Category Archives: Resus

Life-saving medicine

It’s Tamponade – Now What?

You ultrasound the chest of your shocked patient in resus with fluid refractory hypotension. You see fluid around the heart. The right ventricle keeps bowing inwards, which you recall being described as ‘a little invisible man jumping up and down using the RV as a trampoline’, and you know this is in fact a sign of right ventricular diastolic collapse.
 

image courtesy of thebluntdissection.org

The collapse of the right side of the heart during diastole is the mechanism for shock and cardiac arrest due to tamponade, because the high pericardial pressures prevent the right heart from filling in diastole. This patient therefore has ‘tamponade physiology’ on ultrasound. A quick scan of the IVC shows it is dilated and does not collapse with respiration. This confirms a high central venous pressure (as do the patient’s distended neck veins), also consistent with tamponade physiology.
 
A formal echo done in resus confirms your suspicion of a dliated aortic root and visible dissection flap, so the diagnosis is now clear. This is type A aortic dissection with tamponade. The patient remains hypotensive and mottled with increasing drowsiness. Cardiothoracic surgery is based at another hospital site 30 minutes away by ambulance.
 
As the critical care clinician responsible for, or assisting with this patient’s care (emergency physician, intensivist, anaesthetist, rural GP, physician’s assistant, etc.), how do we get this patient to definitive care and mitigate the risk of deterioration en route? Let’s discuss the options using real life case examples, and consider the physiology, the evidence, and the dogma.
 
Here are four key questions to consider:
1. To drain or not to drain the pericardium?
2. To intubate or not to intubate?
3. If they arrest – CPR or no CPR?
4. How to transfer – physician escort or just send in an ambulance on lights and sirens?
 
Here are three scenarios that follow the intial assessment of the above patient. They are based on similar cases shared with me by participants on the Critical Care in the Emergency Department course.
 

Case 1

The patient is obtunded with profound shock and too unstable for transfer. The resus team undertakes pericardiocentesis and aspirates 30 ml of blood. The patient becomes conscious and cooperative and the systolic blood pressure (SBP) is 95 mmHg. The patient is transferred by paramedic ambulance to the cardothoracic centre where he is successfully operated on, resulting in a full recovery.
 

Case 2

As the patient is unconscious and requires interhospital transfer, the decision is made to intubate him for airway protection. He undergoes rapid sequence induction with ketamine, fentanyl, and rocuronium in the resus room. After capnographic confirmation of tracheal intubation he is manually ventilated via a self-inflating bag. The ED nurse reports a loss of palpable pulse and CPR is started. A team member suggests pericardiocentesis but a senior critical care physician says there is no point because ‘it won’t fix the underlying problem of aortic dissection’ and ’the blood will be clotted anyway’. After a brief attempt at standard ACLS, resuscitation efforts are discontinued and the patient is declared dead.
 

Case 3

The patient is hypotensive with a SBP of 90mmHg and drowsy but cooperative. The receiving centre has accepted the referral and an ambulance has been requested. The critical care physician responsible for patient transfers is requested to accompany the patient but declines, on the basis that ‘these cases are just like abdominal aortic aneurysms – they just need to get there asap. If they deteriorate en route we’re not going to do anything.’
The patient is transferred but 15 minutes into the journey he becomes unresponsive and loses his cardiac output. The transporting paramedics provide chest compressions and adrenaline/epinephrine but are unable to resuscitate him.
 
These cases illustrate some of the pitfalls and fallacies associated with tamponade due to type A dissection.
 

Pericardiocentesis

Pericardiocentesis can definitely be life-saving, restoring vital organ perfusion and buying time to get the patient to definitive surgery. Numerous case reports and case series provide evidence of its utility, even in patients in PEA cardiac arrest(1). The authors of the two largest cases series both used 8F pigtail drainage catheters(1,2).
Reports of pericardiocentesis in tamponade due to aortic dissection. From Cruz et al (1)
Reports of pericardiocentesis in tamponade due to aortic dissection. From Cruz et al (1)
One key component of procedural success was controlled pericardial drainage, removing small volumes and reassessing the blood pressure, aiming for a SBP of 90 mmHg. The danger is overshooting, resulting in hypertension and extending the underlying aortic dissection which can be fatal (3).
 
Those still unconvinced by the evidence may be swayed by guidelines. The 2015 European Society of Cardiology Guidelines for the diagnosis and management of pericardial diseases (4) state:
 
“In the setting of aortic dissection with haemopericardium and suspicion of cardiac tamponade, emergency transthoracic echocardiography or a CT scan should be performed to confirm the diagnosis. In such a scenario, controlled pericardial drainage of very small amounts of the haemopericardium can be attempted to temporarily stabilize the patient in order to maintain blood pressure at 90 mmHg. (Class IIa, Level C)”
 

Intubation

Deterioration of tamponade patients following intubation is well described in the literature and the risk is well appreciated by cardiothoracic anaesthetists(5). Once positive pressure ventilation is started, positive pleural pressure is transmitted to the pericardium, where pressures can exceed right ventricular diastolic pressure and prevent cardiac filling. The result is a fall in and possible loss of cardiac output. This is further exacerbated by the addition of PEEP(6). One suggested approach if the patient must be intubated for airway protection but is not yet in the operating room with a surgeon ready to cut, is to consider intubation under local anaesthesia and allow the patient to breathe spontaneously (maintaining negative pleural pressure) through the tube until the surgeon is ready to open the chest(5). Alternatively preload with fluid, use cautious doses of induction agent, and ventilate with low tidal volumes and zero PEEP. However the patient can still crash, so remember that these effects of ventilation on cardiac output in tamponade can be mitigated by the removal of a relatively small volume of pericardial fluid(6).
 

Cardiac Arrest

In cardiac arrest, external chest compressions are unlikely to be of benefit. In a study on baboons subjected to cardiac tamponade, closed chest massage resulted in an increase in intrapericardial pressure. There was an increase in systolic pressure, but a marked decrease in diastolic pressure, with an overall decrease in mean arterial pressure(7).
Pressure changes from CPR during tamponade in baboons. From Möller et al (6)
Pressure changes from CPR during tamponade in baboons. From Möller et al (6)
This would lead to impaired coronary perfusion and would be very unlikely to result in return of spontaneous circulation (ROSC). In the clinical situation described above, it is only relief of tamponade that is going to provide an arrested patient with a chance of recovery.
 

Transport

For patients with cardiac tamponade requiring interhospital (or intrahospital) transfer, it would seem vital therefore that the patient is accompanied by a clinician willing and capable to perform pericardiocentesis in the event of severe deterioriation or arrest en route. This simple life-saving intervention to deliver the patient alive to the operating room should be made available should the need arise.
 
 

Summary

  • Patients presenting in shock from cardiac tamponade often have treatable underlying causes and represent a situation where the planning and actions of the resuscitationist can be truly life-saving.
  • Pericardiocentesis is recommended in profound shock to buy time for definitive intervention. Controlled pericardiocentesis should be performed paying strict attention to SBP to avoid ‘overshooting’ to a hypertensive state in type A aortic dissection. In cardiac arrest, chest compressions are likely to be ineffective and pericardiocentesis is mandatory for ROSC.
  • The institution of positive pressure ventilation often results in worsened shock or cardiac arrest, and this is exacerbated by PEEP. Where possible, avoid intubation until the patient is in the operating room, or use low tidal volumes and no PEEP. Even then pericardiocentesis may be necessary to maintain or restore cardiac output.
  • Patients requiring transport who have tamponade should be accompanied by a clinician able to perform pericardiocentesis in the event of en route deterioration.

References

  1. Cruz I, Stuart B, Caldeira D, Morgado G, Gomes AC, Almeida AR, et al. Controlled pericardiocentesis in patients with cardiac tamponade complicating aortic dissection: Experience of a centre without cardiothoracic surgery. European Heart Journal: Acute Cardiovascular Care. 2015 Mar 19;4(2):124–8.
  2. Hayashi T, Tsukube T, Yamashita T, Haraguchi T, Matsukawa R, Kozawa S, et al. Impact of Controlled Pericardial Drainage on Critical Cardiac Tamponade With Acute Type A Aortic Dissection. Circulation. 2012 Sep 10;126(11_suppl_1):S97–S101.
  3. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic dissection. Is pericardiocentesis harmful? Circulation. 1994 Nov 1;90(5):2375–8.
  4. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. European Heart Journal. 2015 Nov 7;36(42):2921–64.
  5. Ho AMH, Graham CA, Ng CSH, Yeung JHH, Dion PW, Critchley LAH, et al. Timing of tracheal intubation in traumatic cardiac tamponade: A word of caution. Resuscitation. 2009 Feb;80(2):272–4.
  6. Möller CT, Schoonbee CG, Rosendorff C. Haemodynamics of cardiac tamponade during various modes of ventilation. Br J Anaesth. 1979 May;51(5):409–15.
  7. Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamic effects of external cardiac massage in trauma shock. The Journal of Trauma: Injury, Infection, and Critical Care. 1989 Oct;29(10):1430–3.

Difficult Airway? What Kind Exactly?

crazed-nutter-sm
Mention the term ‘difficult airway’ and many of us will conjure mental images of some kind of distorted anatomy. However, airway management may be ‘difficult’ for a number of reasons, and no internationally agreed definition of the term exists. Given the wrong staff and circumstances, an ‘easy’ airway in your or my hands may indeed become very difficult. In their editorial “The myth of the difficult airway: airway management revisited” (1) Huitink & Bouwman state:

“In our opinion, the ‘difficult airway’ does not exist. It is a complex situational interplay of patient, practitioner, equipment, expertise and circumstances.”

Airways that are anatomically difficult (eg. limited mouth opening, short thyromental distance, large tongue, neck immobility, etc.) and physiologically difficult (hypoxaemia, hypotension, acidosis) are well described among FOAM resources (2-4). In addition to these, a third category of difficulty is well worth considering.

At the smaccDUB conference, intensivist and human factors legend Peter Brindley described three types of difficult airway:

  1. Anatomically difficult
  2. Physiologically difficult
  3. Situationally difficult
    brindleysm
    Brindley = Legend

This last category probably surfaces more commonly than realised, particularly outside the operating room.

Imagine attending a cardiac arrest call on a medical ward. The patient is a 70 year old 120 kg male. The nurses have flattened the bed and discarded the pillow to optimise supine position for CPR. Gobs of vomitus splash from the patient’s pharynx with each compression. The wall suction system is disconnected. There is no bougie in the crash cart’s airway drawer. The nearest capnograph is on another floor of the hospital. In this scenario, no matter how excellent the critical care practitioner’s airway skills, this is a damned difficult airway.

I think Brindley’s third category is a term that should catch on, as a way of helping analyse cases that progress suboptimally and to identify factors during pre-intubation checks that can be addressed. It is terminology that I have added to my own Resuscitese Lexicon, particularly for case discussions during morbidity & mortality and airway audit meetings.

I would like to hear the ‘Situationally Difficult Airway‘ become more widely used, as it fills a gap in how we describe this important area of resuscitation practice.

 

 

1. Huitink JM, Bouwman RA. The myth of the difficult airway: airway management revisited. Anaesthesia. 2015 Mar;70(3):244–9. (Full text)

2. LITFL: Airway Assessment

3. EMCrit: HOP Killers

4. PulmCCM: The Physiologically Difficult Airway

The Course I Made For Me

CCED2013sm

My whole career has been about finding ways to optimise resuscitation. Many others also have the bug. The ‘resuscitationist movement’ is sweeping across Europe, with Katrin Hruska and Femke Geijsel about to run amazing courses for emergency teams in Sweden and The Netherlands. I have the honour of joining Clare Richmond in helping them do that. But first Critical Care in the Emergency Department is going to be run in London one more time.

This course contains the stuff I wish someone had told me as a registrar. A synthesis of my learning points in intensive care, prehospital & retrieval medicine, paediatric critical care, and being a front line ED doc for 20 years.

I’ve been running the course for over a decade, including in London, Birmingham, Basingstoke, Dublin, Stockholm, Sydney and Maribor. Each time I try to improve it, and try to squeeze one or two more learning points in. It’s a tough day – just me and fifty or so critical care cases to talk about. But no-one goes to sleep – guaranteed! Everyone has to work – to talk, think, and interact.

It is of course primarily a clinical course, focusing on optimal clinical practice. But consistent feedback from participants is that they get far more from it: a reassurance that they’re not crazy wanting to do more for their patients, and a way forward for remaining inspired and motivated to make changes to their practice and to their departments.

If you’re able to make it to London next Friday 26th August treat yourself to a day of training you’ll never forget. There are no planned future dates for this course in the UK so get it while you still can!

You can register here or read more here

CCED-FBF-sm

 

 

Hilar Twists & Human Error

This engaging scene from ‘Code Blue‘ demonstrates a Helicopter Emergency Medical Service team managing a patient with major thoracic haemorrhage. They have done a right thoracotomy and want to clamp the hilum but there’s some kit missing from the pack.

This scene has some great discussion points for prehospital professionals, even if the specific scenario is somewhat unlikely for most people’s practice:

  • Non-compressible haemorrhage is possibly the biggest single clinical challenge when you’re a long way from hospital
  • Agitated friends and family can be disruptive – allocate a rescuer to look after them
  • Having blood products to give is essential
  • Don’t rely on the memory of individuals, who are fallible, to pack your equipment. “I was sure I put them in” didn’t cut it when the team needed forceps to clamp the pulmonary hilum and stop the bleeding. Checklists are the in thing, for good reason.
  • Luckily, you don’t need to clamp the hilum (which is tricky) in massive unilateral thoracic haemorrhage. You can just twist the lung 180 degrees on the hilum so it’s upside down. This can prevent further haemorrhage and air embolism.

 

What’s a hilar twist then?

The hilar twist manoeuvre, as it’s called, is worth learning if you’re a clinician who is prepared to do resuscitative clamshell thoracotomy for penetrating traumatic cardiac arrest. The clamshell is quick and provides excellent exposure(1) and is preferred to lateral thoracotomy(2).

The primary purpose of clamshell thoracotomy in penetrating traumatic arrest is to relieve cardiac tamponade and control a cardiac wound(3). It is well described and continues to save lives in the prehospital setting(4).

However, sometimes you’ll open the chest and the pericardium will be empty (other than containing the heart of course), and there will be massive haemorrhage on one side of the chest. Although most of these patients will be unsalvageable outside a trauma centre’s operating room, it’s worth trying something once you’ve gone to all the trouble of opening the chest. The hilar twist(5) is probably the best option for the non-surgeon, especially when some muppet’s forgotten to pack a clamp.

In order to make the lung mobile enough to twist, it’s first necessary to cut through the inferior pulmonary ligament. This is also known as simply the pulmonary ligament (because there’s no superior equivalent) and sometimes the inferior hilar ligament. It’s not actually a ligament, but an extension of the parietal pleura extending downwards in a fold from the hilum. Some describe it as hanging down from the hilum like a ‘wizard’s sleeve’, which invariably gets a giggle from some of our trainees from the United Kingdom for some reason.

Hilar Twist

 

After cutting the ligament completely to the level of the inferior pulmonary vein, the lung is then twisted ‘lower lobe towards you’, ie. lower lobe is rotated anteriorly over the upper lobe until the lung is oriented ‘upside down’. The twisted vessels around the hilum become occluded and further haemorrhage from that side should be limited. Other priorities in the arrested patient will be aortic occlusion, internal cardiac massage, and blood products. Packs may be required to keep the lung from untwisting, and if return of spontaneous circulation is achieved, there is a risk of dysrhythmia, right heart failure, and refractory hypoxaemia.

I’ve only done this on pigs and human cadavers so am not speaking from any reassuring level of experience or competence. The literature is out there to read, and it’s up to you to decide how you want to expand or limit your options when you’ve cracked that chest in an arrested patient.

References

1. Flaris AN, Simms ER, Prat N, Reynard F, Caillot J-L, Voiglio EJ. Clamshell incision versus left anterolateral thoracotomy. Which one is faster when performing a resuscitative thoracotomy? The tortoise and the hare revisited. World J Surg. 2015 May;39(5):1306–11.

2. Simms ER, Flaris AN, Franchino X, Thomas MS, Caillot J-L, Voiglio EJ. Bilateral Anterior Thoracotomy (Clamshell Incision) Is the Ideal Emergency Thoracotomy Incision: An Anatomic Study. World J Surg. 2013 Feb 23;37(6):1277–85.

3. Wise D. Emergency thoracotomy: “how to do it.” Emerg Med J. 2005 Jan 1;22(1):22–4.

4. Davies GE, Lockey DJ. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician-Performed Resuscitation Procedure That Can Yield Good Results. The Journal of Trauma: Injury, Infection, and Critical Care. 2011 May;70(5):E75–8.

5. Wilson A, Wall MJ Jr., Maxson R, Mattox K. The pulmonary hilum twist as a thoracic damage control procedure. The American Journal of Surgery. 2003 Jul;186(1):49–52.

Convergent Evolution in the Jungles of Critical Care

boss-of-the-mob-1400090-1279x1923By Stuart Duffin
Expat Brit, intensive care physician and anaesthetist at Karolinska University Hospital in Stockholm, Sweden. Stuart trained in the UK, and spent some time working Australian emergency departments.

One of the most striking things for me about our new/old pan-specialty of critical care, brought into focus by the world-shrinking effects of FOAM and twitter, is just how differently it falls into the domains of the established specialities in different parts of the world. This leads inevitably to comments like, “emergency physicians shouldn’t intubate”, “anaesthetists cant do sick”, “nurses cant be doing such and such”, and so on. All of these statements are clearly equally rubbish because obviously, in certain parts of the world, they do. And they do it really well. Sure there are differences between countries and continents, populations and environments, but when it comes down to it, it doesn’t matter where you are, people still get sick, infected, pregnant, run over, stabbed or hit around the head with heavy things.

All over the world, in our previously quite isolated environments, these same ‘selection pressures’ have forced healthcare providers to evolve by the process of convergent evolution. Although obviously not strictly darwinian, the undeniable effects of simultaneous evolution by survival of the fittest-to-practice can be seen.

Convergent evolution is the process by which, in different parts of the world, completely different species have evolved in parallel to fill similar roles and have similar features. It didn’t matter whether it was a deer, a wildebeest or a kangaroo, there was a vacancy for a fairly big animal who liked eating grass and moved in big groups, and someone stepped up.

Unsurprisingly, critical care resuscitationists are also a little different from country to country and from continent to continent. They have different titles and work in slightly different ways. But when you really look at a critical care doc in action, or talk to one, or follow one on Twitter, we are all cut from the same cloth. I would argue that FOAM has created a critical care zoo in which the kangaroos and antelopes, lemurs and monkeys, aardvarks and echidnas and anaesthetists and emergency physicians are all chucked into the same cage. They’re all looking at each other thinking, “you look like me, but somehow not. We seem to do the same stuff, but we’re not identical – it cant be right!”.

In The United States, the idea of an anaesthetist doing a clamshell thoracotomy would be a little strange. In Scandinavia, an emergency physician doing central lines and fiberoptic intubation in resus would be just as eyebrow raising. A Swedish intensivist and anaesthetist spent some time working in Australia as an ICU senior reg. When attending a patient in resus the emergency physician there announced “we need an airway guy”. My colleague answered “I’m the airway guy”. “No an anaesthetist” replied the emergency physican. “I am an anaesthetist!” “No an….” and so it went on.

The effects of this process are of course by no means limited to doctors. Nurses, paramedics and physiotherapists are all part of this still changing ecosystem. A colleague of mine was showing a visiting Australian emergency physician our trauma bay and describing how major trauma is managed here without the involvement of emergency physicians at all. “When it’s really urgent, it’s anaesthesia and surgery” he explained. I wonder how that went down? There is an element of truth to the statement but the words are wrong. It should have been “When it’s really urgent, it’s airway, access, transfusion, invasive procedures and resuscitation thinking”.

The job title of the person who actually holds the knife/laryngoscope/needle and has what it takes to get it done isn’t important. When the push comes to shove and the bad stuff bounces off the fan, it’s more about skillset and mindset, and less about the collection of letters under your name on your badge, or after your name on your CV.

Advice To A Young Resuscitationist

Advice-to-Young-Resuscitationist

This talk was the opening plenary given at smacc Chicago. The title they gave me was ‘Advice To A Young Resuscitationist. It’s Up To Us To Save The World‘ but I ditched the last half because, as I point out later in the talk, I don’t think it is up to us to save the whole World. Some AV muppetry at the conference centre prevented the smacc team from being able to include the slides, so I’ll post those too at some point. You can hear the talk as a podcast at the ICN or on iTunes

The references for the talk are here

 

Learning To Speak Resuscitese

team-sm

In the resus room, clarity of communication between team members is critical to patient safety and effective resuscitation. We are used to following standardised clinical algorithms for cardiac arrests and many other emergency presentations, but there is no standardisation of vocabulary or communication style. Communication failures are a major source of error in resuscitation, suggesting this is an area in which we need to improve.

Defining your lexicon

A contrast with the aviation industry was drawn by neonatologist Dr Nicole Yamada, who points out that pilots and air traffic controllers use an effective, concise, standardised set of words and phrases that are universally understood, for example ‘stand by’, ‘unable’, ‘read back’, and ‘cancel'(1).  She proposed adapting a similar resuscitation-specific lexicon modelled after aviation communication which ‘would aid in streamlining communication during time-pressured clinical situations when seconds count and errors can kill.‘(2)

table3Yamadasm

Dr Yamada tested this approach in a small study of simulated neonatal resuscitation. Standardised communication techniques were associated with a trend toward decreased error rate and faster initiation of critical interventions.(3)

Avoiding the fluff

In the absence of standardised approaches to communication, humans in the resus room often choose language which indirectly acknowledges social hierarchies. For ad hoc teams, phrases may be chosen which are least likely to offend people with whom we’re unfamiliar, or may be deferential in cases of real or presumed authority and expertise gradients. The consequence of this is the use of ‘mitigating language‘. Examples might be:

“Any chance you could pop a line in?”

“Would someone mind letting me know if they can feel a pulse?”

“Do you want to have a think about setting up for intubation?”

“How about we get some bag-mask ventilation happening at some point?”

“If you could have a look at his abdomen that would be awesome”

These commands (imperatives) phrased obliquely as questions or suggestions are know as ‘whimperatives‘ and are found throughout resus room dialogue, when the team leader does not wish to convey the assumption of a power relationship over her colleagues. These whimperatives are an example of ‘mitigating speech’, which refers to language that ‘de-emphasises’ or ‘sugarcoats’ the command.

In the words of Peter Brindley:

‘The danger of mitigating language illustrates why, during medical crises, we should replace comments such as “perhaps, we need a surgeon” or “we should think about intubating” with “get me a surgeon” and “intubate the patient now.”’(4)

Conclusion

There’s nothing wrong with being polite and respectful, and mitigating language may be helpful in the team building phase. However the more critical the situation, the more an authorative/directive leadership style that clearly delegates critical tasks  is required(5). Standardised terminology (with closed loop communication) is likely to enhance clarity of the message and accelerate the sharing of a team mental model. Avoiding whimperatives and excessive mitigating phrases may further prevent ambiguity and imprecision, reducing the time to critical interventions.

These components of the content of resus room communication – unequivocal, standardised, and direct – should go hand in hand with the delivery of the words. Effective delivery requires optimal delivery speed and ‘command presence’. These factors will be discussed in a future post.

I’d be interested to hear what standard phrases or words you think should be in the resus-room lexicon.

 

1. Yamada NK, Halamek LP. Communication during resuscitation: Time for a change? Resuscitation. 2014 Dec;85(12):e191–2.

2. Yamada NK, Halamek LP. On the Need for Precise, Concise Communication during Resuscitation: A Proposed Solution. The Journal of Pediatrics. 2015 Jan;166(1):184–7.

3. Yamada NK, Fuerch JH, Halamek LP. Impact of Standardized Communication Techniques on Errors during Simulated Neonatal Resuscitation. Am J Perinatol. 2016 Mar;33(4):385–92.

4. Brindley PG, Reynolds SF. Improving verbal communication in critical care medicine. Journal of Critical Care. 2011 Apr;26(2):155–9.

5. Bristowe KK, Siassakos DD, Hambly HH, Angouri JJ, Yelland AA, Draycott TJT, et al. Teamwork for clinical emergencies: interprofessional focus group analysis and triangulation with simulation. Qual Health Res. 2012 Sep 30;22(10):1383–94.

Louisa in London – Prehospital Lessons from LTC2015

The London Trauma Conference remains up there on my list of ‘must go’ conferences to attend. It marks the end of the year, fills me with hope and inspires me for the future. Unfortunately this year I was torn between the conference and the demands of clinical directorship so I could only get to the “Air Ambulance & Prehospital Care Day”. At least this way I’m saved from the dilemma of which sessions to attend!
So what were the highlights of the Prehospital Day? For me, they were Prehospital ECMO,’Picking Up the Pieces’, and the REBOA update.

Prehospital ECMO
Professor Pierre Carli gave us an update on prehospital ECMO. Professor Carli (not to be confused with the equally awesome Professor Carley) is the medical director of Service d’Aide Médicale Urgente (SAMU) in Paris. They’ve been doing prehospital ECMO in Paris since 2011 and the data analysed over three years reveals a 10% survival to hospital discharge rate. We know from the work in Asia that successful outcome following traditional cardiac arrest management and ECPR is related to the speed of the intervention. Transposing the time to intervention from his 2011 – 2013 data onto the survival curve that Chen et al produced explains why the success rate is limited:

LTC2015

The revised 2015 process aims to reduce the duration of CPR, reduce time to ECMO and therefore improve survival to discharge rates. They are doing this by dispatching the ECMO team earlier.

The eligibility criteria for ECPR is also changing; patients >18 and <75years, refractory cardiac arrest (defined as failure of ROSC after 20min of CPR), no flow for < 5 minutes with shockable rhythm or signs of life or hypothermia or intoxication, EtCO2 > 10mmHg at time of inclusion and no major comorbidity.

Already there appears to be an improvement with 16 patients treated using the revised protocol with 5 survivors (31%) – although we must be wary of the small numbers.
A concern that was expressed by the French Department of Health was the fear of a reduction in organ donation with the introduction of ECPR – it turns out that rates have remained stable. In fact the condition of non heart beating donated organs is better when ECMO has been instigated; the long term effects on organ donation are being assessed.

I’m without doubt that prehospital ECMO/ED ECMO is the future although currently in the UK our hospital systems aren’t ready for this. If you want to learn more then look at the ED ECMO site or book on one of the many emerging courses on ED ECMO including the one that is run by Dr Simon Finney at the London Trauma Conference, or if you want to go further afield you could try San Diego (although places are fully booked on the next course).

Picking Up the Pieces
The Keynote speaker was Professor Sir Simon Wessely. He is a psychiatrist with a specialist interest in military psychology and his brief was to describe to us the public response to traumatic incidents. He has worked with the military and in civilian situations. After the 7/7 London bombings the population of London was surveyed: those most likely to be affected were of lower social class, of Muslim faith, those that had a relative that was injured, those unsure of the safety of others, those with no previous experience of terrorism and those experiencing difficulty in contacting others by mobile phone. Obviously there are many factors that we cannot influence however on the basis of the last risk factor our response to incidents has changed – the active discouragement to make phone calls has been changed to a recommendation of making short calls to friends and relatives.
The previous practice of offering immediate psychological debriefing to those involved in incidents was discounted by Prof Wessely – his research demonstrated that this intervention was not only not required but could actually result in harm: only a minority have ongoing psychological distress that can benefit from formal psychological input, which should occur later.
The approach that should be taken is to allow that individual to utilise their own social networks (family, friends, and colleagues) and to accept that in some cases the individual may not want or need to talk. This has led to the development of the Trauma Risk Management (TRIM) system which provides individuals within organisations that are exposed to traumatic events the skills required to identify those at risk of developing psychological problems and to recognise the signs and symptoms of those in difficulty. To a certain extent we naturally do this for our peers – I have spent many a night sitting in the ‘Good Samaritan’ pub with colleagues from the Royal London Hospital and London’s Air Ambulance – but having a more formal system is probably of benefit to enable those who have ongoing difficulties to access additional support.

REBOA update
Finally, the REBOA update – Resuscitative Endovascular Balloon Occlusion of the Aorta. One year on, Dr Sammy Sadek informed us that there are now more courses teaching the REBOA technique than there are (prehospital) patients that have received it. Over the last year only seven patients have qualified for this intervention in London, far fewer than they had anticipated. Another three patients died before REBOA could be instigated. All patients had a positive cardiovascular response. Four of the seven died from causes other than exsanguination. Is it worth all the effort and resource to deliver this intervention when such a select group will benefit?

Obviously there was much more covered in the day, this is just a taste. If you’ve never been to the London Trauma Conference then I definitely would recommend it and even if you have been before there are so many breakout sessions now there is always something for everyone.

More on the London Trauma Conference:

Merry Christmas and see you next year!

Louisa Chan

Dabigatran Reversal Agent – Idarucizumab

Thanks to Rob MacSweeney‘s fantastic Critical Care Reviews I learned of Idarucizumab, a monoclonal antibody fragment that binds the (pesky) anticoagulant dabigatran. Two industry-supported studies this week show rapid, complete reversal of anticoagulation in healthy volunteers(1) and patients who were either bleeding or undergoing procedures(2). The dose given to patients was 5g intravenously.

An accompanying editorial(3) highlights that the clinical study did not have a control group, and these patients had a high mortality. Further controlled studies examining patient-orientated outcomes will be helpful.

Of interest, another editorialist(4) lists other potential antidotes for Non-vitamin-K antagonist oral anticoagulants (NOACs) that have been or are being tested: an antidote against all oral direct factor Xa inhibitors called andexanet alpha (a recombinant activated factor X that binds direct factor Xa inhibitors), and a modified thrombin has been shown to be effective in vitro and in animals for reversal of dabigatran and potentially also other direct thrombin inhibitors.

1. Safety, tolerability, and efficacy of idarucizumab for the reversal of the anticoagulant effect of dabigatran in healthy male volunteers: a randomised, placebo-controlled, double-blind phase 1 trial
The Lancet Volume 386, No. 9994, p680–690, 15 August 2015


BACKGROUND: Idarucizumab is a monoclonal antibody fragment that binds dabigatran with high affinity in a 1:1 molar ratio. We investigated the safety, tolerability, and efficacy of increasing doses of idarucizumab for the reversal of anticoagulant effects of dabigatran in a two-part phase 1 study (rising-dose assessment and dose-finding, proof-of-concept investigation). Here we present the results of the proof-of-concept part of the study.

METHODS: In this randomised, placebo-controlled, double-blind, proof-of-concept phase 1 study, we enrolled healthy volunteers (aged 18-45 years) with a body-mass index of 18·5-29·9 kg/m2 into one of four dose groups at SGS Life Sciences Clinical Research Services, Belgium. Participants were randomly assigned within groups in a 3:1 ratio to idarucizumab or placebo using a pseudorandom number generator and a supplied seed number. Participants and care providers were masked to treatment assignment. All participants received oral dabigatran etexilate 220 mg twice daily for 3 days and a final dose on day 4. Idarucizumab (1 g, 2 g, or 4 g 5-min infusion, or 5 g plus 2·5 g in two 5-min infusions given 1 h apart) was administered about 2 h after the final dabigatran etexilate dose. The primary endpoint was incidence of drug-related adverse events, analysed in all randomly assigned participants who received at least one dose of dabigatran etexilate. Reversal of diluted thrombin time (dTT), ecarin clotting time (ECT), activated partial thromboplastin time (aPTT), and thrombin time (TT) were secondary endpoints assessed by measuring the area under the effect curve from 2 h to 12 h (AUEC2-12) after dabigatran etexilate ingestion on days 3 and 4. This trial is registered with ClinicalTrials.gov, number NCT01688830.

FINDINGS: Between Feb 23, and Nov 29, 2013, 47 men completed this part of the study. 12 were enrolled into each of the 1 g, 2 g, or 5 g plus 2·5 g idarucizumab groups (nine to idarucizumab and three to placebo in each group), and 11 were enrolled into the 4 g idarucizumab group (eight to idarucizumab and three to placebo). Drug-related adverse events were all of mild intensity and reported in seven participants: one in the 1 g idarucizumab group (infusion site erythema and hot flushes), one in the 5 g plus 2·5 g idarucizumab group (epistaxis); one receiving placebo (infusion site haematoma), and four during dabigatran etexilate pretreatment (three haematuria and one epistaxis). Idarucizumab immediately and completely reversed dabigatran-induced anticoagulation in a dose-dependent manner; the mean ratio of day 4 AUEC2-12 to day 3 AUEC2-12 for dTT was 1·01 with placebo, 0·26 with 1 g idarucizumab (74% reduction), 0·06 with 2 g idarucizumab (94% reduction), 0·02 with 4 g idarucizumab (98% reduction), and 0·01 with 5 g plus 2·5 g idarucizumab (99% reduction). No serious or severe adverse events were reported, no adverse event led to discontinuation of treatment, and no clinically relevant difference in incidence of adverse events was noted between treatment groups.

INTERPRETATION: These phase 1 results show that idarucizumab was associated with immediate, complete, and sustained reversal of dabigatran-induced anticoagulation in healthy men, and was well tolerated with no unexpected or clinically relevant safety concerns, supporting further testing. Further clinical studies are in progress.

2. Idarucizumab for Dabigatran Reversal
N Engl J Med. 2015 Aug 6;373(6):511-20


BACKGROUND: Specific reversal agents for non-vitamin K antagonist oral anticoagulants are lacking. Idarucizumab, an antibody fragment, was developed to reverse the anticoagulant effects of dabigatran.

METHODS: We undertook this prospective cohort study to determine the safety of 5 g of intravenous idarucizumab and its capacity to reverse the anticoagulant effects of dabigatran in patients who had serious bleeding (group A) or required an urgent procedure (group B). The primary end point was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after the administration of idarucizumab, on the basis of the determination at a central laboratory of the dilute thrombin time or ecarin clotting time. A key secondary end point was the restoration of hemostasis.

RESULTS: This interim analysis included 90 patients who received idarucizumab (51 patients in group A and 39 in group B). Among 68 patients with an elevated dilute thrombin time and 81 with an elevated ecarin clotting time at baseline, the median maximum percentage reversal was 100% (95% confidence interval, 100 to 100). Idarucizumab normalized the test results in 88 to 98% of the patients, an effect that was evident within minutes. Concentrations of unbound dabigatran remained below 20 ng per milliliter at 24 hours in 79% of the patients. Among 35 patients in group A who could be assessed, hemostasis, as determined by local investigators, was restored at a median of 11.4 hours. Among 36 patients in group B who underwent a procedure, normal intraoperative hemostasis was reported in 33, and mildly or moderately abnormal hemostasis was reported in 2 patients and 1 patient, respectively. One thrombotic event occurred within 72 hours after idarucizumab administration in a patient in whom anticoagulants had not been reinitiated.

CONCLUSIONS: Idarucizumab completely reversed the anticoagulant effect of dabigatran within minutes. (Funded by Boehringer Ingelheim; RE-VERSE AD ClinicalTrials.gov number, NCT02104947.).

3. Targeted Anti-Anticoagulants
N Engl J Med. 2015 Aug 6;373(6):569-71

4. Antidotes for anticoagulants: a long way to go
The Lancet Volume 386, No. 9994, p634–636, 15 August 2015