Comments for Emergency medicine podcasts, reviews and curbside consults Tue, 10 Feb 2015 05:17:40 +0000 hourly 1 Comment on Superficial Thrombophlebitis and other clotting quagmires by Rob Orman Tue, 10 Feb 2015 05:17:40 +0000 This is controversial, but I’ll give you my take on the matter…
Distal clots are not benign. They can cause PE, progress to proximal clots, and recur. Anticoagulating distal DVTs decreases the incidence of all of these. This risk of bad outcome is not as high as it is with proximal clot, but it is still a reality for the patient. I pursue any suspected calf clots and treat for 6 weeks if positive.

Comment on Superficial Thrombophlebitis and other clotting quagmires by drescudero Tue, 10 Feb 2015 05:04:22 +0000 When should we be looking for calf vein clots? My ultrasound techs will not routinely look below the knee unless requested. Should I be pushing for this routinely?

Comment on Superficial Thrombophlebitis and other clotting quagmires by emergencypdx Sun, 01 Feb 2015 01:47:57 +0000 Hi Caroline. Sorry for the delay in reply. Here is the answer from Tom Deloughery…

I based this on three trials. The STTESG trial looked at several doses of LMWH and prophylactic 8-12 was just as good as full dose (1). Then there was a trial of high vs low dose LMWH (2) that again show low dose just as good. They looked at this for a month of therapy. Finally the French looked at prophylactic dose fondaparinux and found benefit when given for 45 days. (3)

So that is why I recommend prophylactic dosing. Based on the STTESG trial I start with 14 days of drug – if you look at the curves of the fondaparinux trial most of the benefit was seen in the first 10 days. So my approach is 40mg of enoxaparin for 14 days – if still symptomatic another 14 days of drug

1. Arch Intern Med. 2003 Jul 28;163(14):1657-63. A pilot randomized double-blind comparison of a low-molecular-weight heparin, a nonsteroidal anti-inflammatory agent, and placebo in the treatment of superficial vein thrombosis. Superficial Thrombophlebitis Treated By Enoxaparin Study Group.
2. J Thromb Haemost. 2005 Jun;3(6):1152-7. High vs. low doses of low-molecular-weight heparin for the treatment of superficial vein thrombosis of the legs: a double-blind, randomized trial. Prandoni P1, Tormene D, Pesavento R; Vesalio Investigators Group.
3. N Engl J Med. 2010 Sep 23;363(13):1222-32. doi: 10.1056/NEJMoa0912072.Fondaparinux for the treatment of superficial-vein thrombosis in the legs.Decousus H1, Prandoni P, Mismetti P, Bauersachs RM, Boda Z, Brenner B, Laporte S, Matyas L, Middeldorp S, Sokurenko G, Leizorovicz A; CALISTO Study Group.

Comment on Is Coronary CT worth it? by Stephen Smith Wed, 07 Jan 2015 15:55:24 +0000 First, remember doing CTCA in the ED applies to chest pain patients at low or moderate risk of ACS, not to patients with known CAD, or known coronary anatomy, and not to patients who have a positive ECG or rule in for MI.

Nuclear Testing (Sestamibi) is slightly more sensitive than stress echo; neither is terribly sensitive, and neither is good for diagnosing thrombus or stenosis that is not hemodynamically significant. A plaque can rupture, result in thrombus, cause pain, then partly lyse and leave an asymptomatic thrombus until it is symptomatic again, and it won’t result in a positive stress test. I and 2 others (Nerenberg, Engineer) have shown that of patients who return to the ED with chest pain within 3 years of a negative stress imaging test, 5-7% have MI. Most are within the first year and many were within the first week after the test. If a CTCA is normal, there is no MI or increased CAD for at least two years (Chang AJEM). Furthermore, repeat future visits to the ED for CP result in fewer admissions because for most patients you know there is no CAD.

The two randomized NEJM studies (Hollander, ROMICAT II) on CTCA in the ED vs. standard management showed much shorter ED stay but more downstream procedures in the CTCA group. Whether the downstream procedures were ultimately beneficial or not is unknown, but one year mortality was the same in both groups.

In an older study of calcium score (Arad Y et al. JACC 46(1):166-72; July 5, 2005), there was benefit to aggressive risk factor treatment for those with a score > 400. I am unaware of any similar randomized trials of patients with CT coronary angiogram (with contrast). Those who had CAD in the two ED studies got more invasive therapy.

ACS without a positive troponin (unstable angina) does still exist and can be very dangerous. Here are 9 death and near death cases (link would not show in this window, but search “unstable angina” in my blog), all with serial negative contemporary troponins; there are many others I never posted and there are no doubt many others I am not aware of. Here are three cases:
two: (transient ST elevation, serial negative troponins, almost sent home. Cath showed 80% thrombotic occlusion.)

And here is one I posted right after Eugene Braunwald asked if it is “time for a requiem” for unstable angina:

Such cases do not substitute for a randomized trial of diagnostic and therapeutic management. All of these cases that I posted could have been found with correct ECG interpretation. That’s the reason that I know of them. There are many others I knew about but did not post. For cases with nondiagnostic ECGs, it is much more difficult.

There is no proof that if you do stress or CTCA imaging on all of these patients that they would be diagnosed by CTCA or by stress testing. Furthermore, it may be that the complications of testing so many negatives, including the resulting false positives, may result in worse outcomes of the entire cohort than there would be with no testing.

No one has ever randomized patients who rule out for MI to no testing vs. selective testing. No one dares.

And that is because of the worry for Unstable Angina. Unstable angina definitely still exists.

Only when we get high sensitivity troponins might we be able to accurately state that unstable angina is largely a think of the past. Studies show that in a significant number of unstable angina cases (contemporary trops negative), high sensitivity troponins have a rise and fall.

If it is ACS, and contemporary trops are negative, and there are no high risk lesions, then medical therapy (aspirin and statin at a minimum) works well (see ICTUS trial below). No intervention is necessary. But how do you find out if there are high risk lesions without further testing? (As my blog posts show, one way is good ECG interpretation during the initial presentation, but that will not solve the whole problem.)

The problem with the excess downstream procedures after CTCA is that many think that any stenosis needs to be stented. In the case of negative trops and non-critical anatomy, that is not true. Even in patients who rule in by positive troponins, a mandatory invasive strategy is not necessarily better: See the ICTUS trial here: In cases that rule out, it is likely that, in the absence of high risk lesions, such medical therapy is as good or better.

Very tight stenoses do predict future death from MI, and certainly non flow obstructing thrombus is dangerous. CTCA can find these high risk lesions. But what differentiates it from stress testing is that it can find other CAD which can guide medical management.

What we need is a large randomized trial of ED CP patients, of CTCA vs. standard management, in which only high risk lesions on CTCA get intervention, and low risk ones get medical therapy.

Until that is done, we don’t know for certain what to do.

Until then, if you work at a place which uses an appropriately selective strategy to downstream testing, I believe that CTCA is the best way to:

1) rule out significant ACS,
2) prevent admission and excessive testing for future ED CP visits
2) diagnose CAD and start patients on medical therapy, and
3) find the critical ACS/CAD that needs hospital admission.

To summarize:
1. More information
2. Faster
3. Less expensive
4. Less radiation than nuclear testing

Finally, there are those who argue against tests that provide too much information. It may lead to unnecessary testing. To me, that is not a valid argument. The proper response is to learn what to do with the information, not to avoid knowing it. Only if a test which provides more information is more expensive or dangerous, which CTCA is not, should it be avoided.

Comment on Pulmonary Nodule: The incidentaloma by Walid outhman Sun, 07 Dec 2014 21:13:06 +0000 wish you the best and i pray for you .i always had a pain in my right side and the stupid docts disnt know what is it and thought it was a cold . today i went for a doctor and he asked me to make a CT test and he told me i have a nudle sized 5mm .. i am 36 yo and i am really scared too. i will quit smoking tomorrow after i finish the last box i have lol. he asked me to make another CT after three months to see the size.

Comment on PEA made simple by Rob Orman Sun, 07 Dec 2014 19:28:56 +0000 I am with you on this. Twelve lead EKG is a luxury and a rarity in a pulseless patient. I initially use the rhythm strip, follow the algorithm, and get a 12 lead as soon as possible.

Comment on Anticoagulation Reversal by Episode 20 – Anticoagulation | FOAMcast Sun, 07 Dec 2014 13:25:51 +0000 […] ER Cast […]

Comment on So, you want to be an ER doc… by Five Tips to Avoid Emergency Medicine Burnout | The Skeptics Guide to Emergency Medicine Wed, 03 Dec 2014 14:19:35 +0000 […] Check out this other video on the topic submitted from the #FOAMed world. Rob Orman also had a excellent post recently on ER Cast called So You Want to Be an ER Doc. […]

Comment on Pulmonary Nodule: The incidentaloma by Becky Seely Tue, 02 Dec 2014 20:24:39 +0000 Jeff,,,Were your nodules calcified or non calcified? I am going for a more advanced CT scan on Thursday..I have one nodule that grew from 1.1 cm to 1.4 cm in 3 months..I am scared to death.

Comment on PEA made simple by donald zweig Tue, 02 Dec 2014 04:07:32 +0000 so how do you actually do this pea evaluation algorithm. i guess you don’t do a 12 lead but just the rhythm strip? then if there is no pulse you hold cpr long enough to get the views? that seems like a long wait.