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There’s a certain symmetry to starting the first journal club of the year studying d-dimer for dissection (last time around, we looked at the PERC rule and d-dimer for PE). This month, Bing examined a paper by Ohlmann and others, called “Diagnostic and prognostic value of circulating D-Dimers in patients with acute aortic dissection” (Crit Care Med. 2006 May;34(5):1358-64. PMID: 16557157). For background, we also read “D-dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study” (Eur Heart J. 2007 Dec;28(24):3067-75. PMID: 17986466) and got some perspective on D-dimer the with Klompas addition to the JAMA rational clinical exam series: “Does This Patient Have an Acute Thoracic Aortic Dissection?” (JAMA 2002;287(17):2262-2272. PMID: 11980527).

The clinical background was useful in delineating the scope of the problem: acute aortic dissection (AAD) is rare — in some rigorous European surveys, incidence is 3-4 / 100,000 and in EDs, 2-3 of 1000 chest pain patients have AAD (so if you see about 1000 chest pain patients in the course of your residency…). We miss it a lot — Klompas said 39% of patients have a delay in diagnosis of more than 24 hours, 10% of autopsies for show missed dissections, and we only suspect AAD properly less than half the time (as low as 15% of the time).

There are a few key features of dissection that should set off alarm bells for AAD — pulse deficits and blood pressure cuff differences > 20 mmHg (positive likelihood ratio 5.7), focal neuro deficits (LR+ 6-33), and a description of “tearing pain” (LR+ 10.8). But many other signs are sensitive but not that specific, or not even that sensitive (and ‘tearing pain’ is only reported 39% of the time, with focal neuro deficits found just 17% of the time). Chest Xrays have a LR+ of around 2, and are only 60-80% sensitive (though a completely normal CXR — normal width mediastinum and normal aortic knob, have a LR- 0f 0.3).

What’s really needed to diagnose AAD is not-so-standard imaging, like CT, TEE, or MRI (all 98% sensitive or greater, with specificies in the high 90’s as well). So there’s an opportunity for a lab test to step in and help us guide decisionmaking. And d-dimer, a substance released by fibrinolytic activity unleashed when the extrinsic pathway is activated in dissection, in theory could work well as a marker.

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Guest blogger Marisa has written up an expert review of our recent Journal Club discussion of clevidipine, as presented by Dr. Joshua Kosowsky of Brigham & Women’s Hospital:

Just last week, Clevidipine (Cleviprex) was approved by the FDA, making it the first new IV drug approved for high blood pressure in the past 10 years. Dr Joshua Kosowsky introduced us to Clevidipine when he discussed the VELOCITY (The evaluation of the effect of ultra-short-acting clevidipine in the treatment of patients with severe hypertension) trial as published in the June 2008 Annals of Emergency Medicine (PMID: 18534716), “Clevidipine, an Intravenous Dihydropyridine Calcium Channel Blocker, Is Safe and Effective for the Treatment of Patients With Acute Severe Hypertension” (residents: the PDF of this journal is online). More below:

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If you missed Sohan’s last lecture as a resident, the June 4th  Journal Club, well, here’s a brief recap. For those of you who were there for his tour-de-force, you’ll no doubt want to refer to these notes from his talk in your future practice.

Sohan discussed the original PERC rule derivation paper and its recent validation — the papers below are accessible using our password system:

Kline JA, et al. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2004; 2: 1247–55. (PMID: 15304025)

Kline JA, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 2008; 6: 772–80. (PMID: 18318689).

Sohan started with a lit review, going back to DeBakey’s 1954 discussion of 3 million PE’s, where it was first noted that PE is tough to diagnose and its prevalence is unclear. Even now, very little has changed. We don’t know the true incidence, we don’t know how many we miss, we don’t know which PE’s are clinically relevant, and we don’t know when to pursue this diagnosis. Even the Well’s criteria, which I mentioned here a couple of years ago, are not too clean — because they give more points to the physician’s judgment than to any other sign or lab result.

So we’ve been left with the unfortunate, all-to-common situation of considering D-dimers for every poor patient who presents with vague chest discomfort or dyspnea. If that dimer is positive, and it often is falsely so, we’re forced down a road of angiography , contrast, radiation, and other potential sources of morbidity.

Is there a way out of this? Is there a simple decision rule we can apply, at the bedside, using nothing but history and physical, to prevent this unnecessary testing?

Kline et al thought so — and the rule they proposed is discussed below.

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Thanks to all who stopped by our Innovations inEM Education booth at SAEM these past few days. Your input and encouragement were appreciated! The abstract is now online and an MS-Word version of our informational pamphlet is available for download.  

 For those of you who wanted to discuss things further, my email is Nicholas.Genes /at/ mssm.edu.

Other EM journal club websites with analyses of articles:

• Washington University (archives)
• University of Michigan (archives)
• Emory (archives)
• East Virginia Medical School

If you know of more, please share! The idea of putting EM Journal Clubs online, for prompt bedside access, goes back a few years…

At our last Journal Club, Tom presented a 2005 paper from JEM on new CT scanners in the evaluation of SAH. The paper was called Subarachnoid Hemorrhage Diagnosis By Computed Tomography and Lumbar Puncture: Are Fifth Generation CT Scanners Better at Identifying SAH? by Boesiger and Shiber, and it appears in Journal of Emergency Medicine (2005: Vol. 29, No. 1 pp23-27).

The article is motivated by the fact that 1% of headache patients in the ED have SAH. Most are traumatic, but those that aren’t are usually from Circle-of-Willis aneurysm ruptures, which often kill or disable otherwise healthy people. EM physicians hate that sort of unsettling risk, and the situation is further complicated by the 20-50% of SAHers who present with a sentinel bleed. So there’s a real opportunity to help some potentially moribund patients —  but if you ask most interns, they’ll say they’re shoving too many needles into the backs of people who probably just needed some exedrin.

Maybe we can change our practice, based on recent upgrades in CT scanner technology. These authors were the first to look at the new scanners with an eye toward sensitivity in SAH diagnosis. More below…

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Lynn was telling me about a case she saw this year – if I recall, it was a young man who developed uncontrollable hiccuping after an inguinal hernia repair. I don’t know what happened to the guy, but I saw my first hiccuping patient shortly thereafter. As I surf the web, I keep coming across remedies for this unusual but vexing complaint:

• Methylcellulose (to expand the stomach) 
• NG Tube (to decompress the stomach)
• An implantable vagal nerve stimulator
• Pressing on the ears while drinking through a straw
• Digital rectal massage (also reported in Annals of EM)
• Chlorpromazine 25-50mg IV (the only FDA-approved agent for intractable hiccups)

Our anesthesia colleagues have looked at this issue, as hiccuping in the OR is a pressing concern. Unfortunately, a systematic review (Kranke, Eur J Anaesthesiol 2003 Mar;20(3):239-44) turned up lots of anecdotes, but only one (inconclusive) RCT:

A large variety of interventions have been proposed for the treatment of hiccup during anaesthesia and sedation. However, perioperative treatment is still based on empirical findings and no treatment is ‘evidence-based’. Thus, no valid recommendations for the treatment of hiccup can be derived. Uncontrolled observations are inadequate to establish treatment efficacy.

More drug suggestions below, along with some background on hiccups…

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Jack tackled a controversial topic at this month’s Journal Club — what’s the evidence for giving antibiotics within four hours for CAP patients? It’s a good question, because how well we perform at this task is a big part of how our hospitals are measured. Ineed, pneumonia antibiotic timing is one of JCAHO’s Core Measures and there are only more such metrics down the road — so we’d like to think that our funding depends on rock-solid science and proven benefits.

Well…

As Jack noted, the 4-hr policy is based primarily on four papers,

1) Kahn et al, JAMA 1990 Oct 17 264(15) 1969-73 with comments 1995-6

2) McGarvey et al, Quality Review Bulletin April 13(4) 124-30

3) Meehan, Houck et al.  JAMA 1997 Dec 17 278(23) 2080-4 

4) Houck et al, Arch Intern Med. 2004; 164(6):637-644.

It’s this last paper we’re going to discuss — a retrospective study derived from a national sample of medicare patients with pneumonia.  

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When I was preparing an M+M last fall, I came across this notable study called Management of Acute Undifferentiated Agitation in the ED: A Randomized Double-Blind Trial of Droperidol, Ziprasidone, and Midazolam . It’s by Martel et al (including Michelle Biros, who’s editor of Academic Emergency Medicine), and appeared in Academic Emergency Medicine in December 2005 (Vol 12, No 12, pp1167 – coincidentally, right after Dr. Richardson’s EMPATH study).

It’s a good study that we might otherwise overlook, because it came out on the eve of the ACEP guidelines for agitation management and thus, wasn’t included in that extensive lit review.

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This week in journal club, Matt reviewed a nice little trial submitted by a group of Texans to the Canadian Journal of Emergency Medicine. They studied IV dexamethasone in preventing benign headache recurrence (Can J Emerg Med 2006;8(6):393-400, PDF) – something I had never tried, but apparently has been bouncing around the neurology and EM literature for 20 years.

It turns out that migraines may not be simply a vascular disorder, but rather an inflammatory disease. And, as Matt pointed out, it’s very difficult to diagnose migraines; it might be simpler for us ED folk to say headaches exist on a continuum between tension and migraine, and maybe ED patients with primary headache would benefit from a steroid.

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