Additional comments:

We should be contacting ARV or PIPER within 60mins for all potential major trauma cases.

In potential Major Paediatric Trauma imaging beyond standard trauma series and USS lungs/ pericardium should not occur before discussion with PIPER.

The Trauma Victoria website is now an excellent education and guideline resource worthy of exploration/ reference. Criteria for cases requiring discussion with ARV and PIPER have been posted in Orange POD and can be accessed via the website.





Any way you look at it ..night shift is hard :(

Emergency Medicine Australasia recently published an article that might make surviving this necessary evil that little bit easier for you and safer for your patients.

Click here to check it out.



LP 8

Lumbar Punctures can be tricky..

Obese patients and less cooperative patients make it even more difficult.

Like many procedures Its hard do them often enough to remain slick and secure but Ultrasound can make it a lot easier!! 

The guys at emDocs have posted a great guide to this technique

Check this out...



We’ve all been there...

Things seem to have ground to a halt...

You look the screen and after a quick glance at the top you can see why... Mr or Mrs Plug may be one of several hypothetical patients with triage comments that make most emergency doctors disappear into the suture room... or down the corridor...Some suddenly feel the need to have a long deep and meaningful with the narcissistic PD in cubicle five...Whatever the strategy the result is an ED Mexican standoff.. That lasts until Mr or Mrs Plug have been seen.

Marty Koolstra, a legendary sheep farming EP from Melbourne’s east introduced me to the plug concept some years ago. The screen had belatedly updated to reveal his code beside the 60year old patient with ‘Intermittent headaches and feeling tired > 6 weeks....’  Things were under control but this patient had been top of the screen for a while. I glanced up somewhat sheepishly as he looked over and said “…sometimes it’s easier to just pull the plug yourself...”

Occasionally, the plug is pulled by an unsuspecting junior doctor but it’s amazing how quickly they catch on. The real reason we allocate patients to interns is not to ensure they swim between the flags but to avoid these plug(s) being left in place for too long. At the end of the day though, an experienced doctor can get in there and sort out the vast majority of these patients very quickly.

Obviously these presentations can be associated with significant pathology. It is important to remain objective and focussed on a hunt for ‘red flags’. Examination of patients in the primary care setting can be cursory or minimal and a diligent but focussed examination should never be bypassed. If investigations are required they should not be part of a fishing expedition but limited to specific tests based on findings of your history or examination. If there are no red flags do not feel compelled to insert an IV and take bloods just because they have presented to a hospital. Be sure to check what has already been done before ordering that erect and supine abdominal x-ray.

The following are a list of additional presentations at high risk of forming a plug: Click on the link for a case, red flags to look out for and some tips to make your management of similar cases efficient and safe.

  1. Fatigue > 2 weeks
  2. Feeling increasingly anxious/ Palpitations
  3. Nonspecific abdominal pain > 1 week
  4. Chronic Pain/ Headache
  5. Dizziness > 2 weeks

After reading these episodes you will all know what to do the next time the screen does doesn’t seem to be moving... and I can get back to trimming my toenails in the Early Assessment Pod... on for a rant about the toughest plug of all..the patient with “medically unexplained symptoms”…

 Patients with unexplained symptoms are more commonly seen in the general practice setting but also appear in every ED and can create a very big plug. We generally  recognise they are suffering but at the same time struggle with our own emotional reaction. Without a ready diagnosis they lack a narrative to make sense of their symptoms and this makes for a very challenging encounter.

Walking that line between honesty, minimisation of iatrogenic harms and provision of adequate empathic interpersonal care is difficult but there are a few strategies that can help:

  • Define the goals of the interaction early – Once you establish that there are no red flags or evidence of impending harm explain this and negotiate an appropriate end-point  e.g. optimisation of analgesia plan and establish a pathway for follow-up.
  • Validate not only the symptoms but the frustration and uncertainty experienced.
  • Establish and maintain clear boundaries e.g. by saying “I cannot address that concern today – you will have to discuss that with your GP/ specialist during your next visit”.
  • Limit iatrogenic harm by focusing on care rather than an exhaustive search for a cause or cure.[1]
  • Include psychosocial factors in explanations for symptoms  - If specific diagnoses are not available then explanatory metaphors such as “stress headaches” are appropriate.
  • Ensure symptomatic relief is optimised – avoid iatrogenic harm by providing “enough but just enough” analgesia
  • Discuss with colleagues or  a supervisor to ensure nothing has been missed


With ready access to web based resources, patients are generally more informed and the role of the doctor has become more an interpreter rather than the sole expert. Patients may be seeking a specific diagnosis and have already invested time and effort in the diagnostic process. We tend to rail against the patient who has strong views regarding their diagnosis and this sets the scene for escalating antagonism as the patient resort to more graphic and emotional language. The result being a contest over the presence or otherwise of a legitimate illness.

We are taught to seek explicit evidence for illness. We also infer much through conversation and other observations:

  • Psychosocial context
  • Personality characteristics
  • Degree of distress
  • Possible motivations (primary and secondary gain)

There is also a strong association between unexplained medical symptoms and past trauma and abuse. The common final pathway is injury to the patient’s overall self. Unfortunately the parallels between the doctor-patient relationship and previous relationship may make the consultation difficult. Displaced hidden feelings, mistrust, anxiety, defensiveness and even hostility commonly result. It saves much time and grief to accept agree wholeheartedly with the symptoms as presented but rather than engage in an extensive series of further tests engage the patient in a discussion of likely explanations.

Formulating this explanation for the symptoms is the key but it is an unappreciated art form.

What is required is not reassurance but a future direction for care. Psychological explanations are useful and can be abstract and incorporate the patient’s model of their illness thus incorporating validation. It should be broad in scope to include reference to physical, psychological and social strategies. Where possible suggest involvement of other members of the multidisciplinary team and maintain the focus on active interventions rather than more tests and invasive treatment options.

Be positive but not dismissive. Suggest that different strategies work for different people and may need to be tried systematically to see what works.

If you can do all this you are on your way to being the complete ED doctor.



[1] Epstein RM, Quill TRE, and McWhinney IR, Somatization reconsidered: incorporating the patient’s experience of illness. Arch Intern Med 1999; 159:215-22



Intraosseous Access  

The NEJM has released a video demonstrating the indications, contraindications/ complications and technical aspects of Intraosseous Access using the EZY-IO

If you are a little unsure about this extremely useful technique it's worth a look..




Airway Management Guideline (Northern ED)

Do not be fooled, intubation in the ED is HIGH RISK business.  Nobody ever wants to be caught red-faced with a blue-faced obstructed patient and sats of 70%, a busted IV and a wonky end-tidal CO2...  any combination of these things can happen to anyone at anytime!  Dr Gerrard Marmor has produced a "get out of trouble" guide to assist emergency doctors and nurses in providing standardized airway care in the ED. 

Check out the "plan, prepare and procedure" algorithm and the SPEEDBOMB checklist and the video laryngoscope video below...



De Winter T waves

Whaaat waves? The De Winter T wave is an under-recognised infarct pattern which reliably predicts the presence of acute LAD occlusion (2% of cases) and saves lives!   It is hallmarked by :

ST depression (precordial leads) + low J-point + peaked symmetrical T waves

... and often accompanied by aVR elevation and reciprocal changes.  It is equivalent to a STEMI, so absolutely call a Code STEMI. 


Summer is here ... and so are the snakes!

There is a useful update on management of snake bites for Victorian Emergency Departments recently released on the ECIICN network.  It has a neat flow diagram (see below) de-emphasizing the role of the venom detection kit (VDK) which can sometimes be confusing and really does not help with which antivenom to give since most Victorian bites are brown and tiger snakes anyway.  It also points out how the recommended timeframes of testing and montoring the "stick-bite" case.

For more information, check out


Adenosine for SVT - the fumble-proof method.

Over the weekend, Safaa put a practice pearl to the test on a patient with SVT. I am not a fan of 3-way taps, and I am sure I'm not the only one.  So we drew up 6mg of adenosine into a 20ml syringe and rammed it straight in - and success!  No need for leaky, fidgety 3 way taps and multiple syringes.

Give it a try and let us know if it worked for you!  Also check out :


True pearls..

Dr Peter Cheng's Small  Things that make a Big Difference was a highlight of this year's regional forum.. To check out his great tips click here..



One of the talks from the Austin this week was a fascinating run through the topic of probiotics in children and adults.. Whilst my celtic ancestry demanded scepticism there was more than enough evidence presented to make me sit up and take notice..

Check out the presentation here to see for yourself..


Turn the Oxygen DOWN!

One of the most common knee jerk reactions in medicine is to give oxygen.  Short of breath?  Oxygen.  Chest pain? O2.  Abdominal pain…. And why not?? Oxygen is harmless, right?  While we do require oxygen to live, and it is 21% of our atmospheric pressure at sea level, oxygen in the medical setting should be considered a drug.  It is a substance that you are administering to treat a medical condition, and it has been shown to cause harm in some settings…  

Situation 1

A 70 year old COPD patient is brought in by MAS with a complaint of worsening shortness of breath.  Sa)2 85% on arrival. 10L/min O2 was commenced via a non-rebreather mask. The Cat 2 doctor ordeedr a salbutamol neb 5mg and hydrocortisone 100mg before you saw him. His Sa02 is up to 98%.  You’re feeling much better about yourself, and you consult the med reg for admission.  An hour later, the med reg shows up raving about admitting an unconscious patient on the trolley. You go back to check on your patient, and he is full-on gorked.  What happened?

 Oxygen has led to hypercapneic respiratory failure.  

The traditional teaching is that COPD patients depend on low oxygen to keep their reparatory rate up and blow off CO2.  Thus, if you cause hyperoxia, you knock out their hypoxic reparatory drive, they retain CO2, and spiral into a coma.  Truthfully, the hypoxic reparatory drive only accounts for about 10-15% of your respiratory drive, while CO2 levels contribute most of the rest.  So what does happen in these people when you give them high levels of O2?

A. The Haldane effect:  When we increase blood oxygen levels, hemoglobin binds to mostly oxygen (instead of CO2), leaving CO2 by itself in the blood.  As it builds up in the blood, the acute COPD patient cannot blow it off.  

B. Reversal of hypoxic pulmonary vasoconstriction: In COPD, hypoxic portions of lung are vasoconstricted to match ventilation and perfusion.  When you cause hyperoxia, this vasoconstriction eases, and you get vasodilation in these areas.  This leads to a V/Q mismatch, and increased dead space in the lung.  This again leads to poor ventilation and an increase in plasma CO2.    

There is probably some effect of decreased hypoxic respiratory drive, especially when you drive the paO2 incredibly high, but it’s true effect on hypercapnea is oven overstated (1).  This has been a contentious topic, especially in the prehospital setting.  Further excellent reference below (2).  While it has its flaws, it showed that patients with true COPD exacerbation who received oxygen titrated to a sat of 88-92% had a significantly lower mortality rate than those who received high flow oxygen (2% versus 9%), and less incidence of hypercapnia.  

So what should you do?  Find out what their normal SaO2 is..lf their baseline is 96% , 96% is fine.  If they live at 88%, that’s ok…put them on nasal cannula and titrate the Fi02 to match  the baseline Sa02.

Situation 2 

You resuscitate a cardiac arrest patient including a slick intubation and you are stoked.  ICU is full and your patient stays in the ED for a few hours.  The ICU reg has some choice words for you when he comes down and finds the FiO2 of 100%.  What’s his problem?

This is another case where oxygen has been shown to be bad for patients.  Hyperoxia following cardiac arrest has been shown to lead to increased free radical production and oxidative stress, alveolar injury and apoptosis, and increased in hospital mortality (3).  With patients spending more time in the ED waiting for an ICU bed, we have to realize that this is not something we can ignore.  Check ABG’s after intubation and titrate your ventilator settings. 

For a more detailed dicussion and further references on this topic read the following recent article from the Journal of Critical Care 

 1. New, A.  Oxygen: kill or cure? Prehospital hyperoxia in the COPD patient.  Emerg Med J. 2006 February; 23(2): 144–146.

2. Austin MA et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: Randomised controlled trial. BMJ 2010 Oct 18; 341:c5462. 

3. Kilgannon JH, et al. Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality. JAMA Vol 303, No 21, June 2, 2010;2165-2171. 


How to suture a V-flap

Take a few moments to watch this great little clip. Learn to suture flaps that look beautiful and without tension.



Fascia Iliaca Block in ED

Long gone are the days when patients with fractured NOFs languish in pain on a trolley or become obtunded from having had too much IV morphine.  Fascia Iliaca Block is fast becoming another indisposable addition to the ED physicians toolkit.  It is fast, easily learnt, superior to standard systemic analgesia and best of all, its effect can last for hours.  Not to mention your nurse will appreciate it even more when her 99yo nursing home patient needs to use the pan just as the Xray tech comes to get her!

Other benefits as suggested by evidence:

  • less sedation 
  • no increase in nausea compared to systemic opioids
  • more marked effect in extracapsular NOFs
  • safe
  • may reduce rates of delirium

Talking about bang for your buck... Femoral nerve blocks are also commonly practiced.  We advocate the FIB as it is a compartment block and is less likely to cause intravascular administration.  US might be used to increase accuracy and safety, although a blind technique is quite acceptable and simple to perform.

Landmarks : divide into thirds the distance between Pubic Tubercle and ASIS and go 2 fingerbreadths caudal to the outer X. You should be well away from femoral vessels.

The Braun pencan 22G pencil point needle (3rd from right) allows the operator to feel 2 pops (fascia lata, fascia iliaca) as the compartment is pierced and local anasthetic is injected without resistance. 








Fascia Iliaca Compartment Blockade for Acute Pain in Hip Fracture Patients : A randomised, placebo controlled trial. Anesthesiology: April 2007 - Volume 106 - Issue 4 - pp 773-778

Comparative Effectiveness of Pain Management Interventions for Hip Fracture: A Systematic Review, Ahmed et al, Annals of Internal Medicine

Mouzopoulos G, et al. Fascia iliaca block prophylaxis for hip fracture patients at risk for delirium: a randomized placebo-controlled study. J Orthop Traumatol. 2009; 10(3): 127-133

Reid N; Stella J; Ryan M; Ragg M; Use of ultrasound to facilitate accurate femoral nerve block in the emergency department, Emergency Medicine Australasia: EMA [Emerg Med Australas] 2009 Apr; Vol. 21 (2), pp. 124-30