Month: December 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

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”

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

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

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

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

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

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