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ED management of the Acutely Agitated patient

We all know what it is like to have an acutely agitated patient present to your ED. It is challenging, intimidating, dangerous and disruptive for your staff and and your other patients.

It can be difficult to take a step back from the evolving situation and assess . You may be consumed by the desire to regain control of the situation. It may be difficult to think about (let alone treat) whatever pathology is underlying.

What is ABD?

ABD = acute behavioural disturbance. There are several similar definitions and terminology used can be confusing (excited delirium, acute agitation or drug intoxicated or drug affected behaviour). My favourite is from the Royal College of Emergency Medicine in UK

  • Sudden onset of aggressive and violent behaviour and autonomic dysfunction
  • Often occurs in the setting of acute drug ingestion or serious mental illness

ABD is a presents as a spectrum of features that includes acute delirium, agitation as well as as adrenergic dysfunction

It is associated with sudden death in 10% cases and there have been several high profile deaths in recent years in several countries

It is important to recognise and to treat it quickly

How many patients are affected in Bendigo and in Victoria?

If we look at 2013/ 14 Victorian ambulance data and assume that crystal methamphetamine-related presentations are resposible for most of our ABD patients then we have

  • 3.4 ambulance attendances per day (0 to 10 patients) in metropolitan Melbourne
  • 0.8 ambulance attendances per day (0 to 6 patients) in regional Victoria
  • Most patients present between midday and 6pm in metropolitan Melbourne, between the hours of 6pm and midnight in regional Victoria
  • The peak day was Sunday in metropolitan Melbourne, the peak day was Saturday in regional Victoria

What are the typical symptoms?

A person can display mildly erratic behaviour ranging to extreme agitation and physical exertion

Things to look out for

  • extreme aggression, violent behaviour
  • excessive strength/ continued struggling with police restraint
  • reduced reaction to pain
  • acute psychotic state
  • hyperthermia, tachypnoea, tachycardia

ABD patients may have symptoms that are similar to other conditions. Other things to think about are

  • hypoxia
  • substance intoxication or withdrawal
  • hypoglycaemia
  • head trauma
  • CNS infection, haemorrhage
  • seizure, stroke or post ictal state

Describe general management principles for this patient group?

The general approach to these patients is very important

Remember you are dealing with one of 3 different types of patients

  • cooperative
  • disruptive not dangerous
  • excited delirium

Listen to Reuben Strayer give a fascinating talk about this at #SMACCDUB in June 2016

General principles that I try to implement

  • Evaluate your patient in safe area – evacuate other patients if this is in the ambulance entrance area
  • Make sure your staff is safe, are there any concealed weapons, can you move the patient to a secluded area, involve your security staff early. Call a Code Grey!

De-escalation techniques are important

  • talk to your patient in a calm and confident voice
  • do not confront your patient
  • do not maintain prolonged eye contact
  • never stand over them
  • offer them food or a cigarette if this is appropriate
  • try reduce the amount of ‘testosterone’ in the room if it is safe to do so

Different patients will respond differently and there is no one approach that fits

Some patients are unsuitable for de-escalation and physical restraint may be required. This is defined as the ‘intentional restriction of a person’s voluntary movement or behaviour by the use of a device, removal of mobility aids or physical force’

In most cases, in ED we will use category 1 restraint (emergency single episode restraint) and documentation must include – reason for restraint, condition prior to restraint (see SAT score), form of restraint applied, details of event, length of time restraint was applied for and condition post restraint. Restraint devices should be removed as soon as the patient is adequately sedated

SAT tool for sedation assessment

The Sedation Assessment Tool is a 7 point scoring system, based on level of arousal and speech patterns

  • It was described in Emergency Medicine Australasia in 2011
  • It ranges from plus 3 which is highly agitated to minus 3 which is heavily sedated
  • Endpoint for sedation is -1 (patient is drowsy but rousable)

 

SEDATION ASSESSMENT TOOL (SAT)
Score Responsiveness Speech Scale
+3 Combative, violent, out of control Continual loud outbursts +1 to +3

Agitation

+2 Very anxious and agitated Loud outbursts
+1 Anxious/restless Normal/talkative
0 Awake, calm Speaks normally 0 = normal
-1 Asleep but rouses if name called Slurring or slowing -1 to -3

Sedation

-2 Responds to physical stimulation Few recognizable words
-3 No response to stimulation Nil

 

What drugs can you use?

Chemical sedation or rapid tranquilisation may also be required for an ABD patient.

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Australia is fortunate to have access to droperidol, this is thought to be the first line agent to treat most cases of  ABD. However it is not available in Ireland, UK or in the USA

The main drug categories I use are benzodiazepines, antipsychotics and sometimes ketamine

Benzodiazepeines are familiar to most emergency doctors, they are safe you can give them via the oral and parenteral route. The main side effect to watch out for is respiratory depression. Lorazepam is not readily available in Bendigo Health and this acts as a useful bridge between (short acting) diazepam and other longer acting agents

Antipsychotic medications include droperidol or olanzepine. They are dopamine receptor antagonists and this is why they may work well in ABD – theory is that is caused by dopamine excess. Be careful with acute dystonic reactions

My treatment approach is based on the patient’s SAT score

  • SAT +1 – patient is cooperative 

Offer them something orally – use diazepam or olanzapine – any sedative will suffice

  •  SAT +2 – patient is agitated, vocal loud and probably hard to reason with

Now they are disruptive (but not yet dangerous) this is a difficult group to treat and requires tactical negotiation and experience

If possible try something oral but you may need IM meds early

Start with droperidol 5 – 10 mg IM and wait 15 minutes to see how this works

Repeat this dose if needed and now add in midazolam 5mg IM as a 2nd line agent

  • SAT+3 – your patient is aggressive and dangerous this is a full blown excited delirium!

Draw up 2 syringes – 10mg IM droperidol and 10mg IM midazolam

Use an IM injection and get your patient to resus to monitor them

What about ketamine – can I use it?

Things to consider

  • In recent years, there has been a splurge in the number of articles written by authors espousing the use of ketamine for the “Chemical takedown”
  • We use IM ketamine sucessfully for paediatric sedation – it is reasonable to consider it’s use in this situation
  • Many of the studies that describe droperidol use are done in Australia – maybe this is why ketamine has not been adopted (yet)
  • Ketamine has been incorporated into Victoria prehospital guidelines as a first line agent in excited delirium – see CPG A0709
  • A suggested single dose agent  is ketamine 5 mg/kg IMI, see Reuben Strayer again
  • My feeling is that ketamine will be introduced on a gradual basis once practitioners become more used to using it

Post sedation care for ABD patients

  • Be careful with a patient that may have taken a combination of drugs – benzos could cause respiratory depression or hypotension in this group
  • If you get IV access once the patient is settled then you could use this for further doses – no need to make this a priority at the start
  • Monitor them as if the have had procedural sedation – this means regular pulse ox, ECG and BP monitoring as well as SAT score
  • If a patient develops a dystonic reaction as a result of antipsychotic use then reach for benztropine 1-2mg IV
  • When the patient is sedated, the care is mainly supportive – check electrolytes, rehydration will often be useful, do a full examination and get imaging if this is indicated

What does the literature say about drugs for ABD?

The science here is pretty scarce

There have been a few papers published in recent years – led by Australian authors

  • The 1st DORM study was published in the Annals of Emergency Medicine in 2010 by Isbister et al. It used 3 arms to compare droperidol, midazolam and the droperidol/ midaz combo for 91 agitated ED patients.It showed that there was no difference in time to sedation when using droperidol, midaz or the combination. There was less top up sedation needed when the combination was used and the incidence of prolonged QT interval was the same in all groups
  • DORM 2 was published in the Annals of Emergency Medicine in August 2015 by Calver et al. It had over 1000 patients in a prospective observational study across 6 Australian EDs. Their main finding was that droperidol was safe to use for sedation – 13 of 1009 patients had abnormal QT intervals and 7 of these were using another medication that could explain this. DORM 2 had it’s limitations but seems to support safety of droperidol
  • The SOOTH study was been published in 2016. This was a RCT in 2 Melbourne metropolitan EDs and included at 349 acutely agitated patients requiring intravenous sedation. The authors found that midazolam and droperidol used IV for sedation is better than monotherapy using either droperidol or olanzapine alone

What about children?

If you are faced with an agitated child the general management principles remain the same as in adults

  • deescalate the situation
  • offer oral sedation first, parenteral sedation if needed

The Royal Children’s Hospital Melbourne guidelines suggest a treatment algorithm

What does #FOAMed say?

There are many fantastic resources listed on this topic – here are my favourite

Listen to some of the experts talk about how you could manage the agitated patient

 

Take home points to consider

  • There are many drug regimens that are available and safe
  • If you are a trainee, there is no need to be too gung-ho to use new drugs that are outside your EDs normal practice, talk to your bosses and choose wisely!
  • If you are a consultant developing a new policy then talk to your colleagues and see what others are using and what you could use in your setting
  • A combination of droperidol and midazolam seem to be the standard in Australia at the moment

Promises from #ACEMVIC16

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If you enjoyed my talk in Torquay and you want to know more about #FOAMed and how you could benefit from using Twitter here are some resources that you will find interesting

Enjoy your journey on Twitter and I hope that you find it as fascinating as I have! Feel free to message me if you have any queries about this

@cianmcdermott

 

 

 

Lost dogs and lessons in fluid tolerance

Winter and spring have been unseasonably wet for central Victoria. With plenty of moisture in the soil, things were looking green and gorgeous so when a friend asked me to farm-sit for him I jumped at it. Looking after horses, a moustachioed cat and a beautiful border collie were a small price to pay for enjoying a landscape of granite boulders and grape vines. That was until the dog ran away.

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Dusk arrived and Annie was still missing in action. Terrified by the idea of telling my friend about his lost dog, I decided to chase her down. I had been warned about the risk of getting bogged if I deviated off track…. meh! The ground seemed solid, I had a decent 4wd, and I clearly knew better. Spotlights on and eyes scanning, I started cruising across the paddocks. But pride comes before the fall. It was only when the ute suddenly stopped moving did I appreciate that the ground was less fluid-tolerant than my gestalt told me.  Lost car, lost dog, lost for words (other than 4-letter ones), I tried to make meaning of the day’s events and realised it was a teachable moment in the management of sepsis in the emergency department.

 

 

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When patients arrive in the ED with febrile hypotension, we routinely prescribe in excess of 20-30cc/kg of salt water. The pseudoaxiom is that fluid bolus therapy will improve macrocirculation (arterial blood pressure), and therefore improve microcirculation (tissue perfusion). This is unlikely to be true. Empirically “aggressively resuscitating” people with fluid boluses probably causes harm.  Like the fool in the Hilux chasing the missing dog, we chase haemodynamic targets with unproven watery therapies (or disproven if you’re a marginalised African child) that are physiologically suspect and warrant close examination.

The pathophysiology of sepsis is complicated. The basic mechanisms of the disease, however, (at least as we currently understand it) are less complex:  vasodilation and glycocalyx (GCX) dysfunction. Organ dysfunction in septic shock can largely be attributed to one or both of these mechanisms. It is not due to hypovolaemia.

Currently there are no treatments for GCX stabilisation (unless you are a Scandinavian neonate having open heart surgery in which high doses methyl-prednisolone seems to reduce concentrations of a plasma syndecan-1; an alleged surrogate for GCX dysfunction). Current treatments for vasodilation include noradrenaline, adrenaline,  vasopressin, methylene blue, and angiotensin-2.  In sepsis, fluids cause organ dysfunction through worsening interstitial oedema due to GCX dysfunction, and cause vasodilation by stimulating release of naturetic peptides. It is therefore bizarre that it should be used as a first line therapy for septic shock.

Pseudoaxiom one: Fill the tank before you squeeze.

There is no tank to fill in sepsis, and a vasodilated state is probably best managed with vasoconstrictors.  Giving a septic patient a fluid bolus will increase cardiac filling pressures, triggering release of naturetic peptides which cause vasodilation.  Thus in sepsis, fluids can be considered a vasodilator therapy.  If clinicians are concerned that there is inadequate preload, the LV end-diastolic volume should be measured with echo.

Pseudoaxiom two: fluids improve stroke volume

Patients with septic shock have a depressed Starling curve with a reduction in recruitable contractility via increased preload. > 50% of patients with septic shock have diastolic dysfunction which responds poorly to fluid therapy.

img_3269Ognibene FP, Parker MM, Natanson C, Shelhamer JH, Parrillo JE. Depressed left ventricular performance: response to volume infusion in patients with sepsis and septic shock. Chest 1988; 93: 903–1

 

Pseudoaxiom three: fluid stays in the circulating volume

In patients with septic shock less than 5% of administered fluid remains in the intravascular space at 1hr. This fluid leaks from the vascular compartment to enter the interstitium, causing organ dysfunction. The Marik-Philips EVLW curve illustrates the respiratory harms of fluid therapy in patients with increasing filling pressures. In the abdomen, increased initerstital oedema causes intra-abdominal hypertension, gut failure and renal failure.

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Pseudoaxiom four: albumin is the answer when crystalloid fails

The disrupted GCX enables translocation of albumin into the interstitium, where it  continues to exert an osmotic effect causing further interstitial oedema.

Lessons Learnt

The concept of fluid tolerance in pursuit of haemodynamic “stability” in shocked septic patients is as ill-fated as a hunt for a lost dog across a muddy paddock in the dark. Even though there was no surface water visible, the ground swallowed up my ute before I even realised I was on a path to trouble. So too do we drive our septic emergency department patients further into multi-organ dysfunction with iatrogenic salt-water drowning.

So how do I manage septic shock in the ED? After antibiotics are on board I perform a focused haemodynamic assessment using echo to examine preload (LVEDD or LVEDA), contractility (fractional shortening or fractional area change), filling pressures (interatrial septal motion), and diastolic function (E/A, E/e prime).  This takes less than 5 minutes. If patients have had no recent oral intake I replace guesstimated deficits (4, 2, 1 method) then commence maintenance fluids (D5W and providing Na, K, Mg as required [N.B. Australian RDI of sodium is 40mmol, not 154mmol]). I concurrently target a MAP of 65-70mmHg using a combination of noradrenaline, vasopressin and adrenaline, depending on the haemodynamic state.

So what happened to the ute you ask? Like the drowned patient needing CRRT and an inpatient bed before they break the NEAT 4-hour rule, I had to phone a critical care colleague who spent 4 hrs helping me dig the car out of the quagmire and haul it to dry ground.  Annie came back on her own volition without intervention and I scored a well earned “told you so” from her master.

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With thanks to Paul Marik, Thomas Woodcock, Rinaldo Bellomo and John Myburgh for inspiring me to care about fluids.

Special thanks to Caitlin Young for helping to dig me out of my stupidity.

The many faces of EM trainees: a quick feelgood post from a proud acting director

We’re looking forward to working with a great team in 2017 and the make up of it demonstrates the extraordinary diversity that makes up Emergency Medicine in Australia. Even the core group of people who have come straight to EM via intern and HMO years (and don’t get me wrong, that was me, falling in love with EM in term 1 of intern year and never toying with anything else) bring a great mix to the team. We have people from tiny rural Australian towns, and big cities, coming from the UK, Asia and Africa and via Canada, writing for the Victorian Institute of Forensic Medicine in their “spare time”, building a craft distillery, and lord knows what else I am yet to discover.

One of our advanced trainees next year is currently in the Pacific, doing a term in developing world EM while one of our new provisional trainees is in Liverpool England, doing a Diploma of Public Health; see her blog post here, describing her vision for a career combining EM and world health.

We’ve also got 4 new full-time consultants starting with us next year, all of them current or previous trainees. They include one of my first ever registrars, one of the first of our international graduate HMOs to be seduced into EM training, and two of our first advanced trainee recruits. I can’t tell you proud I am, of these four people, of the contribution our team was able to make to their development and of the distance that Bendigo ED has come, from a place where we didn’t even have a FACEM on every day and where there were frequently no ACEM trainees on the roster, to a place that has been able to train and retain 4 really high quality emergency physicians who would be a credit to any department anywhere in the world.

Thanks everyone for coming on board for 2017, a new hospital and more fantastic Emergency medicine training.

 

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Social Media workshop

In preparation for our Social Media ‘How to Get Started’ workshop, follow these links

The concept is called ‘flipping the classroom’ – encouraging you to pre-learn before we come together and discuss

The videos are taken from Rob Rogers @EM_Educator (of University of Kentucky EM, iTeachEM and The Teaching Course)

I had the good fortune of attending #TTCAus16 in July & can recommend it to anyone interested in this fascinating side of medical education! It’s on in Melbourne September 2017

@cianmcdermott

 

 

 

 

 

 

 

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Broken ladders and analgesia

What’s the age cut-off for stupid males (or females) to no longer be allowed to climb ladders? As long as it’s under 35 years old I’m safe.

But that’s not the reason for today’s post.  Yesterday I saw half a dozen patients with various painful conditions who at some stage had been prescribed opioids as first line therapy without simple analgesic adjuncts. A quick straw poll of the staff on shift at that time revealed that no-one apart from myself had heard of the WHO pain ladder.

Today is a beautiful spring day in central Victoria. With crisp air, warm sun, and bees happily  gathering digitalis-laden pollen from my foxgloves, it was a good opportunity to get on the roof and clean out the gutters of the house.  Until my ladder broke…. Was it a teachable moment for my personal safety? No.  But it seemed like a teachable moment for how I approach analgesia in the ED.

Climb the ladder to escape pain.

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