Tag Archives: DVT

General

Could Deep Venous Thrombosis (DVT) In Trauma Patients Be Caused By Microparticles?

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Deep venous thrombosis is commonplace after multiple trauma. A systemic inflammatory process is activated, which leads to an increase in cytokine production. We know that a process called microvesiculation occurs, where cells undergoing apoptosis shed small particles that contain active tissue factor. These types of microparticles have been shown to lead to thrombosis in cancer patients, but the role in trauma patients has not been clear.

Researchers at the University of Rochester performed a simple study looking at injured or burned patients with an Apache II score >20 compared to normal controls. They examined blood drawn after day 2 in the hospital, and looked for microparticles using fluorescent microbeads. They concentrated on differences between 3 trauma patients who did not develop DVT and 2 who did.

Patients who developed DVT had nearly 300% more circulating microparticles than matched controls. It is likely that the majority of those microparticles expressed tissue factor as well. 

Bottom line: This exciting work may help explain why trauma patients have a higher DVT rate. Additionally, it may eventually provide us with a blood test that will help pinpoint patients at high risk so we can provide more intensive surveillance and/or more aggressive prophylaxis or prevention.

Reference: Multisystem trauma patients who develop venous thromboembolism have increased numbers of circulating microparticles. Marlene Mathews MD et al. Presented at the 34th Annual Resident Trauma Paper Competition at the AmericanCollege of Surgeons Spring Meeting, Washington DC, 2011.

General

Solid Organ Injury: How Soon Can We Begin Chemical DVT Prophylaxis?

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Nonoperative management of solid organ injury is the norm, and has reduced the operative rate significantly. At the same time, the recognition that development of deep venous thrombosis (DVT) in trauma patients is commonplace creates uncertainty? Is it safe to give chemical prophylaxis with low molecular weight heparin (LMWH)? How soon after injury?

The trauma group at USC+LAC recently published the findings of a retrospective review of 312 patients undergoing nonoperative management for their liver, spleen or kidney injuries. They looked at chemical prophylaxis administration and its relationship to failure of nonop management of solid organ injury.

As expected, as the grade of the solid organ injury increased, so did the failure rate of nonoperative management. Administration of low molecular weight heparin, such as enoxaparin, did not increase failure rate in this study. All but one failure occurred in patients who had not yet received the injections. Likewise, two DVT and two pulmonary embolisms occurred, but only in patients who had not yet received prophylaxis. 

Bottom line: This small study offers some assurance that early prophylaxis is okay, and a few prospective studies do exist. UCSF / San Francisco General is comfortable beginning chemical prophylaxis 36 hours postop, regardless of solid organ injury. Look for more guidance on this issue in the coming year or so. Until then, consider starting LMWH prophylaxis early to avoid complications from DVT or PE.

Reference: Thromboembolic prophylaxis with low-molecular-weight heparin in patients with blunt solid abdominal organ injuries undergoing nonoperative management: current practice and outcomes. J Trauma 70(1): 141-147, 2011.

General

Does Interrupting DVT Prophylaxis Increase Risk for DVT/PE?

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Deep venous thrombosis is a common concern in trauma care. Most trauma centers have well defined protocols for prophylaxis and surveillance. Ongoing use of pharmacologic thromboprophylaxis (PTP) in patients with traumatic brain injury (TBI), or in patients who need surgical procedures is controversial.  We have all experienced some form of “prophylaxis interruptus”, where our orthopedic or neurosurgical colleagues want us to forego or interrupt ongoing administration of heparin products. Does this create new problems?

A trial was conducted at two Denver trauma centers, trying to clarify the optimal administration of PTP in patients with stable TBI. One cohort received PTP, the other did not (either not indicated, short stay, or already on blood thinners). The group receiving PTP was also stratified into those who received it continuously and those who had interruptions in treatment.

They found that the incidence of DVT and PE was similar for patients receiving PTP vs those not receiving it. The two groups were very different, though, because the ones who did not receive it had less severe injuries and were more likely to be ambulating by discharge.  The most interesting finding was that being started on PTP and then interrupting it increased the incidence of DVT fourfold.

What is it about prophylaxis interruptus that is so risky? First, there were only 480 patients in this study, so statistical anomalies could be present. Could it be that the conditions (TBI) and operations that cause it to be interrupted greatly increase the risk? Unfortunately this study can’t answer those questions.

The bottom line: DVT and its prophylaxis is still a muddy concept. What we really need to do is to find out if PTP is really necessary in all the patients in whom we are using it. It would also be helpful if we knew how harmful it really is in patients with significant bleeding in their head, or in patients who need to undergo surgery. One alternative, if this paper pans out, is to begin with mechanical prophylaxis until cleared by neurosurgery and all operations are completed. For now, it’s not yet appropriate to change your existing practice and procedures.

Reference: Interrupted pharmocologic prophylaxis increases venous thromboembolism in traumatic brain injury. J Trauma 70(1):19-26, 2011.The term “prophylaxis interruptus” was coined by Tom Esposito in his discussion of this paper.

General

Pulmonary Embolism and DVT in Trauma

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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.

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:

  1. 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
  2. Many clots originate in the upper extremities. FALSE: most centers do not detect many DVTs in the arms
  3. Leg clots do not break off to throw a PE, they dislodge cleanly and completely. FALSE: cadaver studies have not show this to be true
  4. 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.

The 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.

Velmahos, Spaniolas, Tabbara et al. Arch Surg. 2009; 144(10):928-932.