Tag Archives: DVT

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Brain Injury and DVT Prophylaxis Part II

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I previously wrote about a new review that looked at using chemical prophylaxis for deep venous thrombosis (DVT) in patients with traumatic brain injury (TBI). The authors showed that it was safe to give subcutaneous heparin products within 24 to 48 hours after a stable 24 hour followup CT.

A just-published article now helps to refine the selection of the heparin product. A retrospective review looked at 386 ICU patients with a head Abbreviated Injury Score (AIS) > 2. A total of 57 received mechanical prophylaxis, the remainder received heparin products. Chemical prophylaxis consisted of subcutaneous enoxaparin 30mg bid or unfractionated heparin 5000u tid, at the whim of the attending neurosurgeon.

The heparin group had a slightly but significantly higher Head AIS (4.1 vs 3.8). The drugs were started at the same time post-injury, about 48 hours from admission. Unfractionated heparin was found to be inferior to enoxaparin. The unfractionated heparin patients had both a higher rate of pulmonary embolism, and were more likely to have progression of any intracranial hemorrhage (12% vs 5%). The authors claim a significantly lower DVT rate, but information in their data tables do not support this. Additionally, their overall DVT rate is very low, most likely because they did not routinely screen for it.

Bottom line: The head injury / DVT prophylaxis literature is expanding rapidly. It’s time to start working with your neurosurgeons to initiate chemoprophylaxis early (within 48 to 72 hours from injury once any intracranial bleeding is stable). And it looks like the drug of choice is enoxaparin, not unfractionated heparin.

Reference: Safety and efficacy of heparin or enoxaparin prophylaxis in blunt trauma patients with a head abbriviated injury severity score >2. J Trauma 71(2):396-400, 2011.

Related post: Brain injury and chemical prophylaxis for DVT

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What To Do About Upper Extremity DVT

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Deep vein thrombosis (DVT) is a potential problem for all trauma patients, primarily due to the small but real possibility of a resultant pulmonary embolism (PE). Many trauma programs have protocolized their evaluation and management of DVT, but this usually only involves clot in the lower extremities and pelvis. Unfortunately, up to 10% of DVT occurs in the upper extremities, and they are not usually addressed in the same fashion as lower extremity clot.

The American College of Chest Physicians has issued a number of recommendations for managing upper extremity DVT. This includes the use of anticoagulants in a similar manner as for lower extremities. These recommendations have varying literature support behind them, and it is not clear how well they apply to trauma patients.

Cedars Sinai Medical Center in Los Angeles has just published a paper that prospectively looks at the problem of upper extremity DVT in critically ill trauma and surgery patients. They used an existing protocol to screen and treat lower extremity DVT, but had no such algorithm for the upper extremity. A total of 1269 patients were treated in 2.5 years, and 862 patients were screened for DVT at least once. 

They found 316 DVTs in 198 patients (115 lower extremity, 201 upper extremity). A total of 77 patients with upper extremity DVT met inclusion criteria by have at least one followup duplex ultrasound. Since no protocol existed, management was at the discretion of the individual attending physician. Important findings regarding upper extremity DVT were:

  • Most were nonocclusive (72%) and occurred in the internal jugular vein (52%)
  • The average diagnosis was made on hospital day 19
  • 64% were associated with a central venous catheter, usually double or triple lumen. Removal of the catheter was predictive of improvement by the next duplex exam.
  • Pulmonary embolism occurred in 2.6%
  • Two thirds were treated with prophylactic or therapeutic anticoagulation
  • Anticoagulation did not lead to significant resolution by the final duplex exam

Bottom line: Trauma centers should develop a protocol for screening and treating upper extremity DVT. Anticoagulation may not be necessary, and specific criterial should be developed for its use. The patency and necessity for any central venous catheter associated with upper extremity DVT should be assessed, and preference given to moving or removing it.

Reference: The natural history of upper extremity deep venous thromboses in critically ill surgical and trauma patients: what is the role of anticoagulation? J Trauma 71(2):316-322, 2011.

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General

Brain Injury and Chemical Prophylaxis for DVT

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Deep venous thrombosis (DVT) and its complications are recognized and common problems in trauma patients, particularly those with traumatic brain injury (TBI). We know that giving chemical prophylaxis like heparin and low molecular weight heparin (LMWH) reduces the risk. Unfortunately, trauma professionals (and neurosurgeons in particular) are reluctant to give it after acute TBI for fear of making intracranial hemorrhage worse.

Froedtert Hospital in Milwaukee modified their protocol for TBI patients to allow chemical prophylaxis to start 24 to 48 hours after a 24 hour followup CT that showed no progression of any bleeding. Therefore, prophylaxis could be started 48 to 72 hours after injury. They used subq heparin three times daily, or LMWH twice daily. All others received mechanical prophylaxis and were screened twice weekly by duplex ultrasound. The chemical prophylaxis group was not screened routinely. 

A total of 812 patients were studied, half of whom received early prophylaxis per protocol. The average Abbreviated Injury Score for the head in these patients was 3.4, which represents fairly serious injury. There was a significant decrease in the incidence of DVT in the chemical prophylaxis group (1% vs 3%). More intriguing, there was a lower rate of injury progression in this group as well (3% vs 6%), although not quite statistically significant.

Bottom line: Although this is a small and retrospective study, it was well designed and relatively large compared to most other similar work. It shows that use of chemical prophylaxis works in patients with serious TBI, and appears to be safe. Similar protocols should be considered by trauma program multidisciplinary operations committees to further systematize this process. 

Reference: Safety and efficacy of prophylactic anticoagulation in patients with traumatic brain injury. J Am Coll Surg 213:148-154, 2011.

Related post: Does interrupting DVT prophylaxis increase risk for it?

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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.

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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.