Tag Archives: TBI

EAST 2016: How Long Does VTE Risk Last In TBI?

Most trauma patients
are considered to be at some risk for deep venous thrombosis (DVT) and/or
venous thromboembolism (VTE) during their hospital stay. Trauma professionals
go to great lengths to screen for, prophylax against, and treat these problems.
One of the tougher questions is, how long do we need to worry about it? For
fractures, we know that the risk can persist for months. But what about head
injury?

A group at Brigham
and Women’s Hospital did a large database study looking at the VTE risk in adults
who sustained significant head injury, with only minor injuries to other body
regions. They tried to tease out the risk factors using multivariate regression
models.

Here are the
factoids:

  • Patients were only included if their AIS Head
    was >3, and all other AIS were <3
  • Of the over 50,000 patients in the study,
    overall incidence of VTE was 1.3% during the hospital stay, and 2.8% overall
    within 1 year
    of injury
  • Risk factors for VTE after discharge included
    age > 64 (3x), discharge to a skilled nursing facility (3x), and prolonged
    hospital length of stay
    (2x)
image

Incidence of VTE over time

Bottom line: View this paper as a glimpse of a potential unexpected
issue. The risk of VTE persists for quite some time after head injury (and
probably in most other risky injuries like spine and pelvic fractures. The
three risk factors identified seem to identify a group of more seriously
injured patients who do not return to their baseline soon after injury. We may
need to consider a longer period of screening in select patients, but I believe
further work needs to be done to help figure out exactly who they are.

Reference: How long should we fear? Long-term risk of
venous thromboembolism in patients with traumatic brain injury. EAST 2016 Oral
abstract #28.

EAST 2016: Brain Hypoxia In TBI With Aeromedical Evacuation

I’m sure that most of you have noticed that I very rarely write about animal studies. The problem I have is that the effects generally found are not dramatic, and results seldom carry over to humans the way we think they should. 

But for this paper, I’ve made an exception. It uses a swine model to study the effect of air transport at altitude on TBI. As you may know, most aeromedical transport in the US is via helicopter. 

However, some patients in more rural areas must travel longer distances to get high level trauma care, and may need to fly in fixed wing aircraft. U.S. military transports overseas use fixed wing almost exclusively. 

Medical helicopters typically fly at only 1000-3000 feet above the ground, and the change in air pressure (and hence PaO2) is small. However, fixed wing aircraft fly at much higher altitudes, and the effective cabin altitude may rise to about 8000 feet. This is why your ears “pop” so many times as you ascend. You’ve essentially just climbed Mt. St. Helens in Washington state. The amount of oxygen in cabin air also decreases with altitude.

So what happens to a patient with severe TBI when exposed to these fluctuations in pressure and oxygen levels? A group at the Naval Research Center looked at this issue in anesthetized swine that received a TBI from a percussion device. They received standard TBI and injury-specific care (for pigs?) for two hours, then underwent flight simulation using a hypobaric chamber set to a cabin altitude of 8000 feet for four hours. 

Here are the factoids:

  • Six study pigs underwent the 2 hours at sea level followed by 4 hours at altitude. Six control pigs stayed at sea level after their injury.
  • Mean arterial pressure in the pigs at altitude decreased somewhat, but not significantly.
  • Intracranial pressure (ICP) increased significantly in the TBI group(!)
  • As a result, cerebral perfusion pressure (CPP) dropped in the study group (highly significant result).

Bottom line: Aeromedical transport at typical cabin altitudes significantly increases ICP and decreases CPP in an injured pig model. Although the groups are small, this information is startling and deserves rapid confirmation. This information may have a significant impact on the way we fly patients with head injuries. In particular, this is important for military aeromedical evacuation.

Reference: Brain hypoxia is exacerbated in hypobaria during aeromedical evacuation in swine with TBI. EAST 2016 Oral abstract #2, resident research competition.

Can TBI Be Managed Without Neurosurgical Consultation?

The standard of care in most high level trauma centers is to involve neurosurgeons in the care of patients with significant traumatic brain injury (TBI). However, not all hospitals that take care of trauma patients have immediate availability of this resource. An interesting paper looked at management of these patients by acute care surgeons.

The authors retrospectively reviewed all their patients who had a TBI and positive head CT managed with or without neurosurgery consultation over a two year period. They matched the patients with and without neurosurgical consultation for age, GCS, AIS-Head and presence of skull fracture and intracranial hemorrhage (parenchymal, epidural, subdural, subarachnoid). Neurosurgeons were available to the no-consult group if things went awry.

A total of 180 patients with and 90 patients without neurosurgical involvement were reviewed. Here are the interesting findings:

  • Hospital admission rate was identical for both groups (88%)
  • ICU admission was significantly higher if neurosurgeons were involved (20% vs 44%)
  • Repeat head CT was ordered more than 3 times as often by neurosurgeons (20% vs 86%)
  • Post-discharge head CT was ordered more often by neurosurgeons, but was not significantly higher (5% vs 12%)
  • There were no neurosurgical interventions, in-hospital mortalities, or readmissions within 30 days in either group

Based on this experience, the hospital adopted a set of guidelines for helping determine if neurosurgery should be consulted.

Bottom line: This work raises an interesting question: can general surgeons safely manage select patients with intracranial injury? The answer is probably yes. The majority of patients with mild to moderate TBI with small intracranial bleeds do well despite everything we throw at them. And it appears that surgeons use fewer resources managing them than neurosurgeons do. The keys to being able to use this type of system are to identify at-risk patients who really do need a neurosurgeon early, and having a quick way to get the neurosurgeon involved (by consultation or hospital transfer). Looking at the brain injury guidelines above, I am a little nervous about managing an epidural or contusion without one additional head CT. But this is certainly food for thought. As neurosurgery involvement in acute trauma declines, this concept will become more and more pertinent.

Related posts:

Reference: The acute care surgery model: managing traumatic brain injury without an inpatient neurosurgical consultation. J Trauma 75(1):102-105, 2013.

Treating Headache After TBI

Most patients with mild traumatic brain injury (TBI) recover quickly and have few sequelae. Headache is common during the first few hours or days. But some patients experience significant and sometimes unrelenting headaches after their injury. How should we treat them? Are they the same as other common headaches?

There are several common types of headaches that are not related to brain injury, but many of these can begin after TBI. These include tension headaches from muscle tension or spasm, cervicogenic headaches from strains, sprains or more significant injury to the neck and cervical spine, musculoskeletal headaches from pain in bone or muscle in the head or neck, and headaches related to the TMJ and jaw.

But many patients experience significant headaches without any of these factors. Why? Sometimes it is due to blood in or around the brain, irritating the meninges. But often, there is nothing that we can detect using our current diagnostic technology. However, even if we can’t find a reason, the headache is very real and very concerning to the patient. 

I’ve seen practitioners treat post-TBI headaches with a variety of drugs ranging from acetominophen and NSAIDs to anti-seizure and psychotropic drugs. Unfortunately, there is little literature support for any of them. A review article published in 2012 found only one article with Class II data that showed no lasting effect from manipulation therapy. 

So what do we do? Here is an algorithm suggested by the review article:

  • Consider a workup to rule out intracranial pathology as a source of the headache
  • Categorize the headache. If it is one of the non-TBI types listed above, treat appropriately.
  • If the headache severely limits function, consider time-release opioids
  • For milder headache, consider adetominophen or NSAIDs
  • Treat any comorbidities that may contribute to headache
  • If the headache has migraine-type properties, treat as such
  • If the headache is associated with cervical spine pain, mobilize the neck as appropriate

Bottom line: There is very little guidance for treatment of headache purely associated with TBI. Time-honored drugs like opioids for severe pain and acetominophen and NSAIDs for mild to moderate pain help, but generally do not entirely relieve the pain. Only tincture of time will make things better. And it’s probably best to stay away from prescription drugs other than opioids recommended for the pain. They have not been shown to work, and there are plenty of side effects to worry about.

Related post:

  • Prescription drugs and side effects

Reference: Systematic review of interventions for post-traumatic headache. PM&R. 4(2):129-140, 2012.

Antiplatelet Therapy And Blunt Head Trauma

All trauma professionals are aware of the evils of anticoagulation in patients who sustain traumatic brain injury. Warfarin is one of the most common anticoagulants encountered, but there is also a growing number of poor outcomes in patients with the newer, non-reversible agents.

But what about antiplatelet agents like aspirin and clopidogrel (Plavix)? Many physicians worry about these drugs, but is it warranted? Two Level I trauma centers in the Chicago area reviewed their experience. They retrospectively reviewed the records of patients over 40 years old who sustained blunt head trauma. A total of 1547 patients were identified over a 4 year period. They analyzed these records for in-hospital mortality, need for neurosurgical intervention, and length of stay.

Here are the factoids:

  • 27% of patients were taking antiplatelet agents. Patients also taking warfarin were excluded.
  • 21% were taking aspirin alone, 2% clopidogrel alone, and 4% both drugs
  • Patients taking the drugs averaged about 10 years older than those who were not
  • Overall, injury severity was relatively low (average ISS 10). A disproportionate number of more severely injured patients were not taking antiplatelet agents.
  • There was no difference of incidence of intracranial hemorrhage (45%), neurosurgical intervention (3%), or mortality (6%) between the two groups
  • Hospital length of stay averaged about 6.5 days, but long LOS was a bit more common in the antiplatelet agent group.

Bottom line: This is one more in a series of papers scrutinizing trauma and antiplatelet agents. A few previous studies have shown an adverse effect, but they have been much smaller series. I don’t believe the jury is in yet, so watch these patients carefully. A 6 or 12 hours repeat scan is probably in order, along with frequent neuro monitoring.  It’s probably not worthwhile to actively try to reverse them by giving platelets unless there is obvious life-threatening hemorrhage or sudden neurologic change (see below).

Related posts:

Reference: Outcomes in traumatic brain injury for patients presenting on antiplatelet therapy. Am Surg 81(2):128-132, 2015.