Saturday, August 6, 2022

A man in his 40s with multitrauma from motor vehicle collision

Submitted and written by Andrew Yde MD, peer reviewed by Meyers, Grauer, Smith



A man in his 40s presented after motor vehicle collision in which he was the unrestrained driver in a vehicle moving at high speed. He was found by EMS to be obtunded at the scene of the accident, and was intubated in the field. On initial ED evaluation the patient was found to be hypotensive and tachycardic, with multiple obvious orthopedic injuries. He received emergent transfusion and bilateral chest tubes. FAST exam was indeterminate, but did not show a large amount of free fluid. He was deemed stable for CT scans.


CTs revealed the following injuries: left hemopneumothorax, right pneumothorax, pneumomediastinum, sternal fracture, right anterior rib fractures 2-6, left sided flail chest of ribs 2-9, L2 transverse process fracture, left clavicle fracture, grade 1-2 liver laceration, and a grade 1 splenic laceration. The patient was admitted to the surgical trauma ICU.


That night, he exhibited multiple episodes of ectopy, and what appeared to be NSVT. Electrolytes were found to be within normal limits, and the following EKG was obtained:


What do you think?

 




The patient had no prior EKGs in the system for comparison. The ECG shows sinus rhythm with a right bundle branch block (RBBB). The STD and T waves following the RBBB in V1-V3 are unusual in morphology and potentially excessively discordant compared to normal RBBB. Also, the lateral precordial leads are unusual in that they still have the R', instead of the slurred S wave we see in I and aVL, suggesting that the lateral chest leads are misplaced medially (probably because of the left chest tube in place).


Cardiac contusion was suspected. Remember: other important considerations for ECG changes in the setting of trauma include traumatic coronary dissection or laceration.


A troponin was ordered, along with a repeat EKG, seen below.

Mostly unchanged.

 


The high sensitivity troponin I (normal less than 20 ng/L) resulted at 20,973 ng/L, and cardiology was consulted. Cardiology recommended an echocardiogram and trending troponins, stating that cardiac contusion was their initial impression. 


The repeat troponin overnight into the following morning was＞25,000 ng/L (the lab does not report higher values).


By this time, a formal echocardiogram had been obtained, which revealed normal left ventricular ejection fraction (LVEF), with a severely hypokinetic right ventricle. These findings were interpreted as consistent with cardiac contusion. Cardiology continued to follow, but no cardiac catheterization was deemed necessary. Cardiology cleared the patient for rib plating.

After induction of anesthesia in the operating room, awaiting rib plating, the patient had a run of what was assumed to have been Non-Sustained Ventricular Tachycardia (NSVT), though this telemetry strip was not available for review. He then went into a bradydysrhythmia, and the procedure was aborted. On returning to the ICU, the ECG below was taken, revealing atrial fibrillation with a PVC.

Atrial fibrillation, narrower RBBB than before, one PVC. There appears to be STE and possibly hyperacute appearing T waves in some leads such as I, II, aVF, V6, compared to prior ECGs.




The troponin had begun to downtrend significantly, down to 2,243 ng/L. by hospital day 3. 

A repeat echocardiogram revealed no left ventricular wall motion abnormalities and normal EF, but reduced RVEF and akinesis of the RV free wall and mid ventricle to apex., with biatrial enlargement. The patient was placed on an amiodarone drip, and ultimately converted back to sinus rhythm. He remained hemodynamically stable.


More ECGs were obtained at days 6 and 9 below:





 

These ECGs show progressive resolution of the RBBB and significant improvement in prior concerning ST changes. 

The remainder of the patient’s hospital course was characterized by many complications. He was finally discharged to rehab after about a month in the hospital.


See our other cases of myocardial contusion and related cases (some of which have an important diagnosis OTHER THAN myocardial contusion!):

A Child with Blunt Trauma -- See how the ECG can be definite for myocardial contusion, but subtle, and what happens if you miss it.   















Discussion

This is a case where clinical context is of vital importance, because the EKG manifestations of cardiac contusion are fairly unpredictable. Intramyocardial hemorrhage, edema, and necrosis of myocardial muscle cells are characteristics of cardiac contusion. All of these cause troponin elevation, making troponin a very specific marker for cardiac injury. It is suggested that a troponin that is within normal reference range at about 4-6 hours from the inciting event suggests strongly the absence of cardiac injury in blunt chest trauma (Sybrandy).

The EKG is not generally sensitive for cardiac contusion. The right ventricle comprises the majority of the anterior heart which is most susceptible to direct injury in blunt chest trauma. Cardiac contusion can manifest on the ECG in a number of ways, including: ST segment elevation or depression, prolonged QT, new Q waves, conduction disorders such as RBBB, fascicular block, atrioventricular (AV) nodal conduction disorders (1,2, and 3 degree AV block), and arrhythmias such as sinus tachycardia, atrial and ventricular extrasystoles, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, sinus bradycardia, and atrial tachycardia (Sybrandy). RBBB in blunt chest trauma seems to be indicative of several RV injury. Atrial fibrillation is also a predictor of worse outcomes in this case (Alborzi).

See these publications for more information

Overall, management for cardiac contusion is mostly supportive unless surgical complications develop, involving appropriate treatment of dysrhythmias and hemodynamic instability. Ultimately, a normal ECG and normal troponin at 4-6 hours from initial traumatic incident is highly predictive of a lack of future cardiac complications in blunt chest trauma. Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization. Troponins and EKGs should be trended until normalization (Sybrandy).  

Delayed cardiac rupture is a potential consequence, especially if there is any ST Elevation.  See this case, this case, and this case.  In patient's at risk, physical activity should be limited for several months after the injury.




References

Alborzi, Z., Zangouri, V., Paydar, S., Ghahramani, Z., Shafa, M., Ziaeian, B., Radpey, M. R., Amirian, A., & Khodaei, S. (2016, April 13). Diagnosing myocardial contusion after blunt chest trauma. The journal of Tehran Heart Center. Retrieved July 2, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027160/

Moyé, D. M., Danielle M. Moyé From the Division of Cardiology, Dyer, A. K., Adrian K. Dyer From the Division of Cardiology, Thankavel, P. P., Poonam P. Thankavel From the Division of Cardiology, & The Data Supplement is available at http://circimaging.ahajournals.org/lookup/suppl/doi:10.1161/CIRCIMAGING.114.002857/-/DC1.Correspondence to Poonam Punjwani Thankavel. (2015, March 1). Myocardial contusion in an 8-year-old boy. Circulation: Cardiovascular Imaging. Retrieved July 2, 2022, from https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.114.002857

Sybrandy, K. C., Cramer, M. J. M., & Burgersdijk, C. (2003, May). Diagnosing cardiac contusion: Old Wisdom and new insights. Heart (British Cardiac Society). Retrieved July 2, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1767619/ 






===================================
MY Comment by KEN GRAUER, MD (8/6/2022):
===================================
Excellent review by Drs. Yde and Meyers — regarding multi-trauma with resultant Cardiac Contusion! I focus my comment on a number of additional specific aspects of the serial ECGs obtained in today's case.

As per Drs. Yde and Meyers — the ECG is less than optimally sensitive for detecting cardiac injury following blunt trauma. This is because the anterior anatomic position of the RV (Right Ventricle), and its immediate proximity to the sternum — makes the RV much more susceptible to blunt trauma injury than the LV. But because of the much greater electrical mass of the LV — electrical activity (and therefore ECG abnormalities) from the much smaller and thinner RV are more difficult to detect. To REVIEW (Sybrandy et al: Heart 89:485-489, 2003 — Alborzi et al: J The Univ Heart Ctr 11:49-54, 2016 — and Valle-Alonso et al: Rev Med Hosp Gen Méx 81:41-46, 2018) — ECG findings commonly reported in association with Cardiac Contusion include the following:
  • None (ie, The ECG may be normal — such that not seeing any ECG abnormalities does not rule out the possibility of cardiac contusion).
  • Sinus Tachycardia (common in any trauma patient ...).
  • Other Arrhythmias (PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib).
  • RBBB (as by far the most common conduction defect — owing to the more vulnerable anatomic location of the RV). Fascicular blocks and LBBB are less commonly seen.
  • Signs of Myocardial Injury (ie, Q waves, ST elevation and/or depression — with these findings suggesting LV involvement).
  • QTc prolongation.

  • NOTE: Prediction of cardiac contusion "severity" on the basis of cardiac arrhythmias and ECG findings — is an imperfect science.

Additional KEY Points:
Despite the predominance for RV (rather than LV) injury — use of a right-sided V4R lead has not been shown to be helpful compared to use of a standard 12-lead ECG for detecting ECG abnormalities.
  • In addition to ECG abnormalities related to the blunt trauma of cardiac contusion itself — Keep in mind the possibility of other forms of cardiac injury in these patients (ie, valvular injury, aortic dissection, septal rupture) — as well as the possibility of a primary cardiac event (ie, acute MI may have been the cause of an accident that led up to the trauma).
  • ECG abnormalities may be delayed — so repeating the ECG if the 1st tracing is normal is appropriate when concerned about severe traumatic injury.
  • That said (as per Drs. Yde and Meyers) — IF troponin is normal at 4-6 hours and IF the ECG is normal — then the risk of cardiac complications is extremely low.


How Did YOU Interpret the Initial ECG?
I found the initial ECG in today's case extremely interesting. Clearly, this patient with severe multi-trauma following a motor vehicle accident suffered a cardiac contusion — confirmed by the presence of obvious ECG abnormalities and marked troponin elevation.
  • While the literature acknowledges the difficulty trying to predict "severity" of cardiac contusion from ECG findings — there are a number of concerning ECG abnormalities present in the initial tracing (Figure-1).

Figure-1: I've reproduced and labeled the initial ECG in today's case.


MY Thoughts on the Initial ECG:
  • The rhythm in ECG #1 is sinus (RED arrow in lead II) — at a rate of ~90/minute. 
  • The PR interval looks to be slightly prolonged (especially considering the relatively rapid rate). Among the conduction defects seen with cardiac contusion is 1st-degree AV block.
  • The QRS complex is widened — and the predominantly wide qR pattern in lead V1, in association with the wide terminal S wave in lead I — is diagnostic of RBBB (Right Bundle Branch Block).

  • NOTE: The ECG in Figure-1 provides an excellent example of how QRS width may vary depending on which lead is being looked at. I've added vertical time lines to clarify the beginning and end of the QRS complex (RED and PURPLE dotted lines, respectively). Despite obvious QRS widening — Note how narrow the QRS looks in simultaneously-recorded lead II, due to the fact that much of the last part of the QRS in this lead lies on the baseline.

  • The QRS appears to be very wide and fragmented in leads V1,V2,V3. While I did not find literature to support this degree of widening and amorphous QRS morphology as a predictive factor of cardiac contusion severity — I thought the observation over serial tracings of progressive QRS narrowing, with return to a more normal triphasic RBBB morphology supported the concern regarding this initial tracing.
  • Additional evidence of abnormal ECG findings in Figure-1 was present in the form of: i) Deep Q waves in leads III and aVF; ii) Overly peaked (hyperacute?) T waves in leads I, II, aVL and aVF; and, iii) Excessive ST-T wave depression in the anterior leads (that clearly exceeds that expected with simple RBBB).

  • Did YOU notice how atypical the lateral chest leads are for RBBB? (QRS complexes within the dotted BLUE rectangles). Normally with RBBB — lateral chest leads show an upright R wave with a wide terminal S wave — and not persistence of similar-looking triphasic-notched complexes with persistent ST-T wave depression. I suspect the reason for this atypical QRST morphology in leads V4,V5,V6 — is that electrode lead placement had to be altered in this patient with multi-thoracic traumatic injuries requiring chest tubes, splinting, bandages, etc. NOTE: The relevance of recognizing this atypical RBBB morphology relates to its potential effect on comparing serial ECGs.

  • Did YOU notice the prominent J waves (? Osborn waves) in the inferior leads? There is also prominent negative notching in leads I and aVL (BLUE arrows in the limb leads). We've previously noted how such prominent J waves may be seen not only with hypothermia — but also with other conditions, including myocardial ischemia — and that ischemia-induced J-waves have been found to increase the risk of developing malignant ventricular arrhythmias (See My Comment in the September 23, 2020 post of Dr. Smith's ECG Blog). 
  • J waves have also been shown to be a marker of significant increased risk following penetrating cardiac trauma (Nicol and Navsaria: J Injury 45:112-115, 2014). 
  • Regardless of whether you call these deflections prominent J waves or Osborn waves — I found it "telling" that these deflections were present in both of the first 2 ECGs done in today's case — that an episode of presumed VT, followed by significant bradycardia was seen shortly thereafter in the OR — but that these J-point deflections were no longer seen in the last 3 ECGs (which were done after those life-threatening arrhythmias resolved).


What Happened on Serial ECGs?
I've selected 3 of the 5 ECGs from today's case with the goal of highlighting the evolution of ECGs changes that developed over the course of this patient's hospital admission (Figure-2).

Figure-2: Comparison between 3 of the 5 ECGs recorded in today's case.


MY Thoughts on these Serial ECGs:
I found it interesting to trace progressive improvement of ECG abnormalities over the course of this patient's hospital admission:
  • I've already discussed the notable findings in ECG #1.

  • ECG #3 — was obtained following the episode of presumed VT and marked bradycardia that necessitated stopping the operative procedure. Compared to ECG #1, there is now: i) AFib with a PVC; ii) Some narrowing of the QRS, with appearance of a more distinct triphasic complex in anterior leads (that is now much more typical of RBBB morphology); iii) Much less ST-T wave depression in the anterior leads; iv) Development of significant ST elevation in leads I and II (and to a lesser extent in leads aVL and aVF); v) Loss of the prominent J-point notching that was seen in ECG #1; and, vi) A change in QRS morphology in the lateral chest leads that seems more consistent with an RBBB conduction defect (perhaps a result of improved electrode lead placement?).

  • ECG #4 (done on Hospital Day #6) — There is now: i) Return to normal sinus rhythm at a slower rate; ii) Further narrowing of the QRS — that is now consistent with an incomplete RBBB pattern; iii) Reduced size of the Q wave in lead III — with resolution of the Q wave in lead aVF; and iv) Continued improvement in ST-T wave abnormalities.

  • In SUMMARY: While the literature does not provide us with specific ECG criteria for assessing severity of cardiac contusion — today's case does provide insight as to how clinical correlation with serial ECGs can confirm that the patient is recovering. I thought it significant that this severely injured multi-trauma patient initially showed an extremely wide QRS (with RBBB and an amorphous QRS morphology) — that gradually narrowed and took on a more distinct RBBB morphology (with eventual resolution of the conduction defect). Along the way — the patient manifested ST-T wave elevation and depression, changing size of Q waves, and a series of rhythm changes (VT, bradycardia, AFib, PVCs) — with eventual improvement of all these ECG findings that corresponded with his progressive recovery.




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