Author: Ryan Radecki

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

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

A Snapshot of Chest Pain Waste

The Lown Institute continues their conference today on avoidable care in the U.S., so this study is a lovely glimpse into one of the worst offenders in Emergency Medicine – chest pain.

Coming from the University of Pennsylvania, this is a retrospective review of patients 805 patients for whom an ED observation protocol of rapid rule-out and stress testing was performed.  The supposed point of this article is to demonstrate the potential safety of stress testing after two sets of cardiac troponin 2-hours apart, and, in theory, they do demonstrate this.  Of these 805 patients, 16 patients were diagnosed with acute myocardial infarction on index visit through this protocol – and within 30 days, 1 patient had AMI and 2 received revascularization.

The authors conclusion: “…serial troponins 2 hours apart followed by stress testing is safe and … rapid stress testing represents another option to expedite care of patients with potential ACS”.

789 of 805 patients received serial troponins and a negative stress test to identify a handful of higher than minimal risk folks.  The 16 AMI diagnoses were based on 12 patients with negative troponins and positive stress tests, 1 patient with troponins that rose from <0.02 to 0.16 ng/mL and a negative stress test, and 3 patients with troponins rising from <0.02 to 0.06-0.09 ng/mL and positive stress tests.  But, in order to dredge up these soft diagnoses of ACS, hundreds of thousands of dollars in financial damage were inflicted on the remaining cohort.

These authors feel rapid stress testing is an alternative to CTCA for preventing avoidable admissions.  In the spirit of the Lown Institute, and of Rita Redberg’s NEJM editorial regarding CTCA, the true strategy for preventing an avoidable admission is simply to discharge the majority of these patients.  A less than 2% yield for an expensive observational diagnostic strategy is far more grossly negligent a failure of medicine than an occasional missed minor MI.  We can do nearly as well, for much less cost – but if only we continue to address our “zero-miss” cultural expectations surrounding diagnosis and treatment.

“Safety of a rapid diagnostic protocol with accelerated stress testing”
http://www.ncbi.nlm.nih.gov/pubmed/24211281

Lunacy, Animal Bites, and You

A guest post by Justin Hensley (@EBMGoneWild) of Evidence-Based Medicine Gone Wild.

The word “lunacy” receives its etymology from the belief the moon can cause disorders of the mind.  Multiple things – including crime, crisis incidence, and human aggression – are all positively correlated with the phases of the moon.  It is obvious that the moon affects human behavior, but does it affect other animals?

From 1 January 1997 to 31 December 1999 there were 1621 patients seen at the Bradford Royal Infirmary ambulatory and emergency department with a diagnosis of “bite”. The overwhelming majority of these bites (95.1%) are from dogs, with the rest from cats, horses, and rats in descending order. To break down the 29.530589 day lunar cycle, the authors divided it into 10 periods, 9 with 3 days, and 1 with 2 days. Using that breakdown they were able to get a statistically significant difference in the incidence of animal bites at or about the full moon. 

What to take from this? Well, we can’t determine causation from this study certainly. Is it still human behavior causing increased bites, or are animals also influenced by lunar cycles? Notwithstanding the confidence intervals for the “high period” covering the entirety of their chart, they don’t break down the data for each day of the lunar cycle. Most human behavior differences in the full moon have to do with increased nocturnal light, and this doesn’t apply during the day. No reasons are given for the seemingly arbitrary divisions of the lunar cycle either.

Perhaps “lunacy” is every bit a misnomer as “hysteria”.

“Do animals bite more during a full moon? Retrospective observational analysis”

Lunacy, Animal Bites, and You

A guest post by Justin Hensley (@EBMGoneWild) of Evidence-Based Medicine Gone Wild.

The word “lunacy” receives its etymology from the belief the moon can cause disorders of the mind.  Multiple things – including crime, crisis incidence, and human aggression – are all positively correlated with the phases of the moon.  It is obvious that the moon affects human behavior, but does it affect other animals?

From 1 January 1997 to 31 December 1999 there were 1621 patients seen at the Bradford Royal Infirmary ambulatory and emergency department with a diagnosis of “bite”. The overwhelming majority of these bites (95.1%) are from dogs, with the rest from cats, horses, and rats in descending order. To break down the 29.530589 day lunar cycle, the authors divided it into 10 periods, 9 with 3 days, and 1 with 2 days. Using that breakdown they were able to get a statistically significant difference in the incidence of animal bites at or about the full moon. 

What to take from this? Well, we can’t determine causation from this study certainly. Is it still human behavior causing increased bites, or are animals also influenced by lunar cycles? Notwithstanding the confidence intervals for the “high period” covering the entirety of their chart, they don’t break down the data for each day of the lunar cycle. Most human behavior differences in the full moon have to do with increased nocturnal light, and this doesn’t apply during the day. No reasons are given for the seemingly arbitrary divisions of the lunar cycle either.

Perhaps “lunacy” is every bit a misnomer as “hysteria”.

“Do animals bite more during a full moon? Retrospective observational analysis”

Time to Move to the HEART Score

A couple posts ago I mentioned it was time for the TIMI Risk Score for UA/nSTEMI to go the way of the dodo for evaluation of chest pain in the Emergency Department.  It wasn’t derived from an Emergency Department population, doesn’t have great predictive skill in identifying very-low-risk patients, and includes nonsensical elements (did you take an aspirin within the last 7 days?).

Alternatively, we have the HEART score: History, ECG, Age, Risk factors, Troponin.  This was derived – like the Wells score – from the elements of clinical gestalt, and ought to at least make better intuitive sense than the occasionally frizzy outputs from multivariate logistic regression.  It was initially derived and refined retrospectively, and this represents the prospective validation study.  These authors prospectively enrolled 2,440 patients from 10 centers in the Netherlands and followed them for a primary endpoint of a major adverse cardiac event (AMI, PCI, CABG, death) for six weeks.  They also collected the variables of interest necessary to calculate TIMI and GRACE risk scores for comparison of c-statistic.

Obviously, I’m recommending the HEART score because it outperformed the others – the c-statistic for HEART was 0.83, 0.75 for TIMI, and 0.70 for GRACE.  Most importantly, for the Emergency Department, it was superior at the low-end of the spectrum.  For the 34% of the population that was TIMI 0-1, 23/811 (2.8%) had 6-week MACE.  14.0% had GRACE 0-60, and 10/335 (2.9%) had MACE.  For HEART, 36.4% were 0-3 and ultimately 15/870 (1.7%) had MACE.

Even though there are 2,400 patients in this study, there are few enough in each individual category that confidence intervals for each predictive bucket are still relatively wide.  Then, you can still have a HEART score in the “very low risk” 0-3 range with a troponin >3x the normal limit and an abnormal EKG – which is seemingly counterintuitive.  They also don’t compare their rule to clinical judgment, so we can’t measure the performance of the rule in actual decision-making.

A couple other studies have either prospectively or retrospectively validated these findings with reasonable consistency.  It isn’t perfect – but it’s better than TIMI or GRACE – and it’s what I currently use to support my shared decision-making discussions at disposition of the appropriate chest pain cohort.

http://www.heartscore.nl/en/

“A prospective validation of the HEART score for chest pain patients at the emergency department”
http://www.ncbi.nlm.nih.gov/pubmed/23465250

HINTS vs. ABCD2 in Dizziness

Dizziness in the Emergency Department sends everyone down their favorite diagnostic algorithm, with outcomes ranging from utterly benign to impending permanent disability.  I’ve covered the repurposing of the ABCD2 score for risk-stratification in dizziness before, showing it had some utility in predicting posterior circulation stroke.

However, unsurprisingly, these authors demonstrate examination maneuvers specifically targeted at evaluating cerebellar function outperform risk-stratification.  The HINTS (head impulse, nystagmus type, test of skew) evaluation compared with the ABCD2 (age, blood pressure, clinical features, duration, diabetes) in a convenience sample of 190 prospectively collected patients with acute vestibular syndrome.  Of these 190 patients, 124 had a central cause for their vertigo (stroke, hemorrhage, space-occupying lesion).  The sensitivity and specificity of the ABCD2 score in predicting a central lesion was 58.1% and 60.6%, respectively, while the HINTS score resulted in 96.8% and 98.5%, respectively.

It’s a bit of a straw-man comparison – considering the ABCD2 score was never designed to detect posterior circulation stroke, only to affect probability estimates for cerebrovascular disease.  The prevalence of disease in this sample probably also leads to an overestimation of the specificity of the HINTS exam, but it has otherwise been found to have very good test characteristics.

Visit EMCrit for more information and video footage of the HINTS test, if you’re not already using it.

“HINTS Outperforms ABCD2 to Screen for Stroke in Acute Continuous Vertigo and Dizziness”
http://www.ncbi.nlm.nih.gov/pubmed/24127701

Gender-Specific Symptom Nonsense

This comical, fundamentally flawed publication has already been skewered online in just the handful of days since it hit publication.  But, any press is good press, right?

We’ve been practicing under the prevailing notion women more frequently manifest atypical constellations of symptoms when presenting with acute myocardial infarction.  We’ve inferred this from observational cohort data, and from studies indicating we miss more diagnoses of AMI in women.  So, these authors set to prospectively validate this notion.

It’s rather sad, unfortunately, how much effort and time was spent prospectively enrolling the 2,475 patients recruited for this study.  Each patient underwent a structured clinical interview to determine the presence or absence of specific chest pain features, and these were correlated with final adjucated diagnosis of AMI.  And, in the end, the positive and negative likelihood ratios for AMI for nearly every recorded feature were identical for men and women.

But, when you exclusively enroll patients with “symptoms suggestive of AMI”, you’ve designed precisely the type of study that will never detect atypical presentations of AMI.  If clinicians didn’t suspect acute coronary syndrome associated with an episode of chest pain, these patients are discarded from follow-up.  Unfortunately, then, this work is unable to conclusively answer any question regarding gender-specific symptoms.

To truly evaluate this question, the inclusion criteria would have be far more expansive.  Essentially, nearly all atraumatic patients with a somatic complaint above the pelvis should be screened and followed for a definitive diagnosis of AMI.  Perhaps that study would be too large and unwieldy to successfully execute, but that would be the scope required to answer this question once and for all (within the bounds of external validity).

Finally, I just want to point back to Seth Trueger’s write-up of a lovely ED chest pain study, where expert rheumatologists made gold standard diagnoses of costochondritis in the Emergency Department.  Incidence of AMI in “costochondritis” patients?  6%.

“Sex-Specific Chest Pain Characteristics in the Early Diagnosis of Acute Myocardial Infarction”
http://archinte.jamanetwork.com/article.aspx?articleid=1783306

What Santa Claus, the Tooth Fairy and Low-Dose Dopamine Have in Common

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

We have known for some time that the renal sparring effects of low-dose dopamine is a story we tell to our cardiologists to tuck them in at night. Despite a large meta-analysis published in 2005, finding no evidence of this theoretical renal benefit, the authors of the recent Renal Optimization Strategies Evaluation (ROSE) felt that this question was again worth investigating. Nesiritide, a drug made infamous for causing renal failure, was also examined for its renal sparing attributes.

A total of 360 patients with acute heart failure and renal dysfunction (GFR between 15-60 mL/min) were, in a convoluted fashion (to reduce unnecessary use of central lines), randomized to either low-dose dopamine (2mcg/kg/min), low dose nesiritide (0.005 mcg/kg/min) or placebo infusion for a 72-hour period. The two co-primary end points assessed were urine output and change in cystatin C level over a 72-hour period. There was no benefit of either low dose dopamine or low dose nesiritide when added to standard therapy of acute heart failure in any of the authors’ primary, secondary or tertiary (yes tertiary) endpoints. Though there was no statistical increase in adverse events seen in either the dopamine or nesiritide groups, this is far too small a cohort to truly assess safety.
With the publication of this trial surely it has come time to close the book on low dose dopamine. So next time a consultant requests we start a dopamine infusion for its renal sparring properties, may I suggest we sit him or her down and politely explain that like Santa Claus and the Tooth Fairy, there is no such thing as renal dose dopamine.
“Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction” http://www.ncbi.nlm.nih.gov/pubmed/24247300

What Santa Claus, the Tooth Fairy and Low-Dose Dopamine Have in Common

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

We have known for some time that the renal sparring effects of low-dose dopamine is a story we tell to our cardiologists to tuck them in at night. Despite a large meta-analysis published in 2005, finding no evidence of this theoretical renal benefit, the authors of the recent Renal Optimization Strategies Evaluation (ROSE) felt that this question was again worth investigating. Nesiritide, a drug made infamous for causing renal failure, was also examined for its renal sparing attributes.

A total of 360 patients with acute heart failure and renal dysfunction (GFR between 15-60 mL/min) were, in a convoluted fashion (to reduce unnecessary use of central lines), randomized to either low-dose dopamine (2mcg/kg/min), low dose nesiritide (0.005 mcg/kg/min) or placebo infusion for a 72-hour period. The two co-primary end points assessed were urine output and change in cystatin C level over a 72-hour period. There was no benefit of either low dose dopamine or low dose nesiritide when added to standard therapy of acute heart failure in any of the authors’ primary, secondary or tertiary (yes tertiary) endpoints. Though there was no statistical increase in adverse events seen in either the dopamine or nesiritide groups, this is far too small a cohort to truly assess safety.
With the publication of this trial surely it has come time to close the book on low dose dopamine. So next time a consultant requests we start a dopamine infusion for its renal sparring properties, may I suggest we sit him or her down and politely explain that like Santa Claus and the Tooth Fairy, there is no such thing as renal dose dopamine.
“Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction” http://www.ncbi.nlm.nih.gov/pubmed/24247300