Tuesday, January 3, 2012

Too Many Traumatic Arrests Are Transported

Traumatic arrest in the field - except in the narrowest of circumstances - has universally dismal outcomes.  Yet, As the authors of this study observe, a great number of these patients continue to be transported to hospitals.

This is a retrospective review of a prospective trauma registry at Sinai in Chicago in which all traumatic patients with pre-hospital arrest were considered.  Patients were excluded for pediatrics, medical causes, drowning/electrocution injuries, and if the prehospital time was less than 15 minutes.  Essentially, they were looking at guidelines from the ACS Committee on Trauma for termination of resuscitation in the out of hospital setting - pulseless, apneic, no organized ECG activity, or unresponsive to 15 minutes of resuscitation.

They identified 428 patients in their cohort - and found that 294 of them were transported in violation of guidelines.  Of the inappropriately transported patients, 93% were declared dead in the ED and the remaining 6.8% (20 patients) survived the ED.  Of those 20, 12 died in surgery, 8 made it to the ICU, and 7 died.  A single, neurologically devastated, patient survived to discharge to a long-term care facility with a GCS of 6.

The total hospital charges incurred for the futile resuscitation of these patients totaled $3.8 million - a figure that excludes the EMS charges as well as the long-term care facility charges for the patient with GCS 6.

And this is just a single hospital.

"The Consequences of Noncompliance With Guidelines for Withholding or Terminating Resuscitation in Traumatic Cardiac Arrest Patients"
http://www.ncbi.nlm.nih.gov/pubmed/21986740

Monday, January 2, 2012

Must We Use IV Paracetamol/Acetaminophen?

I've yet to be terribly impressed with the "new" pain control options available to clinicians these days.  We've got tapentadol (Nucynta), which works just about as well as ibuprofen.  We've got companies working on a purified hydrocodone derivative that's 10 times stronger and equally more dependence forming.  And then we have intravenous paracetamol/acetaminophen.

So, it works.  Studies, like this one, show it's reasonably effective and has a minimal side effect profile - at least compared to the mild incidence of nausea seen with IV morphine.  It's slightly faster acting, achieves more reliable plasma levels than oral paracetamol/acetaminophen, and it's presumably as safe - although the safety of any intravenous drug is compromised due to extravasation risks and potential administration errors.  Oral paracetamol/acetaminophen bills a patient a few dollars while IV administration bills around a hundred, and I continue to wonder whether these sorts of "innovations" are worthwhile advances in pain control outside of extremely narrow indications.  I believe we now stock this and intravenous ibuprofen at our hospital - and goodness knows I've never seen anyone use them.  While relief in suffering is undoubtedly one of our most important roles in healthcare, we have to weigh the few moments of physical suffering against the long-term consequences/suffering of the hospital bills that may be passed along to our patients.

Anyone have a favorable experience with these new non-narcotic medications?

"Intravenous paracetamol versus morphine for renal colic in the emergency department: a randomised double-blind controlled trial"
http://www.ncbi.nlm.nih.gov/pubmed/22186009

Saturday, December 31, 2011

The Risks of Missing Dialysis

Hemodialysis patients have an elevated risk of death - and it's even higher for patients on scheduled dialysis during their "weekend."

Most scheduled plans are every other day Mon-Wed-Fri or Tue-Thu-Sat, which leads to a two-day interval between dialysis - resulting in an extra day of fluid retention and electrolyte abnormalities.  Bad hearts + extra fluid results in a much higher incidence of essentially any kind of mortality or morbidity associated with cardiovascular causes - significantly more myocardial infarction, congestive heart failure, stroke, and dysrhythmia.  Overall, there were 22.1 vs. 18.0 deaths per 100 person-years on the long-interval days than the others.  Retrospective registry data-mining, but it probably illuminates a logical truth.

This particular article caught my eye because we have a significant population at our county facility that comes for "compassionate dialysis".  Non-U.S. citizens that do not qualify for scheduled dialysis, they "live" a tortured existence in which they can only receive "emergency dialysis", as in, we routinely wait until they're at the precipice of death - with strict criteria of pulmonary edema, K+ > 6.0, bicarbonate less than 10, etc. - before pulling them back a small increment and sending them home to repeat the cycle in another week.  Barbaric.  I can't even imagine what their outcomes are like....

"Long Interdialytic Interval and Mortality among Patients Receiving Hemodialysis"
http://www.ncbi.nlm.nih.gov/pubmed/21992122

Thursday, December 29, 2011

Yet Another Highly Sensitive Troponin - In JAMA

...peddling the same tired phenomenon of magical thinking regarding the diagnostic miracle of highly sensitive troponins.  However, this one is different because it's been picked up by the AP, CBS News, Forbes, etc. saying: "Doctors are buzzing over a new blood test that might rule out a heart attack earlier than ever before" and other such insanity.  Yes, our hearts are in atrial flutter around the water cooler about a new assay that changes sensitivity from 79.4% to 82.3% at hour 0 and 94.0% to 98.2% at hour 3.


Unless you actually read the article.

Somehow, contrary to every other high-sensitivity troponin study, this particular highly-sensitive troponin had increased specificity as well - which simply doesn't make sense.  If you're testing for the presence of the exact same myocardial strain/necrosis byproduct as a conventional assay, it is absolutely inevitable that you will detect a greater number of >99th percentile values in situations not reflective of acute coronary syndrome.  The only way to increase both sensitivity and specificity is to measure something entirely different.

Or, if it suits your study aims, you can manipulate the outcomes on the back end.  In this study, the final diagnosis of ACS "was adjudicated by 2 independent cardiologists" whose diagnostic acumen is enhanced by financial support including Brahms AG, Abbott Diagnostics, St Jude Medical, Actavis, Terumo, AstraZeneca, Novartis, Sanofi-Aventis, Roche Diagnostics, and Siemens.

I am additionally not impressed by their results reporting - sensitivity and specificity, followed by the irrelevant positive predictive and negative predictive values.  Since the PPV and NPV are determined by the incidence of disease in their cohort, they're giving us numbers that are potentially not externally valid.  Rather, they should be reporting positive and negative likelihood or odds ratios - which are relatively cognitively unwieldy, but at least not misleading, but conceptually facile, like PPV and NPV.

And this is from JAMA.  Oi.

"Serial Changes in Highly Sensitive Troponin I Assay and Early Diagnosis of Myocardial Infarction"

Tuesday, December 27, 2011

How Frequently Is The Cath Lab Cancelled?

In North Carolina - a fair bit, actually.

This is a 14-hospital registry of cardiac catheterization activations for which the authors retrospectively evaluated how many were subsequently cancelled after activation.  They don't delve into a great deal of detail regarding specific findings that accounted for the cancellation - they simply observe the broad categories of cancellation.

Of all cath lab activations, it was judged that 15% were "inappropriate", with the gold standard being the consulting cardiologist opinion.  Of the cancellations, 40% were based on the EMS ECG, 31% were ED ECG, and the remainder were "not cath lab candidates".  The author's main focus in their conclusion is on the difference between EMS ECG cancellation and ED ECG cancellation due to ECG reinterpretation following activation.

What's more interesting from the paper, however, is when they break it down to the precise cohorts of activation and arrival - and note that 24.7% of EMS activations were subsequently judged inappropriate.  It is also interesting that 13% of non-PCI center activations were inappropriate vs 8% of PCI center activations.  Reading between the lines, there's probably some experiential component to the differences in activation rates, but this study doesn't specifically look at volume and training.

"Rates of Cardiac Catheterization Cancelation for ST Elevation Myocardial Infarction after Activation by Emergency Medical Services or Emergency Physicians: Results from the North Carolina Catheterization Laboratory Activation Registry (CLAR)"
http://www.ncbi.nlm.nih.gov/pubmed/22147904

Sunday, December 25, 2011

Happy Holidays!

Holiday break - intermittent and ineloquent blogging will be the norm.  I count 209 blog posts for the year - more than enough to keep anyone busy reading the archives.

But, if you're done with those, Life In The Fast Lane has a lovely Christmas-themed blog post with great articles including:

"What was wrong with Tiny Tim?"
http://www.ncbi.nlm.nih.gov/pubmed/1340779

"Children’s Nomenclatural Adventurism and Medical Evaluation study"
http://www.ncbi.nlm.nih.gov/pubmed/20415998

"No poinsettia this Christmas"
http://www.ncbi.nlm.nih.gov/pubmed/16866065

Saturday, December 24, 2011

Ranitidine Kills Neonates

Specifically, 24 to 32-week premature neonates, but it's still an interesting demonstration of the unanticipated dangers of reducing the body's nonimmune defense mechanisms.

This is a non-randomized, controlled, prospective, observational study from Italy that simply looked at how many premature neonates in their NICU received ranitidine treatment for acid suppression.  The secondary endpoints of the study were any observed associations between ranitidine use/non-use and NEC, mortality, sepsis, length of hospitalization, etc.  This is still non-randomized observational data, so the associations may be affected by other unknown confounders - but mortality in the non-ranitidine group was 1.6% and the mortality in the ranitidine group was 9.8%.  This difference is probably all attributable to infection, considering 25.3% of the ranitidine group developed sepsis compared to 8.7% in the non-ranitidine group.

An impressive difference, even in a non-randomized cohort.  Not a lot of obviously significant differences between groups.  We've seen similar, smaller increases in infection in ICU adults receiving acid-suppression medication - I wonder if these effects extend to young infants on ranitidine as well?

"Ranitidine is Associated With Infections, Necrotizing Enterocolitis, and Fatal Outcome in Newborns"
http://www.ncbi.nlm.nih.gov/pubmed/22157140

Thursday, December 22, 2011

Dexmedetomidine Is Not For ED Sedation

They use alpha-2 agonists for sedation all the time in veterinary medicine - but it doesn't look like it has a role here in the Emergency Department.

This is a small case-series out of Australia in which they gave dexmedetomidine (Precedex) to the acutely behaviorally challenged - a high-risk population in the Emergency Department, both for the patient and for staff.  Patients became eligible for dexmedetomidine if they had acute behavioral disturbance requiring physical and chemical restraint.  In this hospital, their protocol was to use droperidol 10mg IV for chemical sedation, then a second 10mg dose, and then they became eligible for second-line agents.

Their study population is thirteen patient enrollment over 21 months constituting a heterogenous mix of toxicologic and psychiatric agitation.  Five of the thirteen patients received an IV loading dose only, and the remaining eight received loading dose and infusion.  Of the five who received the loading dose, 2 had effective sedation without adverse effects - and the other 3 were not sedated and one became hypotensive.  Of the other eight, three had effective sedation, one of which developed hypotension and atrial fibrillation.  The other five had only transient or no sedation, four became hypotensive, and two were intubated for persistent agitation.

So, in all, five of the thirteen had adequate sedation using dexmedetomidine as rescue after initial attempts at chemical sedation - but seven had adverse effects.  The authors then conclude that, while it provides an additional, reasonable alternative for sedation, monitoring and managing the adverse effects would be too resource intensive.

Seems reasonable enough.

"Dexmedetomidine in the emergency department: assessing safety and effectiveness in difficult-to-sedate acute behavioural disturbance"
http://www.ncbi.nlm.nih.gov/pubmed/22158533

Wednesday, December 21, 2011

Nitroprusside Saves Pigs - How About Humans?

Essentially, no ACLS medication therapy has been shown to be terribly efficacious with regard to meaningful patient outcomes.  Epinephrine - if we could find a way to satisfactorily preserve neurologic and cardiovascular status after return of spontaneous circulation - seems to have a small helpful effect, but has all sorts of deleterious effects on LV function and cerebral perfusion.  Otherwise, nothing is proving useful other than CPR, shock ventricular arrhythmias, and hope for the best.

I posted about this back in April, and it's another article - from the same masters of porcine resuscitation up in Minneapolis - about a second series of protocols they used to evaluate "sodium nitroprusside enhanced CPR"(SNPeCPR).  The CPR is the same.  The SNPe part is multiple doses of IV sodium nitroprusside and an impedance threshold device, along with a more limited role for epinephrine administration.

They ran two protocols for this study.  Protocol A was a ventricular fibrillation model with 6 standard CPR pigs, 6 CPR + impedance threshold, and 12 SNPeCPR pigs.  Protocol A favored ROSC in SNPeCPR - 0/6, 0/6, and 12/12.

Protocol B was a PEA model with 8 pigs of standard CPR vs 8 pigs of SNPeCPR.  Protocol B favored ROSC in SNPeCPR - 0/6 vs. 7/8.

I think they might be onto something here, but I am still a little wary about the results because both these articles are from the same institution and they keep using these idealized perfusion platforms.  Other investigators should heed this research to evaluate whether their methods are externally valid and warrant human trials.

"Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models"
www.ncbi.nlm.nih.gov/pubmed/21725236

Monday, December 19, 2011

Under/Overtesting in Fever Without a Source

A curious study that observes, from the NHAMCS dataset, the testing performed by Emergency Physicians on children who have fever without a source between the ages of 3 and 36 months.

The general point of the authors, while acknowledging the limitations of this sort of data-dredging, is that testing strategies by Emergency Physicians appear to be generally non-conforming with the American Academy of Pediatrics recommendations for testing in otherwise well-appearing children.  They are hesitant to critique the patients who received laboratory testing - because they have no data on how well-appearing the child may have been or other comorbidities that might indicate testing - but they do take issue with the fact that only 43% of females under age 2 with a fever received a urinalysis and culture.  The 2008 Pediatrics guidelines - not endorsed by ACEP - would recommend that all of them receive UA and culture.  Considering the prevalence of UTI in febrile females under 2 years of age ranges from 8-17%, their criticism is probably valid.

Other trivia: 20% of children with no testing performed received antibiotics.  This could be due to missing ICD-9 data about another clinical diagnosis - but more likely due to simply treating fever unnecessarily.  

And, finally, children from zip codes with higher median incomes were more likely to receive CBC and UA.  More UAs, probably good.  More CBCs, probably bad.

Just an interesting summation of observational data.

Sunday, December 18, 2011

Early Heparin Does Not Save Lives in Pulmonary Embolism

Or, if it does, this is not the article that shows it.  It tries to show it - and Rick Bukata, who I love, includes it as part of his PE review in this month's Emergency Physician's Monthly.  It's a year and a half old, but I had to pull it because I've presented other articles showing the diagnosis and treatment of pulmonary embolism isn't changing mortality.

This is from the Mayo clinic, and it's observational, retrospective cohort data, which is red flag #1 for drawing practice-changing conclusions.  They reviewed charts on 400 symptomatic pulmonary embolism identified on CTPA that were subsequently admitted to the hospital and anticoagulated with systemic heparin.  In their introduction, they set out to show that outcomes are improved in pulmonary embolism if you initiate heparin in the Emergency Department.  In the end, their conclusion is essentially summarized by this graphic:


Seems pretty convincing, eh?

And, it's true, there was a significant association between heparin in the ED and 30-day survival.  There was also, however, a significant association between 30-day survival and: tachycardia, Wells score, leukocytosis, elevated troponin, malignancy, recent surgery, ICU admission, and hemorrhagic events.  So, did patients die because they didn't get heparin, or did they die because they were more acutely ill - and/or had a hemorrhagic event after initiating heparin?  The big one for me is the difference between positive (>0.01 ng/mL) troponins - 26.4% in their survivors and 47.8% in the non-survivors.  Considering the criteria for diagnosis of submassive pulmonary embolism - patients who occupy a different level of risk for poor outcomes - includes elevated troponins indicative of right heart strain, I think this study doesn't properly support anything it tries to imply regarding the time to heparin and survival.

"Early Anticoagulation Is Associated With Reduced Mortality for Acute Pulmonary Embolism"
www.ncbi.nlm.nih.gov/pubmed/20081101

Friday, December 16, 2011

Your Residents Would Love a Wiki

It's not a terribly profound paper - along the lines of "we did this and we liked it" sort of thing - but it is a relevant educational application of wikis in medicine.

The BIDMC Internal Medicine department undertook an initiative to essentially convert all their little handbooks and service guides to an online reference.  They chose the wiki interface so anyone could update information or add pages while allowing updates to be tracked and rolled back as necessary.  They promoted it during their intern orientation and made a significant effort both to get people to update it and use it.  And, for the most part, they were successful.  Most residents (92%) thought it was useful, it was mostly used to find phone numbers and rotation specific clinical information, and, overall, about half of the PGY-2 and -3s updated the site during the 2009-10 year.

It probably takes a lot of effort and requires just the right collaborative environment, but there are a lot of residencies, departments, or other clinical organizations that could also probably benefit from something similar - particularly if there are a lot of rotating students/residence between difference services or sites.

"Adoption of a wiki within a large internal medicine residency program: a 3-year experience"
http://www.ncbi.nlm.nih.gov/pubmed/22140210

Thursday, December 15, 2011

Why Aren't You Using Nitrous Yet?

Another massive study reviewing adverse events encountered during procedural sedation - this time with nitrous oxide given in concentrations up to 70%.  It is odd that resistance is encountered regarding high concentrations of nitrous oxide - considering 30% O2 is still greater than the fraction of inspired oxygen on room air - but this, and other studies like it, should help allay any concerns.

Out of their 7,802 nitrous administrations, they recorded 9 "potentially serious" adverse events - eight desaturations and one potential aspiration event requiring oropharyngeal suctioning.  More importantly, a reasonable percentage of these administrations were in children with comorbid diseases or potentially serious illness that needed sedation for significant procedures - LP, CT scans, NG/G-tube placement, and "other" that included EMGs and botulinium toxin injections.  Their rates of serious events are similar to other published series where either zero or <1% potentially serious events occurred - except for the study that reported 30% adverse events, but included "euphoria" and "dreaming" as adverse events.

This is not, however, an ED-only study, and one of the limitations is that they don't specifically record whether they are able to successfully complete the intended procedure with this method - however, one would imagine, if it didn't work the first 7,000 times, they wouldn't have kept doing it...

"Safety of High-Concentration Nitrous Oxide by Nasal Mask for Pediatric Procedural Sedation"
http://www.ncbi.nlm.nih.gov/pubmed/22134227

Tuesday, December 13, 2011

High-Sensitivity Troponin Dead End

Another article trying to work the unworkable - the balance between sensitivity and specificity.

From New Zealand, an attempt to evaluate the Roche Laboratories hsTnT assay in the interests of performing accelerated rule outs in the ED - looking at any combination of initial value, 2-hour value, delta between 0-2 hour value, etc.  And, essentially, any strategy you choose is wrong.

On one hand, you can get up to 91.4% specific for their gold  standard of AMI by requiring a hsTnT  >14 ng/L and a 20% delta change at 2 hours - but your sensitivity will drop to 72%.  Conversely, you can have sensitivity of 98.8% - which is the point of these hsTnT testing strategies - but your specificity drops to 56.4%.  Unless you're doing something intelligent with all those false positives that isn't harmful, expensive, or invasive, the costs of zero-miss are, once again, too high.

"High-sensitivity troponin T for early rule-out of myocardial infarction in recent onset chest pain"

Monday, December 12, 2011

Just Do It - Lytics for STEMI

PCI is fabulous - but only if you get them to the balloon in 90 minutes or less - otherwise, we should be giving thrombolytics for STEMI.  Unlike stroke, and even though many of these studies are manufacturer-supported, we have literally hundreds of thousands of patients randomized to tenecteplase, alteplase, streptokinase, etc. in combination with every different antiplatelet agent under the sun.  I still don't know whether prasugrel and lytics go together, but I'm sure we'll have GUSTO-10,000 soon enough.

Why do I bring this up?  Because it turns out we're terrible at transferring patients to PCI-capable centers fast enough.  This is a retrospective, observational study of CMS OP-3, the door-in, door-out quality measure for STEMI patients receiving transfer.  A grand total of 9.7% patients in this review of 13,776 patient encounters met the quality standard of transfer within 30 minutes.

If you agree with the literature that says a DIDO time >30 minutes is associated with a 56% increased odds for in-hospital mortality, this could be important.

Lytics.  Just do it.

In fact, depending on the recency of symptoms, the location of the infarct, and whether we're off-hours for cath lab activation, I'll give full-dose lytics on arrival while awaiting cath lab transport.  Your mileage may vary, depending on your cardiology team.

"National Performance on Door-In to Door-Out Time Among Patients Transferred for Primary Percutaneous Coronary Intervention"
www.ncbi.nlm.nih.gov/pubmed/22123793

Saturday, December 10, 2011

ED Geriatric CPOE Intervention - Win?

It does seem as though this intervention had a measure of success - based on their primary outcome - but there's more shades of grey throughout the article.

This is a prospective, controlled trial of a contextual computer decision-support (CDS) incorporated into the computerized provider order entry (CPOE) system of their electronic health record (EHR).  They do a four-phase On/Off intervention where the CPOE either suggests alternative medications or dose reductions in patients >65 years of age.  They look at whether the intervention changed the rate at which medication ordering was compliant with medication safety in the elderly, and then, secondarily, at the rate of 10-fold errors, medication cancellations, and adverse drug event reports.

The oddest part of this study is their choice of primary outcome measure.  Ideally, the most relevant outcome is the patient-oriented outcome - which, in this case, ought to be a specific decrease in adverse drug events in the elderly.  However, and I can understand where they're coming from, they chose to specifically evaluate the usability/acceptability of the CDS intervention to verify the mechanism of intervention.  There are lots of studies out there documenting "alert fatigue", resulting in either no change or even increasing error rates.

As far as the main outcome measure goes, they had grossly positive findings - 31% of orders were compliant during the intervention periods vs. 23% of orders during the control periods.  But, 92.5% of recommendations for alternative medications were ignored during the intervention periods - most commonly triggered by diazepam, clonazepam, and indomethacin.  The intervention was successful in reducing doses for NSAIDs and for opiates, but had no significant effect on benzodiazepine or sedative-hypnotic dosing.

However, bizarrely, even though there was just a small difference in guideline-concordant ordering, there was a 4-fold reduction in adverse drug events - most of which occurred during the initial "off" period.  As a secondary outcome, there's much to say about it other than "huh".  None of their other secondary outcomes demonstrated any differences.

So, it's an interesting study.  It is consistent with a lot of previous studies - most alerts are ignored, but occasionally small positive effect sizes are seen.  Their primary outcome measure is one of mostly academic interest - it would be better if they had chosen more clinically relevant outcomes.  But, no doubt, if you're not already seeing a deluge of CDS alerts, just wait a few more years....

"Guided medication dosing for elderly emergency patients using real-time, computerized decision support"
http://www.ncbi.nlm.nih.gov/pubmed/22052899

Friday, December 9, 2011

Dog Bites and Antibiotics

Nicholas Genes of...well, multiple sites of fame, including recurring columns in several EM publications, SAEM leadership, and the long-standing medical blog "blogborygmi" beat me to this ACEP News item from today:

MedPage Today (12/9, Walsh) reports that a study presented in a poster session at the midyear clinical meeting of the American Society of Health-System Pharmacists (ASHP) found that only 64% of the patients presenting to the emergency department with animal bites "were discharged on the appropriate antibiotic."


I won't attempt to replicate his scathing criticism of ACEP News for publicizing a poster from an interim pharmacy conference, just read it for yourself:
http://blogborygmi.tumblr.com/post/13967004314/among-98-patients-seen-with-bites-over-the-course

TEG and Dabigatran

An interesting mini-letter from my institution regarding dabigatran, thromboelastography, and poor outcomes.

It simply notes and reinforces the fact that conventional coagulation studies in patients on dabigatran will be normal - and therefore conventional reversal options are unlikely to be of value.  The only abnormality detected was prolongation of the activated clotting time, corresponding to inhibition of enzymatic clotting.

Multiple patients have presented after traumatic injury to our institution, and they have universally had poor outcomes.

"Acutely Injured Patients on Dabigatran"
http://www.nejm.org/doi/full/10.1056/NEJMc1111095

Thursday, December 8, 2011

Journal Watch: Stroke

Mentioned in Journal Watch: Stroke -


...regarding my recently published article regarding pharmaceutical ties to thrombolysis literature.

No idea what the review says - since I don't subscribe to the service!

Wednesday, December 7, 2011

No More Excuses For Not Giving TPA

Rather than restrict TPA for acute ischemic stroke to the small cohort of patients identified by strict exclusion criteria in the few completed randomized trials, the current crusade is to continue to try and give it to more patients on the fringes of eligibility.

This article promotes giving TPA to patients with "minor or rapidly improving" strokes, because the lead author (sponsored by Genentech) sees this classification of patients is responsible for 50% of the documented reasons why patients were excluded from receiving TPA.  In fact, if patients with mild and improving strokes received TPA, it would immediately double the rate of TPA use - and provide potentially excellent outcomes at 90 days for the manufacturers.

They base their assertions on a retrospective, uncontrolled evaluation of the discharge disposition of patients in this "minor or rapidly improving" cohort - and observe that only 72% of patients in this group were discharged home.  In their mind, patients could do much better (as measured by disposition location) if they had received TPA - and their final conclusion is that this exclusion criteria should be further studied so that it may be revoked.

But, their conclusions are a preposterous farce conjured out of fictionalization of the data.  Considering the median age of their cohort was 72, 30% of whom had prior stroke/TIAs, 26% were diabetic, 76% were hypertensive, etc. - the sheer fact that only 28% went to rehab/SNF/died is probably rather good performance.  The authors also admit they had no information regarding the initial residence of this mostly elderly cohort and have no idea if the patients discharged to nursing facilities originally resided there.  Finally, the article additionally states "outcomes for patients with mild/rapidly improving stroke were better than for rtPA-treated patients with mild stroke (NIHSS score of 0 to 5) but worse for patients with a final diagnosis of TIA."

Yes, they compared this mild stroke cohort data to the mild stroke cohort data that received TPA, and all outcomes - adjusted and unadjusted for NIHSS - significantly favored the non-TPA cohort.

....so the obvious conclusion is to find a way to give more of them TPA.

Lunacy.  Another example of bad literature undermining trust in a probably efficacious treatment.

"Outcomes in Mild or Rapidly Improving Stroke Not Treated With Intravenous Recombinant Tissue-Type Plasminogen Activator"
www.ncbi.nlm.nih.gov/pubmed/21903949

Tuesday, December 6, 2011

It's Another Chest Pain Prediction Rule!

Yet again, the insanity of the race to a zero-miss culture funds another chest pain discharge prediction rule.  In fact, the most telling part of this paper is in the very end when they compare the chest pain admission rates of the Canadian hospitals in this article to the U.S. hospital - 18% and 20% in Canada compared to 96% in the U.S. (combined ED observation status and inpatient).  The difference in those numbers is insane - and I'm sure people could easily debate which is the preferred side of those numbers to be on.

In any event, the study is a prospective, observational data-gathering study of 64 variables related to the presentation of chest pain - some of which are objective and some of which are historical.  It's an interesting read - in part because the inter-observer kappa for a lot of the historical variables is so terrible they weren't even usable.  After collecting all their data, they did 30-day telephone follow-up or vital records review to evaluate the combined endpoint of death, myocardial infarction, or revascularization.

Via the magic of recursive partitioning, a patient without new EKG changes, a negative initial troponin, no history of CAD, atypical pain, and age less than 40 years separated out 7.1% of their study population that had zero 30-day outcomes.  Adding a second negative troponin six hours later for the 41-50 year group gives another 11.2% of patients that had zero outcomes.  So, a facility that admits 96% of their patients could potentially reduce admissions - but it might have less utility in Canada.

I'd rather see a two-hour second troponin than a six-hour one; it might reduce sensitivity, but it's wholly impractical to tie up a bed in the ED for 6 hours for a patient you want to send home.  And, like most of these articles, the combined endpoint of death, MI, and revascularization is irritating.  Considering there were twice as many revascularizations as myocardial infarctions, there really ought to be more granularity in these sorts of studies with regard to the actual coronary lesions identified rather than simply lumping them into a combined endpoint.

"Development of a Clinical Prediction Rule for 30-Day Cardiac Events in Emergency Department Patients With Chest Pain and Possible Acute Coronary Syndrome"
www.ncbi.nlm.nih.gov/pubmed/21885156

Sunday, December 4, 2011

Mistakes In Cardiac Arrest Cause Bad Outcomes

Not surprising, of course, but an interesting analysis of a large data set.

The authors pulled 108,636 in-hospital cardiac arrest cases out of the National Registry of Cardiopulmonary Resuscitation and evaluated them for "errors" - such as multiple intubation attempts, incorrect medication administration, delays in code team activation, etc.  After attempting to control for all the differences (of which there were many) in level of care and type of patient suffering cardiac arrest, they finally find that any documented error in resuscitation led to a 9.9% increase in adjusted hazard ratio for death in non-VF/pVT, and a 34.2% increase in VF/pVT patients.

Specifically, when they break out the different types of errors, essentially all the effect size was related to delays in medication administration for non-VF/pVT, and delays in medication and failure to defibrillate in VF/pVT.

"Impact of resuscitation system errors on survival from in-hospital cardiac arrest"
www.ncbi.nlm.nih.gov/pubmed/21963583