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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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Thank you to our speakers today — Dr. Richardson on research methods, Dr. Weingart on hypothermia, Bing with his journal club presentation (highlighted here), Abiola with trauma talk on the utility of repeat head CTs for recognizing intracranial hemorrhage, and Suzi for her M+M presentation on burn management.

Bing’s journal club presentation and discussion is summarized here — please feel free to add comments.

As for points from Abiola’s and Suzi’s talks, please see below:

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Thanks to Bing, Dr. Okuda and Dr. Strother for a wonderful day of sim cases this week. Special thanks to all who had to tolerate my acting.

A few questions came up during the discussions, and, I’ve been trying to research with limited success.

The first question concerned antibiotics for heat illness. Certainly in ambiguous cases, where there is altered mental status with moderately high temperature, antibiotic coverage is mandated. But in our case, of the athlete on a hot day? It was asserted that the heat stress leads to gut flora dissemination, and antibiotics are warranted. But I could find no reference for this, and my usual sources are silent on the issue of prophylactic antibiotics.

The second question revolved around safety factors for emergent sedation. Specifically, I wondered if the risk of aspiration in emergent procedural sedation had been quantified in adults. It turns out there’s a lot of opinion on this matter, but not a lot of data. More below:

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So, lots of big things were discussed today, but I’m going to focus on Dr. Judd Hollander’s talk, as it was crammed with insight on a very common problem – achieving disposition on the 8 million patients we seen annually with chest pain (this is national, not just Sinai). Of these 8 million, 3 million are sent home and so we admit 60-65% of chest pain, of which only 15% have real disease… Cardiologists hate us for this, but is there an alternative? What’s the evidence behind what we do?

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Hello everyone,

Thank you to those of you who passed up Ponte Vedra or new jobs to come to conference this week. Many thanks to our resident speakers, Matt, Shefali and Bing, and to our faculty presenters — Dr. Spina and Dr. Nassisi. Also thanks to the neurology department for their participation in our joint conference.

Below are some topics from conference that for which I found more resources, or that I just thought warranted repeating.  Feel free to add your own thoughts in the comments section.

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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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This month in Journal Club, we continued our theme of prognostication papers as Corey reviewed two recent ones from Latha G. Stead’s group at Mayo.  One paper ran last year and is called “Initial Emergency Department Blood Pressure as Predictor of Survival After Acute Ischemic Stroke” (Neurology 2005, 65:1179:1183). The second paper is called “Impact of Acute Blood Pressure Variability on Ischemic Stroke Outcome” (Neurology 2006:66:1878-1881).

This is something I frankly hadn’t spent much time thinking about — all the emphasis in stroke guidelines and tPA admin has been about getting BP down into a safe range, not worrying about whose BP is too low. But the big result from the first paper was that a diastolic of < 70 mmHg, a systolic less than 155, or an MAP of less than 100 mmHg was associated with higher mortality at 90 days than those with higher BPs (even after adjusting for age, gender, NIHSS score, etc). The worst relative risk (RR) was for a diastolic less than 70; RR = 2.2 in that case, which the authors find is actually worse than the RR of having a diastolic over 105 (RR=1.9… How about that).   

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I gave a talk last week on the workup of nonsevere sepsis that referenced a bunch of little papers, and a few big ones… We’ll leave the discussion of the landmark 2001 EGDT severe-sepsis talk for another time (sigh). Right now I just wanted to go over an Annals paper (AEM Vol 45, No 5, May ‘05) by Shapiro et al from Beth-Israel Deaconess, about lactate in the ED. They were looking at the value of ED serum lactate levels as a predictor of later mortality – echoing studies on ICU lactate and mortality for patients with septic shock, burns, or trauma.

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Annals was mostly about airway this month, and felt a little sparse (Levitan showed that BURP and cricoid pressure worsen the view compared to bimanual laryngoscopy– stop the presses! Also, a letter to the editor advocated for the mnemonic LEMONS over LEMON — the extra S is for O2 saturation, which of course you might otherwise fail to consider as you're prepping to intubate… sheesh).

So, instead, I thought I'd hit up that other noteworthy periodical, the New England Journal of Medicine. This week (June 1, 2006, Vol 354, No. 22) they've got an article (pdf) from the PIOPED II study about the diagnostic value of CT angio alone, vs. CT angio plus CT venography of leg veins.

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