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
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?
Coagulopathy is a frequent occurrence after severe traumatic brain injury (TBI). There are high levels of tissue factor (TF) in the brain, which can be released with severe injury. This in turn triggers a cascade which can lead to generalized coagulopathy.
The trauma group at LAC+USC looked at the time course of coagulopathy after isolated severe TBI. They identified 278 patients over a 1.5 year period and retrospectively review a number of demographic and outcome variables. Coagulopathy was defined as a platelet count < 100,000/mm3, INR > 1.4, or PTT > 36 sec.
They found the following:
- 46% with blunt trauma and 82% with penetrating injury developed a coagulopathy
- Presence of coagulopathy increased with increasing head injury severity
- Thromobocytopenia as a cause of coagulopathy was less common (17%) than clotting factor problems
- As brain injury severity increased from AIS=3 to AIS=5, median onset of coagulopathy became increasingly earlier (26 hrs, 22 hrs, 10 hrs)
- Mortality increased with earlier coagulopathy (23% after 24 hrs, 39% between 12 and 24 hrs, 56% less than 12 hrs)
- Prehospital: Coagulopathy should be suspected if the patient is bleeding profusely from multiple sites, including your IV needle sticks. This indicates severe brain injury and demands triage to a trauma center with immediate neurosurgical support.
- In-hospital: Coagulopathy that is noted in the ED portends severe injury and poor prognosis. Rapid access to CT scan and your neurosurgical consultant is critical.
Related post: Controlling fever in head injury
Reference: Time course of coagulopathy in isolated severe traumatic brain injury. Injury 41:924-928, 2010.
Clearance of the cervical spine is a complicated topic, with many opinions and anecdotes. EAST developed a set of practice guidelines in 1998 and updated them in 2000 and again in 2008. They are well-accepted and very helpful.
Spine clearance in an obtunded or intoxicated patient is made even more challenging. Here’s an approach based on the EAST guidelines that I find helpful:
- Clear the bones. Obtain a CT of the cervical spine from skull base to T2. Sagittal and coronal 2D reconstructions must be created for review. Conventional images (AP, lateral, odontoid) are of no additional value.
- If a fracture is identified, consult your spine service.
- If a neurologic deficit is present, obtain an MRI and consult your neurosurgery or spine service.
- Clear the ligaments. In the obtunded patient, there are 3 choices: 1) keep the collar on until the patient wakes up enough to be examined, 2) obtain an MRI to evaluate the ligaments, or 3) remove the collar on the basis of CT alone.
In patients that you don’t expect to wake up any time soon, I prefer MRI. Some say that it should be obtained within 72 hours of injury for best accuracy in detecting ligamentous injury. Unfortunately, I have not been able to find any specific literature support for this. If the MRI is negative, the collar can be removed immediately.
There is a growing body of research that suggests that CT alone is sufficient for clearance. My opinion is that this is probably true, but only if the scan is read by a radiologist who is especially skilled in reading CT scans of the cervical spine. A pool radiologist may miss subtle findings that might indicate a ligamentous injury.
Reference: Eastern Association for the Surgery of Trauma practice guideline: Identifying Cervical Spine Injuries Following Trauma – 2009 Update. Click here to download.
Overall, omega-3 fatty acids (O3FA) are thought to be an important and beneficial part of our diet. Recently, the Journal of Neurosurgery published an online paper that looked at the potential benefits of fish oil supplementation on recovery from brain injury.
Originally, axonal damage from TBI was thought to occur at the time of impact. Recent research has shown that the injury is really a progressive event that leads to swelling and axon disconnection during the hours to days after the initial injury. Building on a few animal studies over the past 6 years, a project to look at the effect of omega-3 fatty acid supplementation on brain injury was developed.
The authors performed a controlled study in rats, comparing supplementation with 10 or 40 mg/kg/day of O3FA for 30 days after brain injury with no supplementation. After 30 days, the rats were sacrificed and their brains were examined. The investigators found that a chemical marker of axonal injury (beta amyloid precursor protein) was very significantly decreased in the supplemented animals. The decrease was fairly dramatic and was similar for both doses.
The actual mechanism by which the protective effect of O3FA was not determined in this study. There is speculation that it may be due to stabilization of brain cell membranes and reduction in the number of reactive oxygen molecules.
This research is very intriguing and appears to have been designed and executed well. The only downside to the work is that the senior investigator is the founder and trustee for the Inflammation Research Foundation. The foundation promotes research on the treatment of diseases with nutritional supplements such as fish oil. The Foundation provided the supplements used in this study. Readers must always be careful when interpreting positive data that is funded or supported by an organization that may benefit from positive results.
Bottom line: Interesting study, and certainly one that should be followed up with human studies. As far as we know, fish oil supplements are relatively safe, so it should be a little easier to move this work along to human studies. It is not sufficient to recommend adding O3FA to the nutritional regimen of head injured patients yet.
Reference: Omega-3 fatty acid supplementation and reduction of traumatic axonal injury in a rodent head injury model Laboratory investigation. Sears et al. J Neurosurg online July 16, 2010.