For a long time, we “knew” that pulmonary emboli were a possible and dreaded complication of deep venous thrombosis (DVT). However, we are beginning to discover that this is not always the case. The group in San Diego decided to see if there really are two different types of PE in trauma, and what that means.
Here’s another VTE paper from Scripps Mercy Hospital, a level I trauma center in San Diego. It looked at 5 ½ years of their experience with adult trauma patients who were routinely screened for DVT. Any of these patients who developed a PE within 6 weeks of admission were evaluated further.
Here are the factoids:
Duplex screening from groin to ankle was carried out twice weekly in ICU patients, and once weekly in ward patients
Surveillance was carried out if the patient would be non-ambulatory for more than 72 hours, or were at moderate or higher risk for DVT using the ACCP guidelines
Nearly 12,000 patients were evaluated by the trauma service and 2,881 underwent surveillance
31 patients (1%) developed a PE
12 of these 31 had DVT identified before or immediately after their PE. Clot was below-knee in 9 (!), above-knee in 2, and in the IJ in one.
19 patients had PE but no DVT identified (de novo PE, DNPE)
DNPE tended to be single and peripherally located, and associated with rib fractures, pulmonary contusions, blood transfusions, and pneumonia
DVT + PE were more often found in multiple lobes or bilaterally
Bottom line: Like most, this is not a perfect study, but it’s a really good one. It is looking more and more likely that some PEs arise de novo, without any associated DVT. These clots are more likely to be linked to some type of inflammatory process, and have a tendency toward causing more of the classic signs and symptoms of PE. There are still lots of questions to be answered, like do you need to anticoagulate the de novo PEs? But for now, no change in practice. Just be aware that these might not be as bad as they seem.
Reference: Pulmonary embolism without deep venous thrombosis: de novo or missed deep venous thrombosis? J Trauma 76(5):1270-1281, 2014.
Venous thromboembolism (VTE) is an ongoing problem for trauma professionals. Most trauma programs have settled on their own flavor of screening, prophylaxis, and treatment once the problem actually surfaces in a patient. Most prophylaxis centers around a combination of mechanical (leg squeezers) and chemical (some type of heparin) management.
Aspirin has been used for prophylaxis for elective orthopedic surgery, and occasionally in trauma patients managed by orthopedic surgeons for years. Existing literature supporting this has been sparse and unconvincing. But since VTE involves platelets as part of the process, why not have another look?
A recently published paper from Scripps in San Diego looked tried to gauge the effect of aspirin on trauma patients where taking it before they were injured. Novel idea. Can the findings be useful? The authors performed a retrospective, case-controlled study of patients who developed post-traumatic deep venous thrombosis (DVT). The patients were matched for 7 covariates, and the authors looked at an additional 26 risk factors. Those taking aspirin pre-injury were compared with those who were not.
Here are the factoids:
172 cases were identified over the 5 ½ year study, and 62 (36%) were excluded because a matched control could not be found
7% of the remaining110
patients were taking aspirin (why?)
13% of controls were taking aspirin
7% were taking warfarin, and 4% were taking clopidogrel
The mean age was 52, ISS was 13-14, and hospital stay was 7-10 days (!)
Multivariate analysis showed a significant protective effect from DVT with a risk ratio of 0.17 (!!)
But this effect was found only when used in conjunction with heparin prophylaxis after admission
Bottom line: Interesting findings. What does it mean? First, this is a very small retrospective study. It was conducted over 5+ years, so changes in VTE screening and prophylaxis may have occurred at this hospital. But even so, the finding were compelling. The biggest problem is that we can’t expect people to predict that they will need to start taking aspirin. But the study does raise the interesting question of whether it might be helpful to start taking it as soon as the patient arrives at the hospital. This is one of those thought provoking studies that should prompt someone (hint hint) to design a nice prospective study to see if this ultra-cheap drug might help us bring down our VTE rates even more.
Reference: Aspirin as added prophylaxis for deep vein thrombosis in trauma: A retrospective case-control study. J Trauma 80(4):625-630, 2016.
Our current technology for identifying venous thromboembolism (VTE) / deep venous thrombosis (DVT) consists of duplex ultrasonography, and sometimes, CT angiography. Both are relatively noninvasive and painless (unlike the old-fashioned venography of days gone by.
Researchers at the Massachusetts General Hospital have been working with different chemical probes that could adhere to clot and allow it to be identified on a PET scan. After experimenting with a number of fibrin-targeting peptides they settled upon one called copper fibrin-binding peptide 8 (Cu-FBP8). It was found to have a high affinity for clot, remain stable, and clear quickly from the animal.
A series of rats were subject to a surgically induced thrombus in the carotid or femoral arteries, or a sham operation. The animals were then imaged by CT/PET scan after injection with the Cu-FBP8 probe. The authors found that the probe worked as expected, identifying clot immediately. They were also able to follow resolution over the days following induction.
Here is a whole-body fused CT/PET scan of one of the animals with both carotid artery (yellow arrow) and femoral artery (blue arrows) clot.
Bottom line: This is a potentially exciting tool that could make it much easier for us to identify DVT and VTE. It could also help us understand the etiology and incidence of PE as well. But as with all animal studies, it remains to be seen whether this will translate into a useful test for humans. Stay tuned, as it will probably take about 3 years to find out the answer.
Multisite Thrombus Imaging and Fibrin Content Estimation With a Single Whole-Body PET Scan in Rats. Arterioscler, Thromb, Vasc Biol 35(10):2114-2121, 2015.
We have long assumed that pulmonary emboli start as clots in the deep veins of the legs (or pelvis), then break off and float into the branches of the pulmonary artery in the lungs. A huge industry has developed around how best to deal with or prevent this problem, including mechanical devices (sequential compression devices), chemical prophylaxis (heparin products), and physical devices (IVC filters).
The really interesting thing is that less than half of patients who are diagnosed with a pulmonary embolism have identifiable clots in their leg veins. In one study, 26 of 200 patients developed DVT and 4 had a PE. However, none of the DVT patients developed an embolism, and none of the embolism patients had a DVT! How can this kind of disparity be explained?
Researchers at the Massachusetts General Hospital retrospectively looked at the correlation between DVT and PE in trauma patients over a 3 year period. DVT was screened for on a weekly basis by duplex venous ultrsonagraphy. PE was diagnoses exclusively using CT scan of the chest, but also included the pelvic and leg veins to look for a source. A total of 247 patients underwent the CT study for PE and were included in the study.
Here are the factoids:
Forty six patients had PE (39% central, 61% peripheral pulmonary arterial branches) and 18 had DVT (16 seen on the PE CT and 2 found by duplex)
Of the 46 patients with PE, only 15% had DVT
All patient groups were similar with respect to injuries, injury severity, sex, anticoagulation and lengths of stay
Interestingly, 71% of PE patients with DVT had a central PE, but only 33% of patients without DVT had a central PE.
The authors propose 4 possible explanations for their findings:
The diagnostics tools for detecting DVT are not very good.FALSE: CT evaluation is probably the “gold standard”, since venography has long since been abandoned
Many clots originate in the upper extremities. FALSE: most centers do not detect many DVTs in the arms
Leg clots do not break off to throw a PE, they dislodge cleanly and completely. FALSE: cadaver studies have not shown this to be true
Some clots may form on their own in the pulmonary artery due to endothelial inflammation or other unknown mechanisms. POSSIBLE
An invited critique scrutinizes the study’s use of diagnostics and the lack of hard evidence of clot formation in the lungs.
Bottom line: this is a very intriguing study that questions our assumptions about deep venous thrombosis and pulmonary embolism. More work will be done on this question, and I think the result will be a radical change in our use of anticoagulation and IVC filters over the next 3-5 years.
Reference: Pulmonary embolism and deep venous thrombosis in trauma: are they related? Arch Surg 144(10):928-932, 2009.
As with adults a decade ago, the incidence of venous thromboembolism (VTE) in children is now on the rise. Whereas adult VTE occurs in more than 20% of adult trauma patients without appropriate prophylaxis, it is only about 1% in kids, but increasing. There was a big push in the early 2000′s to develop screening criteria and appropriate methods to prevent VTE. But since the incidence in children was so low, there was no impetus to do the same for children.
The group at OHSU in Portland worked with a number of other US trauma centers, and created some logistic regression equations based on a large dataset from the NTDB. The authors developed and tested 5 different models, each more complex than the last. They ultimately selected a model that provided the best fit with the fewest number of variables.
The tool consists of a list of risk factors, each with an assigned point value. The total point value is then identified on a chart of the regression equation, which shows the risk of VTE in percent.
Here are the factors:
Note that the highest risk factors are age >= 13, ICU admission, and major surgery.
And here is the regression chart:
Bottom line: This is a nice tool, and it’s time for some clinical validation. So now all we have to do is figure out how much risk is too much, and determine which prophylactic tools to use at what level. The key to making this clinically usable is to have a readily available “VTE Risk Calculator” available at your fingertips to do the grunt work. Hmm, maybe I’ll chat with the authors and help develop one!
Reference: A Clinical Tool for the Prediction of Venous Thromboembolism in Pediatric Trauma Patients. JAMA Surg 151(1):50-57, 2016.
Home of the Trauma Professional's Blog
Do you want to get a daily email every time there’s a new post? See what I’m up to.