Cardiac contusion

[coldcoldworld]

Interested in what others are doing for suspected cardiac contusions as the diagnosis and workup is quite nebulous in the literature....and I recently had one which was wildly disagreed upon by my attendings.

My case was as follows:
70 y/o F h/o HLD, OA presents from OSH as Level 2 trauma. Pt was restrained rear seat passenger, rear ended and hit chest on front seat. Had some CP at OSH and 1st trop 0.2, repeat trop in 3 hours 0.8. EKG @ OSH NSR, nml axis, nml intervals, anterior Q waves, poor R wave progression, no arrhythmias. CXR wnl. Pt had no preceding CP, SOB, palpitations, lightheadedness, dizziness, presyncope, syncope prior to the event. Pt was nonsmoker and no FH of CAD. Limited bedside US @ OSH with no evidence of pericardial effusion.

At our ED, full trauma survey negative. No chest pain on exam or subjectively. EKG unchanged from OSH. HR 80s BP 165/85

My understanding of the literature was that cardiac enzymes were neither specific or sensitive for cardiac contusion and didn't prognosticate who would have a serious event and that the real money was in the admission EKG and echo only if unstable.

That said, I admitted her to our obs unit for overnight tele w/ plan to d/c home in am if no tele events. No more trops and no echo as she was hemodynamically stable.

Long story short is that the am obs doc disagreed with this plan but I'll hold off on the final pt outcome until I hear some thoughts.

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[bartleby]

What is the reference interval (normal range) for the troponin assay at your facility?

 

[coldcoldworld]

Ours is <0.12 and I think the OSH had the same cutoff on their assay.

 

[bartleby]

If this is the case, the person doesn't sound dischargeable at the outset, so would seem to be a good obs candidate.

Ours is <0.12 and I think the OSH had the same cutoff on their assay.

 

[coldcoldworld]

Why would you say that? B/c of the elevated trop??

My whole point is that troponins don't tell you anything about if they have a contusion or if they are likely to have a serious event and therefore shouldn't have been ordered @ the OSH in the first place. I would have pushed to send her home had she not just been flown in in the middle of the night.

 

[bartleby]

The corollary to the old legal saw about not asking a question you don't already know the answer to is that in medicine, you shouldn't ask a question if you don't want to hear the answer. Quite often, people ordered a test such as a d-dimer, ESR or cardiac enzymes whose result has no significance in the patient they are caring for. More hours and dollars will then be wasted chasing this abnormal finding.

Whether this patient actually had a myocardial contusion or not (perhaps a mild one), you are obliged to trend cardiac enzymes when you order them and find an abnormal result.

In regard to myocardial contusion itself, it would stand to reason that anything which causes myocardial damage, ischemia, infection or confusion would cause a rise in cardiac enzymes. Indeed, there's a large body of literature which suggests that serum markers, particularly troponin, are indeed elevated in the case of contusion.

Journal
BMJ Heart
Diagnosing cardiac contusion: old wisdom and new insights, Heart 2003;89:485-489 http://heart.bmj.com/cgi/content/abstract/89/5/485

ABSTRACT
Cardiac contusion is usually caused by blunt chest trauma and therefore is frequently suspected in patients involved in car or motorcycle accidents. The diagnosis of a myocardial contusion is difficult because of non-specific symptoms and the lack of an ideal test to detect myocardial damage. Cardiac contusion can cause life threatening arrhythmias and cardiac failure. Many diagnostic methods, such as ECG, biochemical cardiac markers, transthoracic and transoesophageal echocardiography, and radionuclide imaging studies, have been investigated to determine their use in predicting such complications. Recently, cardiac troponin I and T were found to be highly sensitive for myocardial injury. Troponin I and T have also proved to be useful in the stratification of patients at risk for complications. Nevertheless, diagnosis of a cardiac contusion and identification of patients at risk remain a challenge. In this review the current diagnostic tests will be discussed. Also, based on these diagnostic tests, a screening strategy containing data from the latest studies is presented, with the intention of detecting patients at risk.

 

[Painter1]

i'm not sure that you can r/o NSTEMI. the whole incident could've been the patient's stress test that pushed them over.

not familiar with cardiac contussion, i have to read up on it. but if there were no contraindications, i would've gave the patient asa and b-blocker after nl trauma w/u.

 

[overthebars]

Without knowing more about the actual CP this hpi seems low risk for ACS. You've got a cause..."I hit my chest during the accident". No assoc Sx of ischemia or findings to go with and now CP free. It may be worth it to see if the ECG changes are dynamic, those Q's are intermediate risk at best. If there were ST or T changes with the Q's I'd be more impressed. The Tn looks borderline positive, but going up so you are stuck trending it down, if not negative (I'd go with down). NSTEMI drops quickly down the list. Watch 'em and refer for OP stress. ASA and Betablock, but no massive dose of statins b/c I want to CMA and they probably need it anyway.

 

[Painter1]

Without knowing more about the actual CP this hpi seems low risk for ACS. You've got a cause..."I hit my chest during the accident". No assoc Sx of ischemia or findings to go with and now CP free. It may be worth it to see if the ECG changes are dynamic, those Q's are intermediate risk at best. If there were ST or T changes with the Q's I'd be more impressed. The Tn looks borderline positive, but going up so you are stuck trending it down, if not negative (I'd go with down). NSTEMI drops quickly down the list. Watch 'em and refer for OP stress. ASA and Betablock, but no massive dose of statins b/c I want to CMA and they probably need it anyway.

low risk? 70yo by itself is a risk factor. i'm not familiar with "HLD" but if it stands for hyperlipidemia, then again that helps you stratify the patient.

 

[Seaglass]

According to an analysis of the iTRACs database of MI patients, risk factors don't continue to increase your risk after age 55. i.e. - once you're 55 you have as much risk as a 40 year old with all the risk factors.

 

[leviathan]

According to an analysis of the iTRACs database of MI patients, risk factors don't continue to increase your risk after age 55. i.e. - once you're 55 you have as much risk as a 40 year old with all the risk factors.

But does a 55 y/o with all the risk factors not have more risk than a 55 y/o without them?

 

[Seaglass]

linkylinky
Not when you crunch the numbers . . . (FYI - I got my ages a little bit wrong - it was 65, not 55)

 

[overthebars]

according to the AHA 2007 chest pain risk stratification guidelines, which seems to be a good [best - written by Braunwald himself] standard of care. The age of 70 barely makes it intermediate, the Q's are probably intermediate, but maybe not. The HLD doesn't enter into it in the acute setting. This is where you need a better history of a Levine's sign or sob/doe/diaphoresis/syncope/near syncope/etc. I think the whole hitting the chest on the car seat is pretty good to throw off the pretest probabilities, but it is only pretty good and that is why the OP watched this lady - too many bad unknowns. Now let us quash this "...NSTEMI can't be ruled out..." business and go back to Cardiac contusions.

The Q's and their distribution are great for cardiac contusion, the lack of a good clinical picture for ischemia makes a better picture for contusion than not and last, the lady hit her chest.

 

[Painter1]

according to the AHA 2007 chest pain risk stratification guidelines, which seems to be a good [best - written by Braunwald himself] standard of care. The age of 70 barely makes it intermediate, the Q's are probably intermediate, but maybe not. The HLD doesn't enter into it in the acute setting. This is where you need a better history of a Levine's sign or sob/doe/diaphoresis/syncope/near syncope/etc. I think the whole hitting the chest on the car seat is pretty good to throw off the pretest probabilities, but it is only pretty good and that is why the OP watched this lady - too many bad unknowns. Now let us quash this "...NSTEMI can't be ruled out..." business and go back to Cardiac contusions.

The Q's and their distribution are great for cardiac contusion, the lack of a good clinical picture for ischemia makes a better picture for contusion than not and last, the lady hit her chest.

Guidelines come after gestalt. Lastly, the missed MI's that end up in court arent' the obvious: "chest pressure, woke me up from sleep, that radiated to my jaw and left shoulder etc etc"

the ones that end up taking your home and mercedes benz are these: the ones that have confounding factors that steer you away from focusing on the number one cause of death in the U.S.!

again, you can rattle off all these studies, but in the end it comes down to gestalt and by simply reading the case, i think alot of seasoned practioners would disagree with your judgement.

 

[coldcoldworld]

Thanks for the replies. Obviously its hard to paint an good accurate clinical picture of the pt without actually seeing them but she was basically rock solid, wondering what all the fuss was about. Long story short, morning doc gets 2D echo showing akinetic inferior wall and ?? papillary muscle dehiscence. Pt gets admitted to CCU. TEE the same day again shows akinetic wall, overall good EF, valves nml, no dehiscence. Pt goes home that day, f/u with cards in 1 week.

Here's a pretty good review of the most recent literature but obviously a lot of controversy still exists:
http://www.ncbi.nlm.nih.gov/pubmed/17826213?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum