All posts by TheTraumaPro

Aspirin For DVT Prophylaxis In Trauma

The use of mechanical and pharmacologic prophylaxis for prevention of deep venous thrombosis (DVT) and venous thromboembolism (VTE) in trauma patients is nearly universal. However, no matter how closely we adhere to existing guidelines, some patients will develop these conditions. Indeed, about 80% of patient who suffer some type of VTE event were receiving prophylaxis at the time.

Trauma is a major factor in causing hypercoagulability. Although current chemoprophylaxis focuses on clotting factors, platelets play a big part in the clot formation process. Our usual drugs, though (various flavors of heparin), have no effect on them.

What about adding aspirin to the regimen? My orthopedic colleagues have been requesting this for years. There is a reasonable amount of data in their literature that it is effect in patients with knee arthroplasty only. As usual, it is misguided to try to generalize management based on experience from one specific body region or operation.

A single Level I trauma center reviewed its data on aspirin prophylaxis for trauma patients. They reviewed their registry data from 2006 to 2011. They identified 172 trauma patients with duplex ultrasound proven DVT. These patients were matched with 1,901 control patients who underwent at least one duplex and never developed DVT. Matching was performed carefully to ensure that age, probability of death, number of DVT risk factors, and presence of TBI were similar. The total number of matched patients studied was 110.

And here are the factoids:

  • About 7% of patients with DVT were on aspirin at the time of their injury, vs 14% of the matched controls
  • 7% were taking warfarin, and 4% were taking clopidogrel
  • Analysis showed that patients taking aspirin had a significantly decreased chance of DVT after injury
  • On further analysis, it was found that this effect was only significant if some form of heparin was given for prophylaxis as well.

Bottom line: So before you run off and start giving your patients aspirin, think about what this study really said. Patients taking aspirin before their injury and coupled with heparin after their injury have a lower rate of DVT. It gives us no guidance as to whether adding aspirin after the fact, or using aspirin alone, are useful.  And we still don’t know if any of this decreases pulmonary embolism or mortality rates.

Related posts:

Reference: Aspirin as added prophylaxis for deep vein thrombosis in trauma: a retrospective case-control study. J Trauma 80(4):625-30, 2016.

What’s Wrong With My Patient? Final Answer!

I previously described a young man who was recovering from surgery for repair of a stab to the heart. He presented shortly after discharge with fever, a slightly elevated WBC, some EKG changes, and a small pericardial effusion.

Several people tweeted out the answer, which is post-pericardiotomy syndrome (PPS).

PPS is an inflammatory reaction to traumatic and then surgical injury to the pericardium. It is seen in a relatively small percentage of patients who undergo pericardiotomy for trauma, which is why patients who develop it are such a surprise to trauma professionals. A similar condition can develop after myocardial infarction (Dressler syndrome) and was first described in 1956. The classic paper describing PPS after trauma was published five years later (cited below).

Symptoms typically develop 1-6 weeks after surgery, and usually consist of low grade fevers, malaise, chest pain, and occasionally arthralgia. A pericardial friction rub may be present (and where is that stethoscope, BTW?). The WBC is usually elevated, with some degree of left shift. EKG may show some degree of pericarditis, including global ST elevation and T wave inversion.

Chest x-ray is usually nonspecific, but may show pleural effusion or an enlarged heart due to the presence of some pericardial fluid. Ultrasound may confirm a pericardial effusion, but this is not a reliable finding since the pericardium is typically left open at the end of the operation.

Treatment is symptomatic, usually consisting of NSAIDS or aspirin to tone down the inflammatory response.  These drugs are usually given for 4-6 weeks, then tapered. If the effusion is large, pericardiocentesis may be needed.

Bottom line: If your postop heart injury patient presents with these symptoms, consider infectious etiologies first, but remember that they are typically even less common than post-pericardiotomy syndrome. Reassure your patient, then reach for the ibuprofen to get them through it.

Reference: Postpericardiotomy syndrome following traumatic hemopericardium. Am J Cardiology 7(1):83-96, 1961.

What’s Wrong With My Patient? Part 2

In my previous post, I described a young man who had recovered from a stab to the heart. He did well for a week and a half, but then presented to the ED with significant chest pain. It seems to be substernal and somewhat pleuritic. What should you do to work it up further?

There have been a number of helpful comments. The first order of business is to rule out problems which may prove to be life threatening. In his case, ischemic disease and some failure of the repair must be ruled out quickly. Although ischemia or MI are unlikely in this young man, they are possible and should be evaluated.

I recommend the following:

  • Auscultate the chest and heart (remember this from medical school?)
  • PA chest x-ray
  • EKG
  • CBC
  • Troponin
  • FAST exam focusing on the heart

My list is short and simple, and should help me figure out nearly all significant problems.

In this case, the following findings are present:

  • The lungs are clear, and their is a faint cardiac friction rub
  • The chest x-ray is unremarkable
  • EKG shows ST elevations in two of the lateral leads only. Otherwise, it is normal.
  • CBC is normal with the exception of WBC 14,000
  • There is a trace level of troponin present
  • FAST demonstrates a very small pericardial effusion without clot

So what do you make of all this? What’s the diagnosis? What do you need to do? Tweets and comments please.

Answers Monday!

What’s Wrong With My Patient?

I’ve had several requests for this case recently, so I figured I’d put it out there again.

A 25 year old man is involved in some sort of violent, non-productive interpersonal relationship. He sustains a stab to the left chest, and is brought to your trauma center as a trauma team activation. During the FAST exam, a moderate effusion with visible clot is seen in the pericardium.

Appropriately, you run to the OR and prepare for a left thoracotomy. You perform a pledgeted repair of the ventricle (black arrow) and close.

The patient does well and is discharged home five days later. He returns to your clinic the following week and is doing well. You remove the staples.

One week later, he returns to your emergency department complaining of significant chest pain. He describes it as deep, behind his sternum, and it seems to be exacerbated by breathing.

Now what? What are you thinking about? What additional exam do you need. What labs?

Tweet or comment with your answers and suggestions. More on this tomorrow!

Could There Be A Simpler GCS?

The Glasgow Coma Scale (GCS) has been around forever. Or really, for about 45 years. It was actually developed in the early 1970s and known as the Coma Index. It was further refined into the GCS, when 1 was selected as the minimum component score. Ever since, it has been used as a common language among clinicians to communicate gross neurologic function and trends.

But it is still somewhat complicated. Oh no it’s not, you say? Then why do so many trauma resuscitation rooms have it posted on the wall? There are three components, each with a different number of possible values. And frankly, some are harder to remember than others. Decerebrate vs decorticate, right?

So what if someone told you that a single GCS component works just about as well as the whole bunch? Researchers have been piecing this together for years, focusing on the motor component of GCS (mGCS). There are two flavors of simplified score: mGCS and Simplified Motor Score (SMS). The mGCS is just what it sounds like: the full motor component of GCS, ranging from 1-6. The SMS is further simplified from the mGCS: mGCS of 1-4 tranlsates to SMS 0, mGCS 5 = SMS 1, and mGCS 6 = SMS 2. In my opinion, this is actually more complicated because you have to remember not only the 6 mGCS levels, but also the cutoffs to convert it to SMS.

Finally, a group from Oregon Health Sciences University in Portland performed a nice meta-analysis of the best individual studies.

Here are the factoids:

  • Only papers that compared total GCS (tGCS) to mGCS or SMS were included, and only if they analyzed a receiving operator characteristic curve. The statistics appeared sound.
  • tGCS was very slightly better than either mGCS or SMS at predicting:
    • in-hospital mortality
    • neurosurgical intervention
    • emergency intubation
    • severe TBI

Bottom line: Overall, the total GCS is slightly (just a few percent) better at doing the things listed above, compared to the motor score alone or the “simplified” (really?) motor score. Is this clinically significant in the field? Probably not. And its mere simplicity makes it appealing. 

However, there is one major problem to adopting the mGCS for use outside the hospital. Inertia. As I mentioned, we have been using the full GCS score for almost 50 years. Pretty much every trauma professional is familiar with the GCS or knows where to look up the details. But I suspect that those clincicians who assume care of the patient once in the hospital, and especially the intensive care unit (neurosurgeons) will never allow the use of an abbreviated scale. Good idea, but sorry, it won’t catch on in the real world.