Category Archives: Head

Hitting The Brakes May Increase Intracranial Pressure During The Ambulance Ride!

One of the most common injuries encountered by trauma professionals is blunt head trauma, and it’s one of the leading causes of death in young people. Keeping the level of intracranial pressure (ICP) within a specified range is one of the basic tenets of critical neurotrauma care in these patients. Most trauma centers have sophisticated algorithms that provide treatment guidance for various levels of ICP or cerebral perfusion.

The vast majority of patients with severe head injuries are transported to the hospital in some type of ambulance. Obviously, the exact ICP level is not known during transport because no monitoring device is present. We can sometimes infer that ICP is elevated if the patient has a Cushing response (wide pulse pressure and bradycardia) or unequal pupils. But for the most part, we assume that ICP is in a steady state during the ambulance ride.

But here’s something I never considered before: can ambulance acceleration or deceleration change the ICP through shifting of the brain or cerebrospinal fluid?

Patients are generally loaded into ambulances head-first, with their feet toward the back door. Frequently, they must be positioned supine in consideration of possible thoracic or lumbar spine injury. This position itself may lead to an increase in ICP. But what happens when the ambulance is hitting the brakes as it approaches a light or stop sign? As the patient’s weight shifts toward the top of the head, so does the CSF, spinal cord, and brain. Couldn’t this, too, increase ICP?

The anesthesiology group at the Erasmus Medical Center in Rotterdam, Holland performed a very novel study to assess this very thing. They recruited twenty participants in whom they evaluated ICP in various positions during acceleration and deceleration.
No, the subjects did not have an actual invasive ICP monitor inserted.

The authors used a novel way to infer pressures: optic nerve sheath diameter (ONSD). The optic nerves are direct extensions of the brain, and CSF travels freely in the nerve sheath. As ICP rises, the diameter of the nerve sheath increases. The subjects were fitted with a special helmet with two devices mounted on it. The first was a 7.5 Mhz ultra-sound probe focused on the back of the eye. The second was an arm with an orange dot on the end. This was adjusted so that the ultrasound probe was pointing at the optic nerve sheath when the other eye was focused on the dot. Subjects just watched the dot and measurements streamed in! Crude but very effective.

Baseline measurements were taken without acceleration or deceleration, then repeated when accelerating to 50 km/hr and decelerating to a stop.

Here are the factoids:

  • A total of 20 subjects were tested, and their oxygen saturation, blood pressure, and pulse were identical pre- and post-test
  • Baseline ONSD was about 5mm; a relevant change in diameter was determined to be more than 0.2 mm
  • Lying supine, the ONSD in nearly all subjects increased from an average 4.8 to 6.0 mm during deceleration
  • With the head raised to 30º, most values remained steady (from 4.8 to 4.9 mm) during deceleration

The left block shows the increase in size of the optic disk with braking while supine. The right one demonstrates that this effect is neutralized by elevating the head 30º.

Bottom line: This is a small, simple, and creative study, yet the results are very interesting! It is clear that optic nerve sheath diameter increases significantly during deceleration in patients who are supine. And this effect is eliminated if the head of bed is elevated 30º.

Unfortunately, we have no idea how the change in ONSD corresponds to absolute values of, or relative increases in, ICP. Does a change of 1.2mm indicate a 5 torr increase in ICP? A 5% increase? Is it proportional to the absolute ICP? We just don’t know.

But the data is clear that a measurable change does occur. Until better data is available, it may be desirable to transport patients with serious head injuries with the head elevated to 30º if there are no concerns for lower spine injury. Or failing that, make sure the driver does not have a lead foot!

Reference: Ambulance deceleration causes increased intra cranial pressure in supine position: a prospective observational prove of principle study. Scand J Trauma Open Access 29:87, 2021.

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Best Of AAST 2021: Validating The “Brain Injury Guidelines” (BIG)

The Brain Injury  Guidelines (BIG) were developed to allow trauma programs to stratify head injuries in such a way as to better utilize resources such as hospital beds, CT scanning, and neurosurgical consultation. Injuries are stratified into three BIG categories, and management is based on it. Here is the stratification algorithm:

And here is the management algorithm based on the stratification above:

The AAST BIG Multi-Institutional Group set about validating this system to ensure that it was accurate and safe. They identified adult patients from nine high level trauma centers that had a positive initial head CT scan. They looked at the the need for neurosurgical intervention, change in neuro exam, progression on repeat head CT, any visits to the ED after discharge, and readmission for the injury within 30 days.

Here are the factoids:

  • About 2,000 patients were included in the study, with BIG1 = 15%, BIG2 = 15%, and BIG3 = 70% of patients
  • BIG1: no patients worsened, 1% had progression on CT, none required neurosurgical intervention, no readmits or ED visits
  • BIG2: 1% worsened clinically, 7% had progression on CT, none required neurosurgical intervention, no readmits or ED visits
  • All patients who required neurosurgical intervention were BIG3 (20% of patients)

The authors concluded that using the BIG criteria, CT scan use and neurosurgical consultation would have been decreased by 29%.

Bottom line: This is an exciting abstract! BIG has been around for awhile, and some centers have already started using it for planning the management of their TBI patients. This study provides some validation that the system works and keeps patients safe while being respectful of resource utilization. 

My only criticism is that the number of patients in the BIG1 and BIG2 categories is low (about 600 combined). Thus, our experience in these groups remains somewhat limited. However, the study is very promising, and more centers should consider adopting BIG to help them refine their management of TBI patients.


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Screening For BCVI

In my last post, I described how common we think blunt carotid and vertebral injury (BCVI) really is. Today, I’ll review how we screen for this condition.

Currently, there are three systems in use: Denver, Expanded Denver, and Modified Memphis. Let’s look at each in detail.

Denver BCVI Screening

There is an original Denver screening system, and a more recent modification. The original system was divided into mechanism, physical signs, and radiographic findings. It was rather rudimentary and evolved into the following which uses both signs and symptoms, and high-risk factors.

Signs and symptoms

  • potential arterial hemorrhage from the neck, nose, or mouth
  • cervical bruit in patients <50 years of age
  • expanding cervical hematoma
  • focal neurologic deficit (transient ischemic attack, hemiparesis, vertebrobasilar symptoms, Horner syndrome) incongruous with head CT findings
  • stroke on CT

Risk factors

  • Le Fort II or III mid-face fractures
  • Cervical spine fractures (including subluxations), especially fractures involving transverse foramen or C1-C3 Vertebrae
  • Basilar skull fracture and involvement of carotid canal
  • Diffuse axonal injury with GCS <8
  • Near hanging with anoxic brain injury
  • Seat belt sign (or other soft tissue neck injury) especially if significant associated swelling or altered level of consciousness

The Denver group reviewed their criteria in 2012 and found that 20% of the patients who had identified BCVI did not meet any of their criteria. And obviously, this number cannot include those who were never symptomatic and therefore never discovered.

Based on their analysis, they added several additional risk factors to the original system:

  • Mandible fracture
  • Complex skull fracture/basilar skull fracture/occipital condyle fracture
  • TBI with thoracic injuries
  • Scalp degloving
  • Thoracic vascular injuries
  • Blunt cardiac rupture

The downside of these modifications is that they are a little more complicated to identify. The original criteria were fairly straightforward yes/no items. But “TBI with thoracic injuries?” Both the TBI part and the thoracic injury part are very vague. This modification casts a wider net for BCVI, but the holes in the net are much larger.

Memphis BCVI Screening

Let’s move on to the modified Memphis system for identifying BCVI. It consists of seven findings that overlap significantly with the Denver criteria. The underlined phrases indicated the modifications that were applied to the original criteria.

  • base of skull fracture with involvement of the carotid canal
  • base of skull fracture with involvement of petrous temporal bone
  • cervical spine fracture (including subluxation, transverse foramen involvement, and upper cervical spine fracture)
  • neurological exam findings not explained by neuroimaging
  • Horner syndrome
  • Le Fort II or III fracture pattern
  • neck soft tissue injury (e.g. seatbelt sign, hanging, hematoma)

Interestingly, these modifications were first described in an abstract which was never published as a paper. Yet somehow, they stuck with us.

So there are now two or three possible systems to choose from when deciding to screen your blunt trauma patient. Which one is best?

Let’s go back to the AAST abstract presented by the Birmingham group this year that I mentioned previously. Not only did they determine a more accurate incidence, but they also tested the three major screening systems to see how each fared. See Table 1.

Look at these numbers closely. When any of these systems were applied and the screen was negative, the actual percentage of patients who still actually had the injury ranged from about 25% to 50%! Basically, it was a coin toss with the exception of the Expanded Denver criteria performing a little better.

If you are a patient and you actually have the injury, how often does any screening system pick it up? Oh, about one in five times. Again, this is not what we want to see.

So what to do? The Expanded Denver screen has a lower false negative rate, but the total number of positive screens, and hence the number of studies performed, doubles when it is used.

Here’s how I think about it. BCVI is more common than we thought in major blunt trauma. If not identified, a catastrophic stroke may occur. Current screening systems successfully flag only 50% of patients for imaging. So in my opinion, we need to consider imaging every patient who is already slated to receive a head and cervical spine CT after major blunt trauma! At least until we have a more selective (and reliable) set of screening criteria.


  • (Denver) Optimizing screening for blunt cerebrovascular injuries. Am J Surg. 1999;178:517–522.
  • (Expanded Denver) Blunt cerebrovascular injuries: Redefining screening criteria in the era of noninvasive diagnosis. J Trauma 2012;72(2):330-337.
  • (Memphis) Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg. 2002, 236 (3): 386-393.
  • (Modified Memphis) Diagnosis of carotid and vertebral artery injury in major trauma with head injury. Crit care. 2010;14(supp1):S100.
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How Common Is BCVI, Really?

Blunt carotid and vertebral artery injuries (BCVI) are an under-appreciated problem after blunt trauma. Several screening tools have been published over the years, but they tend to be unevenly applied at individual trauma centers. I will discuss them in detail in the next section.

For the longest time, the overall incidence of BCVI was thought to be low, on the order of 1-2%. This is the number I learned years ago, and it has not really changed over time.

But how do we know for sure? Well, the group at Birmingham retrospectively reviewed every CT angiogram (CTA) of the neck they did in a recent two-year period. They did this after adopting a policy of imaging each and every one of their major blunt trauma patients for BCVI. Each patient chart was also evaluated to see if the patient met any of the criteria for the three commonly used screening systems.

During the study period, a total of 6,287 of 6,800 blunt trauma patients underwent BCVI screening with CTA of the neck. They discovered that 480 patients (7.6%) were positive for BCVI!

This is a shocking 8x higher than we expected! Why hasn’t this been obvious until now? Most likely because we were previously only aware of patients who became symptomatic. Luckily, many of these patients dodge the proverbial bullet and never exhibit any symptoms at all.

So why should we be worried? This is one of those clinical entities like blunt thoracic aortic disruption that potentially has terrible consequences if ignored. Although the number of patients who develop sequelae from their BCVI is small, suffering a stroke can be catastrophic.

Should we perform a screening study for all blunt trauma patients? Seems like overkill, or is it? Is there any way we be more selective about it?

In the next post, I’ll review the three current screening tools  used to determine which patients should receive CTA, and how good they are.

Reference: Universal screening for blunt cerebrovascular injury. J Trauma 90(2):224-231, 2021.

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It’s BCVI Week!

This post will kick off a series of posts on BCVI. What is that, you ask? There seems to be some confusion as to what the acronym BCVI actually stands for. Some people believe that it means blunt cerebrovascular injury. This is not correct, because that term refers to injury to just about any vessel inside the skull.

The correct interpretation is blunt carotid and vertebral artery injury. This term refers to any portion and any combination of injury to those two pairs of vessels, from where they arise on the great vessels, all the way up into the base of the skull. Here’s a nice diagram:

Note that we will be excluding the external carotid arteries from this discussion, since injuries to them do not have any impact on the brain. They can cause troublesome bleeding, though.

These arteries are relatively protected from harm during blunt trauma. But given enough energy, bad things can happen. Fortunately, injuries to these structures are not very common, but unfortunately many trauma professionals under-appreciate their frequency and severity.

Over the next four posts, I’m going to provide an update on what we know about BCVI. I will try to tease out the true incidence, review the (multiple) screening systems, and discuss various ways to manage these injuries.

In the next post, we’ll explore the incidence of this injury. Is it truly as uncommon as we think?

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