My talk at the SmaccGOLD conference in March 2014
Here are the slides:
A paediatric trauma centre study showed that in their system, seven people at the bedside was the optimum number to get tasks done in a paediatric resuscitation. As numbers increased beyond this, there were ‘diminishing marginal returns’, ie. the output (tasks completed) generated from an additional unit of input (extra people) decreases as the quantity of the input rises.
The authors comment that after a saturation point is reached, “additional team members contribute negative returns, resulting in fewer tasks completed by teams with the most members. This pattern has been demonstrated in other medical groups, with larger surgical teams having prolonged operative times and larger paramedic crews delaying the performance of cardiopulmonary resuscitation.“
There are several possible explanations:
In my view, excessive team size results in there being more individuals to supervise & monitor, and hence a greater cognitive load for the team leader (cue the resus safety officer). More crowding and obstruction threatens situational awareness. There is more difficulty in providing clear uninterrupted closed loop communication. And general resuscitation room entropy increases, requiring more energy to contain or reverse it.
However, for paediatric resuscitations requiring optimal concurrent activity to progress the resuscitation, I do struggle with less than five. Unless of course I’m in my HEMS role, when the paramedic and I just crack on.
More on Making Things Happen in resus.
Factors Affecting Team Size and Task Performance in Pediatric Trauma Resuscitation.
Pediatr Emerg Care. 2014 Mar 19. [Epub ahead of print]
OBJECTIVES: Varying team size based on anticipated injury acuity is a common method for limiting personnel during trauma resuscitation. While missing personnel may delay treatment, large teams may worsen care through role confusion and interference. This study investigates factors associated with varying team size and task completion during trauma resuscitation.
METHODS: Video-recorded resuscitations of pediatric trauma patients (n = 201) were reviewed for team size (bedside and total) and completion of 24 resuscitation tasks. Additional patient characteristics were abstracted from our trauma registry. Linear regression was used to assess which characteristics were associated with varying team size and task completion. Task completion was then analyzed in relation to team size using best-fit curves.
RESULTS: The average bedside team ranged from 2.7 to 10.0 members (mean, 6.5 [SD, 1.7]), with 4.3 to 17.7 (mean, 11.0 [SD, 2.8]) people total. More people were present during high-acuity activations (+4.9, P < 0.001) and for patients with a penetrating injury (+2.3, P = 0.002). Fewer people were present during activations without prearrival notification (-4.77, P < 0.001) and at night (-1.25, P = 0.002). Task completion in the first 2 minutes ranged from 4 to 19 (mean, 11.7 [SD, 3.8]). The maximum number of tasks was performed at our hospital by teams with 7 people at the bedside (13 total).
CONCLUSIONS: Resuscitation task completion varies by team size, with a nonlinear association between number of team members and completed tasks. Management of team size during high-acuity activations, those without prior notification, and those in which the patient has a penetrating injury may help optimize performance.
London Trauma Conference Day 4 by Dr Louisa Chan
It’s the last day of the conference and new this year is the Neurotrauma Masterclass running in parallel with the main track which focuses on in-hospital care.
We heard a little from Mark Wilson yesterday. He believes we are missing a pre-hospital trick in traumatic brain injury. Early intervention is the key (he has data showing aggressive intervention for extradural haemorrhage in patients with fixed dilated pupils has good outcomes in 75%).
Today he taught us neurosurgery over lunch. If you have a spare moment over then go to his website and you too can learn how to be a brain surgeon!
Dr Gareth Davies talks about Impact Brain Apnoea. Many will not heard of this phenomenon. Clinicians rarely see patients early enough in their injury timeline to witness
Essentially this term describes the cessation of breathing after head injury. It has been described in older texts (first mentioned in 1894!) The period of apnoea increases with the severity of the injury and if non fatal will then recover to normal over a period of time. Prolonged apnoea results in hypotension.
This is a brain stem mediated effect with no structural injury.
The effect is exacerbated by alcohol and ameliorated by ventilatory support during the apnoeic phase.
Associated with this response is a catecholamine surge which exacerbates the cardiovascular collapse and he introduces the concept of Central Shock.
So how does this translate into the real world?
Well, could we be miscategorising patients that die before they reach hospital as succumbing to hypovolaemic when in fact they had central shock?
These patients essentially present with respiratory arrest, but do well with supported ventilation. Identification of these patients by emergency dispatchers with airway support could mean the difference between life and death.
Read more about this at: http://www.sciencedirect.com/science/article/pii/S0025619611642547
Prof Monty Mythen spoke on fluid management in the trauma patient after blood (not albumin, HES or colloids) and Prof Mervyn Singer explained the genetic contribution to the development of MODS after trauma.
1. Task focus kills
2. Situational awareness saves lives
3. The best communication is non verbal
4. Train yourself to listen
Prof Susan Brundage is a US trauma surgeon who has been recruited into the Bart’s and the London School of Medicine and the Royal College of Surgeons of England International Masters in Trauma Sciences for her trauma expertise.
She tells us that MOOCs and FOAM are changing education. Whilst education communities are being formed, she warns of the potential pitfalls of this form of education with a proportion of participants not fully engaged.
The Masters program is growing and if you’re interested you can read more here.
This has been a full on conference, with great learning points.
Hopefully see you next year!
There was a jam-packed line up for the Pre-hospital and Air Ambulance Day which was Co-hosted by the Norwegian Air Ambulance Foundation.
My highlights were:
Dr Rasmus Hesselfeldt works in Denmark where they have a pretty good EMS system with ambulances, RRV’s and PHC doctors. Road conditions are good with the longest travel distance of 114 miles. So would the introduction of a HEMS service improve outcomes? He did an observational study looking at year of data post-trial and compared this with 5 months pre-trial. Trauma patients with ISS > 15 and medical emergencies greater than 30 min by road to the Trauma Centre (TC). Primary endpoint was time to TC, secondary outcomes were number of secondary transfers and 30 day mortality.
Results: Increase in on scene time 20 min vs 28 min, time to hospital increased but time to TC was less – 218 min vs 90 min, reduced mortality, increased direct transfer to TC and fewer secondary transfers.
Full article here: A helicopter emergency medical service may allow faster access to highly specialised care. Dan Med J. 2013 Jul;60(7):A4647
Prof Dan Davis ran through pre-hospital intubation. It seems that this man has spent his life trying to perfect airway management. Peter Rosen was his mentor and imprinted on him that RSI is the cornerstone of airway management.
So surely pre-hospital intubation saves lives. The evidence however begs to differ, or does it? As with all evidence we need to consider the validity of the results and luckily Prof Davis has spent a lot of time thinking through the reasons why there no evidence.
During his research he opened a huge can of worms:
1. Hyperventilation was common – any EtCO2 <30mmHg lead to a doubling in mortality.
2. First pass intubation is great, but not if you let your patient become hypoxic or hypotension or worse still both!
3. Hospital practice had similar issues.
So really the RSI processes he was looking at weren’t great.
The good news is that things have improved and he can now boast higher first pass rates and lower complication rates for his EMS system. His puts this success down to training.
The AIRPORT study was discussed at last years LTC. This year we have the results. 21 HEMS services in 6 countries were involved in the data collection including GSA HEMS. The headline findings are that intubation success rates are high (98%) with a complication rate of 10-12%. The more difficult airways were seen in the non-trauma group. 28.2% patients died (mainly cardiac arrest).
Matt Thomas reported on REVIVE – a pre-hospital feasibility study looking at airway management in OHCA (I-Gel vs LMA Supreme vs standard care). It was never powered to show a difference in these groups, the main aim was to see if research in this very challenging area was possible. And the answer is YES. The paramedics involved recruited more patients than expected and stuck to the protocol (prob better that docs would have!). A randomised controlled trial to look at the I-Gel vs ETT is planned.
Finally, Pre-hospital Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) seems eminently possible – Dr Nils Petter Oveland showed us the training manikin they developed for training. Through training on this manikin they achieved an average skin to balloon time of 3.3mins. Animal data supports this procedure as a bridge to definitive care in non compressible haemorrhage.
London HEMS will be starting (P)REBOA in the New Year.
So now it’s stand up science, I’m off for my glass of wine…………….
Check out what they’re saying about the London Trauma Conference on Twitter
London Trauma Conference 2013 – Day 2 by Dr Louisa Chan
So I find myself torn today: do I join the the main track with a Major incident theme or the Cardiac Masterclass? I never liked the thought of missing out on anything so I went to a bit of both.
A lot of people probably think that managing cardiac arrest isn’t challenging and a bit dull because the patient is dead. But the Cardiac Masterclass would inspire you to think of a bright future for cardiac arrest management.
Mark Whitbread reminded us of how important dispatch is in the chain of survival. How much focus do we put on improving bystander CPR rates? Dispatcher assisted CPR has been shown to improve outcomes and needs to be skilfully done.
Ajay Jain pushes for all OHCA patients to be taken to a Cardiac Arrest centre for PCI. Why? Because the results he has from his centre for PCI in OHCA patients results in 77% (101/132) patients surviving to hosp discharge, 65% neurologically intact.
More data from TOPCAT shows us that non survivors of OHCA are easy to cool.
And maybe we should be cooling DURING cardiac arrest to minimise the reperfusion injury.
For persistent VF Prof Redwood says revascularisation is the key; when that doesn’t work then reducing LV volume may help so aspiration or an Impella may work. Failing that – ECMO.
Major Incidents by their nature do not happen every day, so experience in these incidents is limited. The challenge then is how can we learn from incidents?
A standardised reporting system for a major incident database would be a good idea – www.majorincidentreporting.org – is where you will find the standard report form and open access database.
And then all I can suggest is that you need to come to the LTC and listen to the accounts of those who have been there. We heard about the Tokyo Sarin attack, Mumbai, and a very compelling story of multiple drownings from Steen Barnung.
Lessons from Tokyo – Sarin attack:
It will happen again
It will be chaos
Crowds cannot be controlled
Comms will fail
Clinical diagnosis – need a senior clinician
Treatment must be immediately available – 3min to absorb sarin
Decontamination – get naked, 90% decon with clothes removal.
Empower the man on the ground.
The Norwegians won on the equipment front with their Mobile Stroke Unit. It’s due to go on line in 2014.
So TTFN and more from me on Day 3 of #LTC2013
Our inside reporter Dr Louisa Chan provides an update from Day One of the London Trauma Conference:
At risk of sounding like a resuscisaurus, last year was my first foray into the world of blogging. I’m proud to say that the genetic make up of most emergency physicians allows us to adapt so that others do not die! And so here I am again, making my way into the big smoke to report on the great developments of 2013.
I’ve struggled in the past to prise myself away from the main trauma track, it is after all the London Trauma Conference, which has left me curious as to the content of the Cardiac arrest symposium, this year it has been integrated, so I finally get to scratch that itch.
Prehospital Cardiac Arrest Management in Scotland
In Scotland, of 50 cardiac arrests, 6 will survive to hospital and only 1 will survive to hospital discharge. The survival to hospital discharge in the UK is getting worse (4.8% 1995- 0.7% 2007)
Spurred on by these dreadful figures and a personal quest to improve cardiac arrest care (his father succumbed to a cardiac arrest in his forties)
All in all he has studied 400 cardiac arrest patients pre hospital. So what has he learnt?
Echocardiography in cardiac arrest
Prof Tim Harris spoke about his passion – echocardiography in resuscitation. If you were in any doubt before then you would leave convinced.
Of course echo should not interfere with CPR so it should be done during the rhythm check with a 10 sec count down.
He covered the usual uses; PEA vs EMD in prognostication (92% sensitivity and 82% specificity to ROSC), Circulation assessment and an estimation of EF (Normal function – anterior mitral valve leaflet hits the septum or is within 5mm , EF 30-45% between 5mm- 18mm and >18mm ant mitral valve leaflets – 30% EF)
Cardiogenic shock after cardiac arrest
Professor Deakin: optimising cardiac function after ROSC revolves around the three elements of preload, SVR and myocardial contractility. For those who can still remember how, he recommends preload should be optimised to a LA pressure 15-20mmHg (2-12 normal) with a Swan Ganz catheter.
SVR and contractility can be manipulated thereafter using traditional vasopressors and inotropes or more novel agents like Levosimendan.
Mechanical devices such as IABP, Impella, TandemSupport are useful if available.
Where does the future lie? Perhaps synchronised pacing, hypothermia, extrathoracic ventilation and gene therapy.
Prof Karim Brohi: external chest compressions have been around since the 1960′s. Without a doubt external compressions generate a cardiac output, but is this the best way?
Over the last 10 years the priorities in traumatic cardiac arrest have changed – chest compressions are not instituted until after reversible causes have been addressed.
In non traumatic arrest how could we improve?
In canine models coronary perfusion pressure is five times better with internal cardiac massage, providing better survival rates with intact neurology.
There are a few human studies showing marked differences in cardiac index: 1.31 in the open group vs 0.61 in the closed group. In a Japanese study (1993), ROSC was achieved in 58% in open vs 1% closed.
The technique is two handed and the same as that taught in thoracotomy training. The difference is that in medical cardiac arrest you can use a smaller incision ( left lateral).
Who should we use open cardiac massage on? Perhaps in tamponade and pulmonary embolism?
How about when? When 10-15min with “standard care” has failed?
Perhaps it is time for a trial?
Post cardiac arrest syndrome and neuro protective measures
Prof Simon Redwood and Matt Thomas had overlapping talks on this . The bottom line is don’t have too much or too little CO2 or O2. The therapeutic hypothermia debate continues, what is evident is that there should be temperature control to avoid hyperthermia but what temperature? And there may be other benefits to hypothermia eg. limitation of infarct size.
What has been evident from all the speakers today is that it is an integrated system that saves lives and in order to guide the development of your system you need data and the belief that you can improve cardiac arrest outcomes.
More from me tomorrow!
The final one is the most contentious: Pharmacologically assisted laryngeal mask insertion: a consensus statement(1). Here is the summary:
They qualify the first point with the statement: The consensus group felt that, in the hands of a specific set of practitioners and in certain circumstances, patients would benefit from the technique. It was recognised that pre-hospital airway management can be very challenging, and deeming the technique unacceptable could deprive patients of a potentially life saving intervention. It was felt that having another tool available to clinicians which could potentially improve patient outcome was important. This was despite the lack of a robust evidence base. It was felt that the technique is indicated in, and should be limited to, a very specific set of circumstances as described below
The publication lists some ‘Organisations represented at the consensus meeting’, which include some commercial training and equipment companies.
It also states that ‘The Royal College of Anaesthetists, although represented at the initial meeting, was unable to support the outcomes agreed by the other represented organisations.‘
This is a very interesting development. I can see the pros and cons of this. Since practitioners are out there doing PALM anyway, it is in the interests of patients to produce a statement that encourages monitoring, checklists, training, and data collection. To meet all the requirements, one must undergo ‘training in the transfer of critically ill patients’, which would normally necessitate more advanced airway and anaesthesia skills anyway.
A tough one – what would you want if there was no RSI capability but you were hypoxic with trismus and basic airway maneouvres were failing? An all out ban on PALM, or PALM provided by someone trained in surgical airway if it fails (as per the consensus recommendations)?
This and some of the other statements can be downloaded in full at the Faculty of Pre-hospital Care site
1. Pharmacologically assisted laryngeal mask insertion: a consensus statement
Emerg Med J. 2013 Dec;30(12):1073-5
It’s nice to have big randomised trials to guide critical care practice. The age-old crystalloid/colloid debate (is that still going?) has fueled a multicentre and multinational study in 2857 patients with hypovolaemic shock on intensive care units. Patients were classified as having sepsis, trauma, or other causes of hypovolaemic shock.
In the crystalloids group, allowed treatments included isotonic or hypertonic saline and any buffered solutions. In the colloids group, gelatins, albumin from 4-25%, dextrans, and hydroxyethyl starches were permitted.
The primary outcome of 28 day mortality was no different between groups. The study had an open-label design and recruitment took place over nine years.
This finding – no clinical benefit from colloids in critically ill patients – is in keeping with other major ICU trials of colloid therapy: Saline versus Albumin Fluid Evaluation (SAFE), Efficacy of Volume Substitution and Insulin Therapy in Severe Sepsis (VISEP), Scandinavian Starch for Severe Sepsis/Septic Shock (6S), and the Crystalloid versus Hydroxyethyl Starch Trial (CHEST).
Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial
JAMA. 2013 Nov 6;310(17):1809-17
IMPORTANCE: Evidence supporting the choice of intravenous colloid vs crystalloid solutions for management of hypovolemic shock remains unclear.
OBJECTIVE: To test whether use of colloids compared with crystalloids for fluid resuscitation alters mortality in patients admitted to the intensive care unit (ICU) with hypovolemic shock.
DESIGN, SETTING, AND PARTICIPANTS: A multicenter, randomized clinical trial stratified by case mix (sepsis, trauma, or hypovolemic shock without sepsis or trauma). Therapy in the Colloids Versus Crystalloids for the Resuscitation of the Critically Ill (CRISTAL) trial was open label but outcome assessment was blinded to treatment assignment. Recruitment began in February 2003 and ended in August 2012 of 2857 sequential ICU patients treated at 57 ICUs in France, Belgium, North Africa, and Canada; follow-up ended in November 2012.
INTERVENTIONS: Colloids (n = 1414; gelatins, dextrans, hydroxyethyl starches, or 4% or 20% of albumin) or crystalloids (n = 1443; isotonic or hypertonic saline or Ringer lactate solution) for all fluid interventions other than fluid maintenance throughout the ICU stay.
MAIN OUTCOMES AND MEASURES: The primary outcome was death within 28 days. Secondary outcomes included 90-day mortality; and days alive and not receiving renal replacement therapy, mechanical ventilation, or vasopressor therapy.
RESULTS: Within 28 days, there were 359 deaths (25.4%) in colloids group vs 390 deaths (27.0%) in crystalloids group (relative risk [RR], 0.96 [95% CI, 0.88 to 1.04]; P = .26). Within 90 days, there were 434 deaths (30.7%) in colloids group vs 493 deaths (34.2%) in crystalloids group (RR, 0.92 [95% CI, 0.86 to 0.99]; P = .03). Renal replacement therapy was used in 156 (11.0%) in colloids group vs 181 (12.5%) in crystalloids group (RR, 0.93 [95% CI, 0.83 to 1.03]; P = .19). There were more days alive without mechanical ventilation in the colloids group vs the crystalloids group by 7 days (mean: 2.1 vs 1.8 days, respectively; mean difference, 0.30 [95% CI, 0.09 to 0.48] days; P = .01) and by 28 days (mean: 14.6 vs 13.5 days; mean difference, 1.10 [95% CI, 0.14 to 2.06] days; P = .01) and alive without vasopressor therapy by 7 days (mean: 5.0 vs 4.7 days; mean difference, 0.30 [95% CI, -0.03 to 0.50] days; P = .04) and by 28 days (mean: 16.2 vs 15.2 days; mean difference, 1.04 [95% CI, -0.04 to 2.10] days; P = .03).
CONCLUSIONS AND RELEVANCE: Among ICU patients with hypovolemia, the use of colloids vs crystalloids did not result in a significant difference in 28-day mortality. Although 90-day mortality was lower among patients receiving colloids, this finding should be considered exploratory and requires further study before reaching conclusions about efficacy.
The observation that patients with haemorrhagic trauma in military and civilian settings do better if they receive coagulation factors and platelets is yet to be replicated in a randomised trial. It has been suggested that the effect may in part be a consequence of survivor bias – ie. that if a patient lives long enough to received some thawed fresh frozen plasma, then they were already more likely to be a survivor and therefore more survivors will be represented in the ‘FFP’ groups vs a ‘no-FFP’ comparison group.
An attempt to eliminate survivor bias was made in the PROMMTT study, which documented the timing of transfusions during active resuscitation and patient outcomes in adult trauma patients who received a transfusion of at least 1 unit of RBCs within 6 hours of admission.
Increased ratios of plasma:RBCs and platelets:RBCs were independently associated with decreased 6-hour mortality, when haemorrhagic death predominated. In the first 6 hours, patients with ratios less than 1:2 were 3 to 4 times more likely to die than patients with ratios of 1:1 or higher.
A prospective trial is underway to identify the optimal ratio of blood products, in the PROPPR study, in which 1:1:1 ratio of plasma:platelets:RBC will be compared with 1:1:2.
The Prospective, Observational, Multicenter, Major Trauma Transfusion (PROMMTT) Study
Arch Surg. 2012 Oct 15:1-10
Objective: To relate in-hospital mortality to early transfusion of plasma and/or platelets and to time-varying plasma:red blood cell (RBC) and platelet:RBC ratios.
Design: Prospective cohort study documenting the timing of transfusions during active resuscitation and patient outcomes. Data were analyzed using time-dependent proportional hazards models.
Setting: Ten US level I trauma centers.
Patients: Adult trauma patients surviving for 30 minutes after admission who received a transfusion of at least 1 unit of RBCs within 6 hours of admission (n = 1245, the original study group) and at least 3 total units (of RBCs, plasma, or platelets) within 24 hours (n = 905, the analysis group).
Main Outcome Measure: In-hospital mortality.
Results: Plasma:RBC and platelet:RBC ratios were not constant during the first 24 hours (P < .001 for both). In a multivariable time-dependent Cox model, increased ratios of plasma:RBCs (adjusted hazard ratio = 0.31; 95% CI, 0.16-0.58) and platelets:RBCs (adjusted hazard ratio = 0.55; 95% CI, 0.31-0.98) were independently associated with decreased 6-hour mortality, when hemorrhagic death predominated. In the first 6 hours, patients with ratios less than 1:2 were 3 to 4 times more likely to die than patients with ratios of 1:1 or higher. After 24 hours, plasma and platelet ratios were unassociated with mortality, when competing risks from nonhemorrhagic causes prevailed.
Conclusions: Higher plasma and platelet ratios early in resuscitation were associated with decreased mortality in patients who received transfusions of at least 3 units of blood products during the first 24 hours after admission. Among survivors at 24 hours, the subsequent risk of death by day 30 was not associated with plasma or platelet ratios.
Further talks from the SMACC conference are available for free download on iTunes.
Here are the accompanying slides: