Sunday, July 22, 2012

A Child with Blunt Trauma

A 6 yo girl had significant trauma from  an MVC, with head injury (initial GCS 10, but no intracranial bleeding) and mild orthopedic injuries.  She was intubated.  A FAST exam was normal (no pericardial or peritoneal fluid).  As part of her workup, this ECG was recorded:

What do you think?

Interpretation:  There is sinus tachycardia, with right bundle branch block (RBBB).  This would be an unusual baseline finding in a child, and therefore myocardial contusion should be highly suspected.  There appears to be lead misplacement, V2 to V3, as the R' wave disappears in V2, then reappears in V3.  V1 and V2 (labelled V3) have the typical downsloping ST depression of RBBB, with a typical negative T-wave.  However, V3 (labelled V2) has ST segment elevation, which is not normal for RBBB.  Notice lead aVL also has ST elevation.  Normal RBBB has no ST elevation in any lead, though sometimes there is an exception when there is abscnce of R'-wave, as in V2 here.

Course: A CT of the head, neck, chest, abdomen and pelvis showed no other unanticipated injuries and she was admitted to the ICU.

Blunt cardiac injury my result in:
1) Acute myocardial rupture with tamponade
2) Valve rupture (tricuspid, aortic, mitral)
3) Coronary thrombosis or dissection (and thus Acute MI) from direct coronary blunt injury
4) Dysrhythmias of all kinds.
5) Myocardial contusion (edema and hemorrhage in the myocardium) which may result in dysrhythmias, blocks (especially RBBB as here), and poor cardiac contractility, including wall motion abnormalities.  Localized bleeding from contusion could cause hemopericardium even without rupture.

The literature on myocardial contusion is confusing, as, unless there are hemodynamic or dysrhythmic events at presentation, it is difficult to predict who will have complications except for those who have echocardiographic abnormalities.  There is no reference standard for diagnosis in patients without such echocardiographic abnormalities, and there are no definite clinical findings (with the probable exception of ST elevation or depression on the ECG) which consistently predict adverse events in succeeding hours or days.  Patients may have positive biomarkers (troponin) from the related stress of multisystem trauma, and low levels of troponin probably do not predict adverse events any better than the patients clinical condition.  Hemodynamic instability in trauma is usually due to bleeding, but if ultrasound shows poor contractility, then this may be due to cardiac contusion.   More commonly, however, ECG and/or echo wall motion abnormalities are due to pre-existing disease, especially coronary disease complicating trauma.

The finding of RBBB on this ECG is highly suggestive, if not diagnostic, of myocardial contusion.  The much more subtle finding of the ST elevation, not noticed by any physician caring for her, is further suggestive of significant contusion.  There is some old literature which I read in the 1980's (but cannot find now), that suggested that ST abnormalities due to myocardial contusion have the highest risk of any ECG finding for adverse outcomes and a higher risk than positive cardiac biomarkers (at that time, the biomarker was CK or CK-MB).  

Inpatient stay: She quickly awoke and was observed for a couple days, treated for minor orthopedic injuries, and recovered well from the head injury.  No further ECG, troponin, or echocardiogram was done because she was asymptomatic, and had a normal rhythm and rate.  She was discharged to home feeling just fine.


Three weeks later, shortly after having been physically active (bouncing on a trampoline), she was found unresponsive.  She was pulseless, with a narrow complex tachycardia on the monitor.  In the ED, ultrasound showed hemopericardium with tamponade.  An ED thoracotomy was done and the pericardium drained and internal compressions continued.  A cardiothoracic surgeon was called and together they found a 2 mm hole in the LV high in the circumflex distribution (corresponds to the STE in aVL) with a large amount of surrounding thinned, necrotic muscle.  This was too macerated to be repaired and she could not be resuscitated.

Needless to say, all involved were emotionally devastated.

Could the myocardial damage have been diagnosed by echo?  If it had been, could this outcome have been anticipated?  I am aware of no similar case reports in the literature (of delayed myocardial rupture after cardiac contusion), but I have not done an exhaustive review.  If a wall motion abnormality had been found, what could have been done to prevent the rupture?  If anticipated, would a prescription of bedrest have prevented it?  Was there traumatic circumflex artery occlusion that contributed?  Could an angiogram have found this?  And, then, so what?  Could subsequent myocardial rupture have been predicted or suspected?   

Before this case, I doubt any such outcome could have been anticipated, even though myocardial contusion (due to RBBB and STE) is evident.

After this case, were I to see a similar one, I would:

1) do a formal echocardiogram on anyone with new significant ECG abnormalities.
2) consider an angiogram if there is ST elevation (as here) and a wall motion abnormality
3) measure troponins, as a very high peak troponin would confirm large territory of contusion
3) limit physical activity if there is concern for a large area of contusion.

I do think this ECG gave a solid clue to the pathology.  ST elevation is an alarming finding of myocardial contusion. ST elevation is difficult to notice in the context of RBBB and one must specifically look for it to notice it.  In this case, it appears that the over-reading cardiologist also did not see it.

Finally, this may just be an incredibly rare event that none of us will ever see again. 


  1. I'm hoping that it is a rare entity, whatever occurred.

    I have a virtual pile of papers on the topic from a review I did during residency. Perhaps the reference you were looking for was:
    "Suspected myocardial contusion. Triage and indications for monitoring." (

    "Conduction abnormalities on admission electrocardiogram predicted serious arrhythmias. Echocardiography and creatine phosphokinase isoenzyme levels, although frequently positive, did not predict morbidity."

    1. Thanks for the great reference. Unfortunately, it does not specifically comment on ST elevation (or depression) or echocardiographic wall motion abnormalities. Does your pile contain any papers on these?

      Thanks, Steve Smith

  2. I believe this is the article you were referencing:

    The electrocardiographic and clinical diagnosis of myocardial contusion

    Intensive Care Medicine
    Volume 4, Number 2 (1978), 99-102, DOI: 10.1007/BF01684393

    R. D. Cane and N. Buchanan

    My college's library article database only goes back to 1980 for this journal. I found a preview of the article, the link is listed below.

    1. Thanks, David. It may be one of them, anyway.

  3. THANK YOU Steve for this excellent, soul-searching post with the tragic outcome you report in this unfortunate 6yo girl. Credit to you for extracting the teaching points, with suggestion of how a future approach might be improved. I don't know that anything could have prevented the ultimate tragic outcome. That said - I do agree that this ECG is not normal - and support your emphasis that complete RBBB is not an expected usual "normal baseline" in a 6yo child suffering significant trauma from MVC.

    I'd ADD one suggestion to the 4 you listed re potential future approach:
    5) Repeat the ECG (more than once) to see if baseline abnormalities resolve or evolve.

    Hindsight is admittedly 100% in the "retrospectoscope" - but to me - there are a few additional abnormalities I see on this initial (and only) ECG:
    i) Not only is the ST segment elevated in lead aVL - but it is coved, and there is a hint of T wave inversion. There is also a Q wave (though I'm not sure what that means in this lead ...).
    ii) There appears to also be ST elevation in lead I (the J point is clearly elevated in lead I).
    iii) I think there is reciprocal ST depression in lead III and probably also in aVF. This is challenging to assess, given the unusual terminal shape of the QRS complex in these leads - but I think the ST depression is real.
    iv) The angled step-off between the end of the S wave and beginning of the ST segment in leads V4 and V5 (and possibly V6) may also reflect ST depression ....
    v) I agree that lead V2 looks to be mislabeled. It makes no sense appearing between V1 and V3 as it does here. IF this lead is in fact mislabeled - then perhaps IF leads had been correctly mounted there would have been precordial ST elevation in MORE than just a single precordial lead ...

    As stated - I make the above observations AFTER learning the outcome you describe. I'm not sure I would have called all of this had I been "on the scene" - but like you, I would be concerned that this RBBB tracing is not "the usual" for a 6yo trauma patient. Some ECG abnormalities may have been increased by the tachycardia. In any event - a few REPEAT ECGs would clearly have been helpful.

    Thank you again for your soul-searching and insightful review of the highly challenging entity of myocardial contusion.


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