Category: Resuscitation

Alas, EGDT, We Hardly Knew Ye

Twitter and the usual accelerated knowledge translation sites have been abuzz with the release of several important articles regarding resuscitation in severe sepsis.

The one garnering the most press is ProCESS, a 1:1:1 randomization of patients with severe sepsis into Early Goal-Directed Therapy, protocol-based aggressive fluid resuscitation, or “usual care”.  Many detailed analyses and sub-analyses will likely be written, but, the basic gist – it appears the critical innovation coming out out of Rivers’ EGDT is awareness of the importance of any aggressive early recognition and treatment.  The primary outcome – in-hospital mortality at 60-days – was similar across each group.  And, the minor variations in secondary outcomes probably support simply paying close attention to individual patient physiology.

This is not specifically practice-changing in many critical care settings – there has been plenty of skepticism regarding the specific interventions in the Rivers’ algorithm.  The search will certainly go on regarding ways to improve upon the 20% modern mortality in severe sepsis, but it is now easily defensible to eschew the Edwards’ catheter, blood transfusions, and dobutamine from Rivers’ specific protocol.

“A Randomized Trial of Protocol-Based Care for Early Septic Shock”
http://www.nejm.org/doi/full/10.1056/NEJMoa1401602

Still Muddling Through Massive Hemorrhage

The last few years have given way to a paradigm shift in the resuscitation of traumatic hemorrhage.  Using observational data from military settings, resuscitation strategies utilizing reactive correction of coagulopathy have given way to strategies mimicking whole blood transfusion.  Limited evidence suggests PRBC:FFP:Platelet ratios nearing 1:1:1 may be beneficial in resuscitation from traumatic hemorrhage.

This observational study of trauma patients followed lactate levels and measures of coagulopathy during the acute resuscitative phase from major trauma.  106 patients with median Injury Severity Score of 34 received a median of 8 units of PRBCs, 6 units of FFP, and a smattering of platelets and cryoprecipitate transfusions.  Lactate levels, as compared by median and IQR, did not significantly normalize following the initial transfusion, requiring a full day of therapeutic intervention to improve.  Likewise, measures of coagulopathy did not reflect improvement in the acute phase, tending to normalize only after a full day.  It did not matter whether patients received a small, moderate, or large amount of resuscitation.

This study only comments on surrogate outcomes – serum lactate, markers of coagulopathy – and not patient-oriented outcomes, but it serves as a reminder the science is clearly not settled regarding the optimal, cost-effective fashion to resuscitate patients from traumatic hemorrhage.  While many centers have fully adopted whole blood-style resuscitation strategies, it would be incorrect to conclude we have any sort of certainty in the matter.

“Hemostatic resuscitation is neither hemostatic nor resuscitative in trauma hemorrhage”
http://www.ncbi.nlm.nih.gov/pubmed/24553520

No LVADs Were Harmed in the Making of This Blog Post

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Do not perform chest compressions on an LVAD patient in arrest is a pseudoaxiom for the 21st century. The concern is the force of the compressions will dislodge the cannula, turning a critically ill patient into a critically ill patient with an LVAD-sized hole in their left ventricle. The manufacturers staunchly warn against performing compressions at the risk of causing the sky to fall, our patient’s chest to explode, and an incredibly enraged cardiothoracic surgeon to magically appear at bedside spewing hellfire and brimstone.

Authors of this recent retrospective case series attempt to disprove this modern day axiom. This series describes 8 LVAD patients who presented to their facility, Sharp Memorial Medical Center, in arrest over a 4 year span, all of whom received external chest compression as part of the resuscitative efforts. They assessed device integrity post-arrest in two fashions, either by blood flow data from the LVAD control monitor or examination of the device itself on autopsy (a poor prognostic indicator for the patient). 7/8 patients had flow data post-arrest recorded, all of which indicated a functionally intact VAD. 3/8 had an autopsy performed, including the patient with missing flow data. All confirmed an anatomically intact VAD. The authors conclude that at least in this small case series no VADs were harmed during chest compressions. Whether they were helped is another question all together. These are complex patients with multiple variables including the function of both the VAD and the patient’s intrinsic heart. In this series, 5 out of 8 patients arrested due to pump malfunction, 4 of which were due to accidental disconnection (yikes!). Even in this cohort of a seemingly correctable malady (just plug the thing back in), only one patient had return of neurological function.

A case series of 8 patients is clearly not a large enough n to prove chest compressions are safe in the LVAD patient.  What can be said for sure is the sky did not fall and no angry cardiothoracic surgeons materialized from thin air spewing fire and brimstone. Well, at least a half a psuedoaxiom disproven…

“Chest compressions may be safe in arresting patients with left ventricular assist devices (LVADs).” www.ncbi.nlm.nih.gov/pubmed/24472494

2-Handed BVM – Many Hands Make Light Work

A guest post by Anand Swaminathan (@EMSwami) of EM Lyceum and Essentials of EM fame.

I’ve been teaching ACLS and airway workshops for years and I always make a point of focusing on the proper technique for bag-valve-mask (BVM) ventilation. I’ve always taught people both the 1-handed and the 2-handed techniques and said that they’re basically equivalent as long as you feel like you’re getting a good seal. This study brings the efficacy one-hand BVM into question.

The authors performed an interesting study. They took a group of providers (EM residents, attendings, nurses, paramedics and ICU nurses) and had them hold face masks on simulation mannequins with 1-handed and 2 different 2-handed techniques. A ventilator provided a 600 ml tidal volume and then measured the volume returned. Since this is a closed circuit, the volume returned should be equal to the set tidal volume – whatever leaked around the “seal” created by the provider.
What they found was surprising. For the 1-handed only 31% of the set tidal volume was expired while that number was 85% for both of the 2-handed techniques. This difference was found to be statistically significant and I imagine it would also be clinically significant. A study done earlier last year by Hard et al had similar findings.1
So what stands in the way of us completely stopping the teaching and application of 1-handed BVM (unless necessary due to staffing) and embracing 2-handed BVM? Unfortunately, the study is done on simulation mannequins and not on people. What we prefer is to see the application of the study to human patients. But this isn’t always possible. In the same issue of Annals, Wang and Yealy comment in an editorial that not only would it be virtually impossible to do this study in real human patients but also that it’s likely unnecessary.2 BVM is a technique that lends itself well to being studied in a simulation model.
What we have here are two studies showing benefit of a 2-hand BVM technique on mannequins that requires no increased equipment and a minimal increase in necessary resources. Using a 2-hand system is likely a better way to bring the mandible forward and open the nasopharynx allowing for nasal oxygenation. Since we’re unlikely to see a study done on actual patients, this should be enough to change practice.
Article:
“Comparison of Bag-Valve-Mask Hand-Sealing Techniques in a Simulated Model.”
References:
1. “Face Mask Ventilation: A Comparison of Three Techniques.”
2. “Emergency Airway Research: Using All Tools to Bridge the Knowledge Gaps.”

The Great Sugar Wars of Pediatric Critical Care

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Kids are just small adults, or so says the Control of Hyperglycemia in Pediatric Intesive Care (ChiPS) trial. This impressively large RCT of 1369 pediatric ICU patients (under 16 years old) requiring at least 12 hours of vasoactive support and mechanical ventilation, examined how controlling blood glucose levels affects outcomes. Subjects were randomized to either tight glucose control (72-126mg/dL) or conventional control (less than 216 mg/dL). Patients were followed for 30 days to see if mortality and rates of ventilator dependence differed between the two groups.

Simply put the trial was negative. Though the tight glucose control group received more insulin and had lower mean daily blood glucose levels during the first 10 days after randomization, there was no statistical difference between days alive and off the ventilator between the two groups. Patients in the tight glycemic control group were less likely to receive renal replacement therapy (an odds ratio of 0.64 CI 0.45-0.89), but conversely were far more likely to suffer an episode of severe hypoglycemia (below 36mg/dL) with an absolute difference of 4.8%.

Unfortunately thanks to the authors’ spectacular display of subgroup analysis there is nothing simple about this publication. 60% of the population was admitted to the ICU after cardiac surgery. The remaining 40% were there for other reasons, though further details were not specified. A multitude of endpoints in both the cardiac and non-cardiac subgroups were examined. As with the entire cohort, there was no difference in mortality or ventilator-free days in either subgroup.  The authors did observe a decrease in length of stay and mean healthcare costs in the subgroup of patients who did not undergo cardiac surgery and were treated using the tight glycemic parameters. 

Though the authors conclude that these findings are at best hypothesis building and should not be used to guide therapy, this subgroup analysis will inevitably be misinterpreted, suggesting that pediatric ICU patients who have not undergone cardiac surgery will benefit from a strict glycemic regimen. This is clearly not the case. What this trial amounts to is a negative study with both negative primary and secondary endpoints that upon subgroup analysis uncovered statistical differences equally likely to be caused by chance as by the aggressive glucose management. 

This trial is a reminder of our continued insistence of applying disease-oriented outcomes with questionable efficacy over the long term to an acutely ill population. The NICE-SUGAR trial established that tight glucose control was detrimental in an acutely ill adult population, the ChiP trial has demonstrated these lessons can now be applied to our smaller counterparts.

“A Randomized Trial of Hyperglycemic Control in Pediatric Intensive Care” www.ncbi.nlm.nih.gov/pubmed/24401049













A Rapid Response Fantasyland

Rapid response teams sound good in theory – specifically skilled nurses as back-up providers for floor emergencies, intervening and escalating patients in times of unexpected deterioration.  However, the largest cluster-randomized trial and multiple meta-analyses have failed to show any benefit to rapid response teams.

The response to this high-quality evidence?  Irresponsible conclusions based on low-quality retrospective data.

These authors have so much enthusiasm for their product – a rapid response team that proactively rounds on patients – they’re blind to the most obvious holes in their data.  They try to retrospectively compare pre- and post-RRT implementation outcomes, despite having essentially only data on floor codes.  And, backing up their main conclusion, floor codes are lower post-RRT proactive rounding – of course, floor codes were already trending downwards at the time of implementation.

What happened when the RRT intervened?  The same thing as all other studies show – they moved patients to a higher level of care.  How did patients fare in the ICU?  A third died or were transferred to hospice.  Utterly overlooked in the discussion, in which these authors praise their product and their RRT nurses profusely, is the end result of their RRT product appears to be an unchanged mortality – a simple shuffling around the location of in-hospital deaths.  Their title implies a result that is simply demonstrated nowhere in the article, yet they continue to lavish themselves with accolades right up through the final conclusion:

“Our study demonstrates proactivity and innovation as an overall approach to inpatient cardiac arrests  ….  Innovation stems from a dedicated managerial team who routinely evaluates trends in the code data and creatively seeks ways to prevent cardiac arrest from occurring.”

Managerial buzzword self-aggrandizing nonsense.

“Proactive rounding by the rapid response team reduces inpatient cardiac arrests”
http://www.ncbi.nlm.nih.gov/pubmed/23994805

The Shock Index is a Shockingly Poor Predictor of Peri-Intubation Arrest

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.
This retrospective analysis of 410 patients undergoing RSI is a helpful reminder of how a statistically significant association does not implicitly translate into a clinically useful one.

The authors of this paper attempted to identify factors that would predict peri-intubation cardiac arrest using a cohort of patients requiring emergent intubation in a large urban emergency department. Specifically does the Shock Index accurately predict those who will suffer post-intubation cardiac arrest? The Shock Index (HR/systolic BP) is essentially an attempt to quantify a patient’s volume status and cardiac reserve into simple ratio. These same authors have examined this score’s ability to predict peri-intubation hypotension in the past and found similar predictive capabilities.

Given the pedigree of the authors (Dr. Alan Jones and company) it is no surprise their chart review methods were next to flawless. Using standardized data collection forms, a single trained extractor identified patients who underwent ED intubations over a one year period. To ensure inter-observer reliability, 10% of this data was randomly audited by a second extractor blinded to the trials hypothesis. Backwards stepwise regression was utilized to determine what factors were independently associated with peri-intubation cardiac arrest (defined as cardiac arrest up to 60 minutes after intubation).

In this cohort, the rate of cardiac arrest after intubation was 4.2%, or 17 patients. 10 out of these 17 events occurred within 10 minutes of the intubation and, in 15 of the 17 events the initial arresting rhythm was PEA.  As one would expect, patients who experienced peri-intubation cardiac arrest had faster a heart rate, lower blood pressure and more frequent incidence of pre-RSI hypotension. The only two metrics that were found to be independently associated with cardiac arrest were the patient’s body weight and pre-intubation Shock Index. The Shock index was found to have an odds ratio of 1.16 with a confidence interval ranging from 1.003 to 1.3. Put in another manner, it was found to have an AOC of 0.73, rendering it essentially clinically useless.

Given these test characteristics, if we were to use a Shock Index of 0.88 (as suggested by the authors) to determine who is at risk for peri-intubation arrest than we would be left unprepared for an unacceptable quantity of patient who will decompensate during the procedure. This should be inherently obvious, as a formula that incorporates only heart rate and systolic blood pressure is incapable of encapsulating all the many reasons a patient may code peri-intubation. Not to mention that this study does not tell us whether the patients whom the Shock Index identifies as “at risk” will actually benefit from our added vigilance and pre-intubation hemodynamic optimization. Or does the Shock Index merely highlights a spectrum of the more critically ill patients who will inevitably deteriorate despite our clairvoyant best efforts?

Tachycardic, hypotensive patients are at increased peril for peri-intubation arrest. Sicker patients, older patients, and patients with poor cardiac reserve are all at higher risk. Most importantly, the Shock Index does not accurately predict who will and will not arrest after intubation. Similar to tools meant to predict difficult airways (not accurate enough to depend on clinically), we must be prepared for peri-intubation arrest in the majority of the patients requiring emergent intubation. Once a patient reaches the critical juncture of requiring intubation, we should be aware of all the perils this procedure involves and plan accordingly.

“Incidence and Factors Associated with Cardiac Arrest Complicating Emergency Airway Management”
www.ncbi.nlm.nih.gov/pubmed/23911630

Man vs Machine: A CPR Battle to the…

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Presenting the LUCAS 2.0, the latest and greatest in CPR technology! The LUCAS device “provides the same quality for all patients and over time, independent of transport conditions, rescuer fatigue, or variability in the experience level of the caregiver.” Or at least that is what the manufacturer, Physio-Control Inc, will have you believe.

High quality CPR and early defibrillation have been the cornerstones of cardiac arrest management since the AHA published their “Chain of Survival”. Reducing the time off the chest is of utmost importance in the current CPR mantra. So a machine that not only performs consistent high quality CPR, but delivers countershocks without interrupting compressions was sure to show benefit in patient oriented outcomes. What follows is a Paul Bunyan-like contest of man against machine. One in which the makers of the LUCAS device strived to prove modern technology’s superiority over good old fashion manpower. In a delightful twist on the original tale the fancy new mechanical CPR device was found to be no better than traditional CPR.

The trial published in JAMA in November 2013, randomized 2,589 subjects to either traditional CPR following the 2005 European Resuscitation Council guidelines or a mechanical compressions protocol. Patients in the mechanical CPR group received traditional compressions until the device could be deployed, at which point compressions were continued mechanically. Ninety seconds after deployment the device delivered a countershock regardless of the initial rhythm. After which the rhythm was checked every 3-minutes and, if appropriate, a shock was delivered after a 90-second delay.

Despite the obvious advantages the LUCAS device provides, no difference was found in survival at 4-hours, ICU discharge, 1-month, or 6-months. The authors claim victory in a single positive endpoint that reached significance. The number of patients with a CPC score of 1 at 1-month was 2.6% in the traditional CPR vs 4.2% in the mechanical CPR group (p-value of 0.04). This is, of course, just post-hoc dredging of innumerable secondary outcomes, and nothing more than statistical noise. To the authors’ credit, they do not revisit this positive finding.

Despite their claims that the LUCAS device would free up rescuers to do other life sustaining actions, patients in the manual CPR group were defibrillated sooner, intubated faster, transported earlier, and arrived at the hospital in a swifter fashion than those in the mechanical CPR group.

The authors conclude “CPR with this mechanical device using the presented algorithm can be delivered without major complications but did not result in improved outcomes compared with manual chest compressions.” Given that there were only 7 major adverse events in the mechanical CPR group vs 3 in the tradition CPR group this does seem to be the case. Though I would caution, with the low incidence of adverse events, this trial was not powered to truly assess safety of the mechanical delivered CPR. 

“Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest: The LINC Randomized Trial” www.ncbi.nlm.nih.gov/pubmed/24240611

Man vs Machine: A CPR Battle to the…

A guest post by Rory Spiegel (@CaptainBasilEM) who blogs on nihilism and the art of doing nothing at emnerd.com.

Presenting the LUCAS 2.0, the latest and greatest in CPR technology! The LUCAS device “provides the same quality for all patients and over time, independent of transport conditions, rescuer fatigue, or variability in the experience level of the caregiver.” Or at least that is what the manufacturer, Physio-Control Inc, will have you believe.

High quality CPR and early defibrillation have been the cornerstones of cardiac arrest management since the AHA published their “Chain of Survival”. Reducing the time off the chest is of utmost importance in the current CPR mantra. So a machine that not only performs consistent high quality CPR, but delivers countershocks without interrupting compressions was sure to show benefit in patient oriented outcomes. What follows is a Paul Bunyan-like contest of man against machine. One in which the makers of the LUCAS device strived to prove modern technology’s superiority over good old fashion manpower. In a delightful twist on the original tale the fancy new mechanical CPR device was found to be no better than traditional CPR.

The trial published in JAMA in November 2013, randomized 2,589 subjects to either traditional CPR following the 2005 European Resuscitation Council guidelines or a mechanical compressions protocol. Patients in the mechanical CPR group received traditional compressions until the device could be deployed, at which point compressions were continued mechanically. Ninety seconds after deployment the device delivered a countershock regardless of the initial rhythm. After which the rhythm was checked every 3-minutes and, if appropriate, a shock was delivered after a 90-second delay.

Despite the obvious advantages the LUCAS device provides, no difference was found in survival at 4-hours, ICU discharge, 1-month, or 6-months. The authors claim victory in a single positive endpoint that reached significance. The number of patients with a CPC score of 1 at 1-month was 2.6% in the traditional CPR vs 4.2% in the mechanical CPR group (p-value of 0.04). This is, of course, just post-hoc dredging of innumerable secondary outcomes, and nothing more than statistical noise. To the authors’ credit, they do not revisit this positive finding.

Despite their claims that the LUCAS device would free up rescuers to do other life sustaining actions, patients in the manual CPR group were defibrillated sooner, intubated faster, transported earlier, and arrived at the hospital in a swifter fashion than those in the mechanical CPR group.

The authors conclude “CPR with this mechanical device using the presented algorithm can be delivered without major complications but did not result in improved outcomes compared with manual chest compressions.” Given that there were only 7 major adverse events in the mechanical CPR group vs 3 in the tradition CPR group this does seem to be the case. Though I would caution, with the low incidence of adverse events, this trial was not powered to truly assess safety of the mechanical delivered CPR. 

“Mechanical Chest Compressions and Simultaneous Defibrillation vs Conventional Cardiopulmonary Resuscitation in Out-of-Hospital Cardiac Arrest: The LINC Randomized Trial” www.ncbi.nlm.nih.gov/pubmed/24240611

Mostly Dead is All Dead – Neuro Outcomes in OHCA Without Prehospital ROSC

A guest post by Anand Swaminathan (@EMSwami) of EM Lyceum and Essentials of EM fame.

Over the last two weeks there has been a lot of buzz around the NEJM study on targeted temperature management in out of hospital cardiac arrest (OHCA) with return of spontaneous circulation (ROSC). This blog has been no exception. This article we’re going to discuss here addresses the care of a very different population: the patient with OHCA without ROSC in the field.

Over four years, 398,121 adults with OHCA and no ROSC in the field were prospectively entered into a database. The overall survival was dismal (1.89%) with even fewer patients having a good neurologic outcome (0.49%).  Neurologic outcome was defined using the Cerebral Performance Category (CPC) scale with a CPC 1 or 2 as a good neurological outcome. Using logistic regression, the authors identified nine factors that were associated with a CPC 1 or 2 outcomes. The authors further stated that there were four critical factors predictive of a good neurological outcome in these patients: initial non-asystole rhythm; age < 65 years, EMS witnessed arrest and hospital arrival time (from call) < 24 minutes. They further broke down the outcomes by type of non-asystolic rhythm:

There are a number of interesting findings in this study. If there’s no ROSC in the field, the chance of achieving good neurologic status is minimal. Survivors were 3-4 times more likely to have a poor neurologic outcome (i.e. severe cerebral disability, coma or brain death) than a good one (1.89% vs. 0.49%). The presence of the previously mentioned four factors was associated with a higher incidence of better outcomes. In particular, a presenting rhythm of ventricular fibrillation had an adjusted OR of 9.37 for a good outcome. Additionally, this study showed, as others have in the past, that epinephrine use increased the rate of ROSC but did not increase the rate of good neurological outcomes (see also Stiell 2004, Hagihara 2012).

How does this change what we do? We’ve all been working when EMS brings in an unwtinessed arrest patient that never had ROSC. The entire ED team mobilizes to care for this patient even though we know the potential for a good outcome is miniscule. This study provides preliminary information on which patients are more likely to have a good neurologic outcome. It should be the basis of further studies looking at protocols to stop resuscitation in the field and avoid transport to the hospital.

References
Goto Y, Maeda T, Nakatsu-Goto, Y. Neurological outcomes in patients transported to hospital without prehospital return of spontaneous circulation after cardiac arrest. Critical Care 2013; 17:R274 doi: 10.1186/cc13121 [Open Access]

Stiell IG et al. ACLS in OHCA. NEJM 2004; 351: 647-56.

Hagihara A et al. Prehospital Epinephrine Use and Survival Among Patients with OHCA. JAMA 2012; 307(11): 1161-68