Comments for ercast.org http://blog.ercast.org Emergency medicine podcasts, reviews and curbside consults Fri, 13 Mar 2015 02:23:51 +0000 hourly 1 http://wordpress.org/?v=4.1.1 Comment on No CPR in Trauma Arrest? by SAM GHALI (@EM_ResUS)http://blog.ercast.org/no-cpr-trauma-arrest/#comment-953 Fri, 13 Mar 2015 02:23:51 +0000 http://blog.ercast.org/?p=4877#comment-953 Hi Rob,

Great cast with Swami on a fantastic topic!

I think one of the main issues here revolves around the following question: What the hell defines a “traumatic arrest” in the first place? I don’t think it’s very well-realized, but in most of these circumstances where the decision has been made to aggressively push forward with resuscitation of a “traumatic arrest”, we are in essence talking about “PEA”. Asystole is the common final pathway, and V-Tac/V-Fib happens, (especially in the “medical traumas” as you guys discussed) *but by and large these patients have what could/should be a perfusing rhythm, yet .. wait for it… someone can’t quite feel a pulse. This is a subset of “PEA”. The “Traumatic PEA” if you will (only with a much more narrow differential- generally, HOTT) Are we really going to continue to call these “arrests” just as we damagingly do in medical “PEA”?

In my opinion, the term “PEA Arrest” is one of the most illogical and dangerous terms in all of medicine.

I had a recent case at Resus General: Young lady brought in from scene s/p GSW to epigastrum. She was in shock with a pulse of 135; Non-invasive BP of 70/40. Tube placement confirmed via great End-Tidal Waveform, and b/l breath sounds. There was excellent sliding bilaterally (no pneumos), and no pleural fluid(no hemos). Cardiac view showed no effusion (no tamponade) & furthermore a hyperdynamic left ventricle. The heart was going CRAZY trying to pump out what little blood there was. While products were being hung, one of the team was feeling for a pulse and couldn’t quite feel one and announced this to the room. Another member of the team instinctively jumped on the chest and started closed chest CPR as if they’d done this drill time and time again before. I took over by stopping this right away. I was adamant. There was no way I was gonna allow this to happen. It turned out to be one of the greatest “ah,ha” teaching/learning moments for all. I put the probe back on the chest and showed them the walls of the left ventricle slamming together and pumping with the most vigor you’ll ever see a heart pumping-- I said “of course you don’t feel a pulse! This patient is in shock….hemorrhagic shock. She’s bleeding into her belly” I think at that moment, with my explaining as we watched the Echo, everyone in the room (*including the surgery team who completely bought into it as well) truly could see & grasp that the only potential effect chest compressions could have was to impair the filling of a heart that in no way needed help beating-- it needed products. It was like lightbulbs went on in everyone’s head. As products poured in her pulses quickly became much more palpable. A quick chest x-ray confirmed my ultrasound findings. Now she needed immediate hemorrhage control. She went straight up to OR for ex-lap w/ongoing resus and actually did great.

This is how the “traumatic arrest” should go down. If she had pneumo(s)/hemo(s) we would’ve entered the chest. Tamponade? Would’ve cracked the chest. For the reasons you guys discussed I don’t think we will ever see “quality evidence” for this, but not sure we need any to know that the last thing this lady needed was someone pumping on her chest & pumping her full of epinephrine just bc someone at some moment couldn’t quite feel a pulse.. She didn’t even need her chest cracked.

We will never see RCT’s on this. We must attain a better understanding of the pathophysiology taking place in the crashing patient in front of us, use logic & ultrasound to guide specific goal-oriented resuscitation, and realize the craziness & danger of using someone’s subjective finger sense to determine what the most (in)appropriate next course of action is.

Rob- sorry for rant. This is one topic in Emergency Medicine I am most passionate about. Hope you’re doing well my friend.

Sam

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Comment on PEA made simple by The Simplified Approach to PEA (non-traumatic) | First10EMhttp://blog.ercast.org/better-way-manage-pea/#comment-952 Thu, 12 Mar 2015 15:10:48 +0000 http://blog.ercast.org/?p=3614#comment-952 […] PEA made simple at ERCAST […]

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Comment on Amal Mattu on Low Risk Chest Pain by Steve Foy (@SteveFoyMD)http://blog.ercast.org/amal-mattu-low-risk-chest-pain/#comment-948 Tue, 10 Mar 2015 04:42:45 +0000 http://blog.ercast.org/?p=4709#comment-948 Which troponin assay are they using? The regular lab trop, the iStat troponin, or one of the new ultrasensitive assays?

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Comment on Amal Mattu on Low Risk Chest Pain by dchttp://blog.ercast.org/amal-mattu-low-risk-chest-pain/#comment-947 Mon, 09 Mar 2015 04:56:28 +0000 http://blog.ercast.org/?p=4709#comment-947 Curious whether in deriving the HEART score they found any difference regarding onset of chest pain and troponin results. all i could see from the articles were that they drew the troponins on admission to the ED. So are they implying that timing of CP does not matter for troponin interpretation?

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Comment on Superficial Thrombophlebitis and other clotting quagmires by Rob Ormanhttp://blog.ercast.org/superficial-thrombophlebitis-clotting-quagmires/#comment-930 Tue, 10 Feb 2015 05:17:40 +0000 http://blog.ercast.org/?p=2674#comment-930 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.

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Comment on Superficial Thrombophlebitis and other clotting quagmires by drescuderohttp://blog.ercast.org/superficial-thrombophlebitis-clotting-quagmires/#comment-929 Tue, 10 Feb 2015 05:04:22 +0000 http://blog.ercast.org/?p=2674#comment-929 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?

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Comment on Superficial Thrombophlebitis and other clotting quagmires by emergencypdxhttp://blog.ercast.org/superficial-thrombophlebitis-clotting-quagmires/#comment-920 Sun, 01 Feb 2015 01:47:57 +0000 http://blog.ercast.org/?p=2674#comment-920 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.

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Comment on Is Coronary CT worth it? by Stephen Smithhttp://blog.ercast.org/coronary-ct-worth/#comment-907 Wed, 07 Jan 2015 15:55:24 +0000 http://blog.ercast.org/?p=3660#comment-907 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:
one: http://hqmeded-ecg.blogspot.com/2014/12/it-is-far-too-early-for-requiem-for.html
two: http://hqmeded-ecg.blogspot.com/2014/12/transient-st-elevation-rules-out-for-mi.html (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: http://hqmeded-ecg.blogspot.com/2014/04/unstable-angina-dr-braunwald-asks-if-it.html.

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: http://www.nejm.org/doi/full/10.1056/NEJMoa044259. 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.

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Comment on Pulmonary Nodule: The incidentaloma by Walid outhmanhttp://blog.ercast.org/pulmonary-nodule-incidentaloma/#comment-901 Sun, 07 Dec 2014 21:13:06 +0000 http://blog.ercast.org/?p=2455#comment-901 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.

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Comment on PEA made simple by Rob Ormanhttp://blog.ercast.org/better-way-manage-pea/#comment-900 Sun, 07 Dec 2014 19:28:56 +0000 http://blog.ercast.org/?p=3614#comment-900 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.

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