Category Archives: ICU

Stuff relevant to patients on ICU

Sepsis research – let's get some answers

There’s so much debate on which components of Early Goal Directed Therapy in sepsis really make a difference. The good news is that three randomised controlled trials in the UK, Australasia, and North America, aim to answer the question, and the study design from the outset has been a collaboration that will allow the results to be pooled.
ProMISe is taking place in the UK, ProCESS in the US, and ARISE in Australasia.

sepsistrialssm

The Australasian study (ARISE) and is nearing completion. If you can recruit patients then please do. Listen to a podcast on this fantastic study with lead investigator Dr Anthony Delaney.

London Trauma Conference Day 4

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.
LTC-BrohiProf Brohi gave us the lowdown on trauma laparotomies – not all are the same! With important human factors advice:
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!

London Trauma Conference Day 3


Dr Louisa Chan reports on Day 3 of the London Trauma Conference
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:

HEMS

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
 
Airway
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.
 
 
AIRPORT-LTCThe 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.
 
(P)REBOA
ReboaLTCFinally, 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 Day 2

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.
 
Cardiac Masterclass
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.
He also tells us that the ECG post arrest is a very poor predictor of PCI findings (although STEMI predicts a positive result) so they all should have PCI.
Lyon-survivors
 
More data from TOPCAT shows us that non survivors of OHCA are easy to cool.
 
LTC-mice
 
 
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
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.
Stream casualties
Empower the man on the ground.

 
Gadgets
LTC-MSUThe great thing about the London Trauma Conference is that it’s not just about the content of the tracks, there’s the networking and the opportunity to see new pieces of equipment.
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

London Trauma Conference 2013

FDIA_ImageOur 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
The conference was kicked off by Richard Lyon‘s inspirational description of his TOPCAT study.
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?

  • Precise application of the chain of survival to your own system is vital in the delivery of Quality CPR.
  • He started in the ambulance control room analysing calls (CPR starts at step 11 so more experienced dispatchers skip thee quicker) and worked his way through the chain of survival.
  • The TOPCAT study revealed a 3 min delay to compressions where early intubation and cannulation were performed. Through an education program delivering knowledge and skills with individualised feedback they were able to increase on-chest time.
  • LEADERSHIP was a big factor. Having a clinician dedicated to managing the team improved on chest time and is now delivered by paramedics manning a car response in Edinburgh.
  • Breaks in CPR during movement are overcome by a mechanical chest compression device on carry sheet.
  • Non technical skills are monitored by camera feed
  • These changes have led to a survival to hospital discharge rate of 38% for patients in VF
  • This could translate into an extra 300 lives saved in Scotland when these changes are rolled out nationally.
  • And now there is a move to transport patients who are in VF after the third shock then straight to cath lab.

 
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.
LTC-BrohiOpen chest cardiac massage
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!
Louisa Chan

Therapeutic hypothermia does not improve arrest outcome

A paper published today represents to me what’s great about science.
I am impressed with those investigators who had the wherewithall to subject previous therapeutic hypothermia studies to skeptical scrutiny and then design and conduct a robust multicentre trial to answer the question.
One of the criticisms of the original two studies was that those patients who were not actively cooled did not have their temperature tightly controlled, and therefore some were allowed to become hypERthermic, which is bad for brains.
This latest study showed no difference in survival or neurological outcome after cardiac arrest between target temperatures of 33°C and 36°C.
So controlling the temperature after cardiac arrest is still important, but cooling down to the recommended range of 32-4°C is not.
Cool.
Read the full study at the NEJM site.

Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest

NEJM November 17, 2013 Full text
[EXPAND Abstract]


BACKGROUND Unconscious survivors of out-of-hospital cardiac arrest have a high risk of death or poor neurologic function. Therapeutic hypothermia is recommended by international guidelines, but the supporting evidence is limited, and the target temperature associated with the best outcome is unknown. Our objective was to compare two target temperatures, both intended to prevent fever.

METHODS In an international trial, we randomly assigned 950 unconscious adults after out-of-hospital cardiac arrest of presumed cardiac cause to targeted temperature management at either 33°C or 36°C. The primary outcome was all-cause mortality through the end of the trial. Secondary outcomes included a composite of poor neurologic function or death at 180 days, as evaluated with the Cerebral Performance Category (CPC) scale and the modified Rankin scale.

RESULTS In total, 939 patients were included in the primary analysis. At the end of the trial, 50% of the patients in the 33°C group (235 of 473 patients) had died, as compared with 48% of the patients in the 36°C group (225 of 466 patients) (hazard ratio with a temperature of 33°C, 1.06; 95% confidence interval [CI], 0.89 to 1.28; P=0.51). At the 180-day follow-up, 54% of the patients in the 33°C group had died or had poor neurologic function according to the CPC, as compared with 52% of patients in the 36°C group (risk ratio, 1.02; 95% CI, 0.88 to 1.16; P=0.78). In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups (risk ratio, 1.01; 95% CI, 0.89 to 1.14; P=0.87). The results of analyses adjusted for known prognostic factors were similar.

CONCLUSIONS In unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a targeted temperature of 33°C did not confer a benefit as compared with a targeted temperature of 36°C.

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Double balloon pump fail

IABPicon
Two recent trials question the ongoing use of intra-aortic balloon pumps: in patients with acute myocardial infarction with cardiogenic shock undergoing revascularisation(1), and patients with poor left ventricular function undergoing coronary artery bypass surgery(2).
Editorialists Krischan D Sjauw and Jan J Piek from the Netherlands make the following commentary(3) in reference to one of the studies:
Although the results of IABP-SHOCK II question the usefulness of IABP therapy in cardiogenic shock, there still might be an indication for initial stabilisation of severely compromised patients, especially in centres without facilities for early revascularisation, as an adjunct to thrombolytic therapy, or to allow transport to specialised tertiary centres.
So retrieval specialists like me may still be up in the night transferring patients with balloon pumps, but these studies suggest this should be restricted to those with cardiogenic shock pending corrective therapy (eg. revascularisation for AMI or surgery for acute mitral valvular dysfunction). Unless the ECMO team gets to them first, of course.

1. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial
The Lancet, Volume 382, Issue 9905, Pages 1638 – 1645
[EXPAND Abstract]


BACKGROUND: In current international guidelines the recommendation for intra-aortic balloon pump (IABP) use has been downgraded in cardiogenic shock complicating acute myocardial infarction on the basis of registry data. In the largest randomised trial (IABP-SHOCK II), IABP support did not reduce 30 day mortality compared with control. However, previous trials in cardiogenic shock showed a mortality benefit only at extended follow-up. The present analysis therefore reports 6 and 12 month results.

METHODS: The IABP-SHOCK II trial was a randomised, open-label, multicentre trial. Patients with cardiogenic shock complicating acute myocardial infarction who were undergoing early revascularisation and optimum medical therapy were randomly assigned (1:1) to IABP versus control via a central web-based system. The primary efficacy endpoint was 30 day all-cause mortality, but 6 and 12 month follow-up was done in addition to quality-of-life assessment for all survivors with the Euroqol-5D questionnaire. A masked central committee adjudicated clinical outcomes. Patients and investigators were not masked to treatment allocation. Analysis was by intention to treat. This trial is registered at ClinicalTrials.gov, NCT00491036.

FINDINGS: Between June 16, 2009, and March 3, 2012, 600 patients were assigned to IABP (n=301) or control (n=299). Of 595 patients completing 12 month follow-up, 155 (52%) of 299 patients in the IABP group and 152 (51%) of 296 patients in the control group had died (relative risk [RR] 1·01, 95% CI 0·86-1·18, p=0·91). There were no significant differences in reinfarction (RR 2·60, 95% CI 0·95-7·10, p=0·05), recurrent revascularisation (0·91, 0·58-1·41, p=0·77), or stroke (1·50, 0·25-8·84, p=1·00). For survivors, quality-of-life measures including mobility, self-care, usual activities, pain or discomfort, and anxiety or depression did not differ significantly between study groups.

INTERPRETATION: In patients undergoing early revascularisation for myocardial infarction complicated by cardiogenic shock, IABP did not reduce 12 month all-cause mortality.

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2. A Randomized Controlled Trial of Preoperative Intra-Aortic Balloon Pump in Coronary Patients With Poor Left Ventricular Function Undergoing Coronary Artery Bypass Surgery
Crit Care Med. 2013 Nov;41(11):2476-83
[EXPAND Abstract]


BACKGROUND: Preoperative intra-aortic balloon pump use in high-risk patients undergoing surgical coronary revascularization is still a matter of debate. The objective of this study is to determine whether the preoperative use of an intra-aortic balloon pump improves the outcome after coronary operations in high-risk patients.

DESIGN: Single-center prospective randomized controlled trial.

SETTING: Tertiary cardiac surgery center, research hospital.

PATIENTS: One hundred ten subjects undergoing coronary operations, with a poor left ventricular ejection fraction (< 35%) and no hemodynamic instability.
INTERVENTIONS:
Patients randomized to receive preincision intra-aortic balloon pump or no intervention.

MEASUREMENTS AND MAIN RESULTS: The primary outcome measurement was postoperative major morbidity rate, defined as one of prolonged mechanical ventilation, stroke, acute kidney injury, surgical revision, mediastinitis, and operative mortality. There was no difference in major morbidity rate (40% in intra-aortic balloon pump group and 31% in control group; odds ratio, 1.49 [95% CI, 0.68-3.33]). No differences were observed for cardiac index before and after the operation; at the arrival in the ICU, patients in the intra-aortic balloon pump group had a significantly (p = 0.01) lower mean systemic arterial pressure (80.1 ± 15.1 mm Hg) versus control group patients (89.2 ± 17.9 mm Hg). Fewer patients in the intra-aortic balloon pump group (24%) than those in the control group (44%) required dopamine infusion (p = 0.043).

CONCLUSIONS: This study demonstrates that in patients undergoing nonemergent coronary operations, with a stable hemodynamic profile and a left ventricular ejection fraction less than 35%, the preincision insertion of intra-aortic balloon pump does not result in a better outcome. Given the possible complications of intra-aortic balloon pump insertion, and the additional cost of the procedure, this approach is not justified.

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3. Is the intra-aortic balloon pump leaking?
Lancet 2013;382:1616-7

Beta blockers potentially beneficial in septic shock

Counterintuitive as it sounds, this is pretty cool. I blogged about these guys before when they published their findings on microcirculatory flow in septic patients given beta blockers.
It’s a small study – 77 patients with septic shock and a heart rate of 95/min or higher requiring high-dose norepinephrine to maintain a mean arterial pressure of at least 65 mm Hg were randomised to receive a continuous infusion of esmolol titrated to maintain heart rate between 80/min and 94/min for their ICU stay. 77 patients received standard treatment. It should be noted the primary outcome (target heart rate) was not a patient-oriented endpoint. Interestingly though, there were no increased adverse events in the beta blocker group, which demonstrated improved left ventricular stroke work, lower lactate levels, decreased noradrenaline and fluid requirements, improved oxygenation, and a lower mortality.
Caution is appropriate here though: this study was a small, single-centre open-label trial. It will be very interesting to see if these effects are reproduced and whether they will ultimately translate to meaningful outcome benefits.
Read more about the study at the PulmCCM site.
There is also a great critical appraisal of the study at Emergency Medicine Literature of Note/a>.
Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial
JAMA. 2013 Oct 23;310(16):1683-91
[EXPAND Abstract]


IMPORTANCE: β-Blocker therapy may control heart rate and attenuate the deleterious effects of β-adrenergic receptor stimulation in septic shock. However, β-Blockers are not traditionally used for this condition and may worsen cardiovascular decompensation related through negative inotropic and hypotensive effects.

OBJECTIVE: To investigate the effect of the short-acting β-blocker esmolol in patients with severe septic shock.

DESIGN, SETTING, AND PATIENTS: Open-label, randomized phase 2 study, conducted in a university hospital intensive care unit (ICU) between November 2010 and July 2012, involving patients in septic shock with a heart rate of 95/min or higher requiring high-dose norepinephrine to maintain a mean arterial pressure of 65 mm Hg or higher.

INTERVENTIONS: We randomly assigned 77 patients to receive a continuous infusion of esmolol titrated to maintain heart rate between 80/min and 94/min for their ICU stay and 77 patients to standard treatment.

MAIN OUTCOMES AND MEASURES: Our primary outcome was a reduction in heart rate below the predefined threshold of 95/min and to maintain heart rate between 80/min and 94/min by esmolol treatment over a 96-hour period. Secondary outcomes included hemodynamic and organ function measures; norepinephrine dosages at 24, 48, 72, and 96 hours; and adverse events and mortality occurring within 28 days after randomization.

RESULTS: Targeted heart rates were achieved in all patients in the esmolol group compared with those in the control group. The median AUC for heart rate during the first 96 hours was -28/min (IQR, -37 to -21) for the esmolol group vs -6/min (95% CI, -14 to 0) for the control group with a mean reduction of 18/min (P <  .001). For stroke volume index, the median AUC for esmolol was 4 mL/m2 (IQR, -1 to 10) vs 1 mL/m2 for the control group (IQR, -3 to 5; P = .02), whereas the left ventricular stroke work index for esmolol was 3 mL/m2 (IQR, 0 to 8) vs 1 mL/m2 for the control group (IQR, -2 to 5; P = .03). For arterial lactatemia, median AUC for esmolol was -0.1 mmol/L (IQR, -0.6 to 0.2) vs 0.1 mmol/L for the control group (IQR, -0.3 for 0.6; P = .007); for norepinephrine, -0.11 μg/kg/min (IQR, -0.46 to 0.02) for the esmolol group vs -0.01 μg/kg/min (IQR, -0.2 to 0.44) for the control group (P = .003). Fluid requirements were reduced in the esmolol group: median AUC was 3975 mL/24 h (IQR, 3663 to 4200) vs 4425 mL/24 h(IQR, 4038 to 4775) for the control group (P < .001). We found no clinically relevant differences between groups in other cardiopulmonary variables nor in rescue therapy requirements. Twenty-eight day mortality was 49.4% in the esmolol group vs 80.5% in the control group (adjusted hazard ratio, 0.39; 95% CI, 0.26 to 0.59; P < .001).
CONCLUSIONS AND RELEVANCE: For patients in septic shock, open-label use of esmolol vs standard care was associated with reductions in heart rates to achieve target levels, without increased adverse events. The observed improvement in mortality and other secondary clinical outcomes warrants further investigation.

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Colloids again: still no benefit.

fluidinheloiconIt’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
[EXPAND Abstract]

 

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.

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Prehospital ECLS – it's happening

Patients with refractory (>30 mins) cardiac arrest underwent prehospital cannulation for extracorporeal life support in a French feasibility study. A physician-paramedic team responded by car in Paris to cardiac arrest cases that met inclusion criteria. Mechanical CPR devices (Autopulse or LUCAS) were applied during cannulation. Femoral venoarterial ECMO was instituted using a Maquet Cardiohelp system. Blood products and inotropes, echocardiography, and hypothermia were included in the prehospital management package.
Seven patients were treated, with a mean age of 42 (+/- SD of 16, no median given). ECLS was started an average 57 min (±21) after the onset of ACLS. One patient survived to discharge neurologically intact. Two brain dead patients became organ donors. The survivor had hypertrophic cardiomyopathy with refractory ventricular fibrillation.
Safety and feasibility of prehospital extra corporeal life support implementation by non-surgeons for out-of-hospital refractory cardiac arrest
Resuscitation. 2013 Nov;84(11):1525-9
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BACKGROUND: Extra corporeal life support (ECLS) has been recently introduced in the treatment of refractory cardiac arrest (CA). Several studies have assessed the use of ECLS in refractory CA once the patients reach hospital. The time between CA and the implementation of ECLS is a major prognostic factor for survival. The main predictive factor for survival is ECLS access time. Pre hospital ECLS implementation could reduce access time. We therefore decided to assess the feasibility and safety of prehospital ECLS implementation (PH-ECLS) in a pilot study.

METHODS AND RESULTS: From January 2011 to January 2012, PH-ECLS implementation for refractory CA was performed in 7 patients by a PH-ECLS team including emergency and/or intensivist physicians and paramedics. Patients were included prospectively and consecutively if the following criteria were met: they had a witnessed CA; CPR was initiated within the first 5min of CA and/or there were signs of life during CPR; an PH-ECLS team was available and absence of severe comorbidities. ECLS flow was established in all patients. ECLS was started 22min (±6) after the incision, and 57min (±21) after the onset of advanced cardiovascular life support (ACLS). In one patient, ECLS was stopped for 10min due to an accidental decannulation. One patient survived without sequelae. Three patients developed brain death.

CONCLUSIONS: This pilot study suggests that PH-ECLS performed by non-surgeons is safe and feasible. Further studies are needed to confirm the time saved by this strategy and its potential effect on survival.

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