Wednesday, February 7, 2018

ST Elevation after Stab Wound to the Heart

A young man presented after a stab wound to the chest.  Rapid ED diagnosis of cardiac penetrating trauma was made by ED ultrasound, and the patient went to the OR and had a wound to the right atrium repaired.  There was no laceration of any coronary vessel.  He did well.  Because of tachycardia, this ECG was recorded at day 3:

There is sinus tach with diffuse ST elevation, and a bit of ST depression in lead III.  There is PR depression, especially in leads II and V5.  QTc is 383 ms.
This diffuse ST elevation is clearly due to pericarditis, especially given the clinical scenario.  It is slightly unusual, though: The ST vector is directly lateral (highest STE in lead I, with some reciprocal ST depression in lead III).  

[It is unusual to have any ST depression in percarditis, and, if the scenario is one of possible ACS, it would not be wise to assume that diffuse ST elevation is pericarditis without first considering high lateral MI.]

Other ECG factors also support pericarditis: short QTc, significant PR depression, and especially the high ST elevation to T-wave amplitude ratio (in other words, the T-waves are relatively flat, thus non-ischemic).  There is no Spodick's sign (downsloping TP segment).

2 weeks later, his ECG had evolved:
There is resolution of ST elevation, except in V1-V3, and there is now T-wave inversion in V1-V3.

This looks a lot like a common normal variant, and it may actually be, even if it is not seen on the 4 month ECG below.

4 months after the stab wound, it was all resolved:

2 months later (6 months after the stab wound), he again presented with pain typical of pericarditis:
This is more typical: inferolateral ST elevation (ST vector towards lead II), with no reciprocal ST depression.  PR depression is again present.

He was treated with colchicine and NSAIDs, and discharged.

1 comment:

  1. Great case study with insightful serial tracings on this patient with recurrent pericarditis. I’d add the following points. Point i) A good history goes a LONG WAY toward making the diagnosis of acute pericarditis. As emphasized often by Dr. Smith in his blog posts — there is a tendency to overdiagnose acute pericarditis. In many of the “overdiagnosed” cases that I have observed over the years, a history truly suggestive of acute pericarditis is wanting — and the misdiagnosis is made solely on the basis of ST elevation on ECG. Cardiac trauma in this case clearly sets the scene for a pericarditis diagnosis. Point ii) Typical acute pericarditis produces ST elevation in virtually all leads except what I call the “right-sided” leads ( = leads III, aVR and V1). A favorite “pearl” of mine is that the appearance of the ST-T wave in lead II tends to look more like that in lead I with acute pericarditis (as it does here) — whereas with acute MI, lead II tends to look more like lead III. Point iii) In theory — ST segments in Stage II acute pericarditis (ie, the Stage after diffuse ST elevation) — tend to return to the baseline, after which in Stage III there is generalized T wave inversion. So the 2nd ECG here is a bit atypical, in that the coved ST segments in leads V1,V2 are still elevated at the SAME time that there is now frank T wave inversion. Point iv) The last ECG (done 2 months after the stab wound) shows subtle ST elevation that BY ITSELF would not be diagnostic of acute pericarditis! It is really because of the HISTORY plus the serial evolution we see in the 3 prior tracings that we can definitively say there is new and fairly diffuse more-subtle-but-definitely-present ST elevation that in this context clearly tells us this patient is having a recurrence. THANKS for presenting this insightful case!


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