Category Archives: Head

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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What Is The Zumkeller Index in TBI?

I learned something new today: the Zumkeller index. Exciting! Most trauma professionals who take care of serious head trauma have already recognized the importance of quantifying extra-axial hematoma thickness (HT) and midline shift (MLS) of the brain. Here’s a picture to illustrate the concept:

Source: Trauma Surgery Acute Care Open

Zumkeller and colleagues first described the use of the mathematical difference between these two values in prognosticating outcomes in severe TBI in 1996.

Zumkeller Index (ZI) = Midline shift (MDI) – Hematoma thickness (HT)

Intuitively, we’ve been using this all along. At some point, we recognized that if the degree of midline shift exceeds the hematoma thickness, it’s a bad sign. The easiest way to explain this is that there is injury to the brain that is causing swelling so the shift is greater than the size of the hematoma. 

The authors of the current paper from Brazil decided to quantify the prognostic value of the ZI by doing a post-hoc analysis of a previously completed prospective study.  They limited their study to adult patients with an acute traumatic subdural hematoma confirmed by CT scan. It used data from the 4-year period from 2012-2015.

They compared demographics and outcomes in three cohorts of ZI:

  • Zero or negative ZI, meaning that the midline shift was less than the size of the hematoma
  • ZI from 0.1 mm to 3.0 mm
  • ZI > 3.0 mm

And here are the factoids:’

  • A total of 114 patients were studied, and the mechanism of injury was about 50:50 from motor vehicle crashes vs falls
  • About two thirds were classified as severe and the others were mild to moderate, based on GCS
  • Median initial GCS decreased from 6 in the low ZI group to 3 in the highest ZI group, implying that injuries were worse in the highest ZI group
  • Mortality (14-day) was 91% in the highest ZI group and only in the low 30% range in the others
  • Regression analysis showed that patients with ZI > 3 had an 8x chance of dying within 14 days compared to the others

Source: Trauma Surgery Acute Care Open

Bottom line: This study confirms and quantifies something that many of us have been unconsciously using all along. Of course there are some possible confounding factors that were not quantified in this study. Patients with the more severe injuries tended to also have subarachnoid hemorrhage and/or intra-ventricular blood. Both are predictors of worse prognosis. But this is a nice study that quantifies our subjective impressions.

The Zumkeller Index is an easily applied tool using the measuring tool of your PACS application. It can be used to determine how aggressively to treat your patient, and may help the neurosurgeons decide who should receive a decompressive craniectomy and how soon.

Reference: Mismatch between midline shift and hematoma thickness as a prognostic factor of mortality in patients sustaining acute subdural hematomaTrauma Surgery & Acute Care Open 2021;6:e000707. doi: 10.1136/tsaco-2021-000707

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What You Need To Know About: Frontal Sinus Fractures

Fracture of the frontal sinus is less common than other facial injuries, but can be more complex to deal with, both in the shorter and longer terms. These are generally high energy injuries, and facial impact in car crashes is the most common mechanism. Fists generally can’t cause the injury, but blunt objects like baseball bats can.

Here’s the normal anatomy:

sinus-fracture-treatment

 

Source: www.facialtraumamd.com

There are two “tables”, the anterior and the posterior. The anterior is covered with skin and a small amount of subcutaneous tissue. The posterior table is separated from the brain by the meninges.

Here’s an image of an open fracture involving both tables. Note the underlying pneumocephalus.

frontal_sinus1

A third of injuries violate the anterior table, and two thirds violate both. Posterior table fractures are very rare. A third of all patients will develop a CSF leak, typically from their nose.

These fractures may be (rarely) identified on physical exam if deformity and flattening is noted over the forehead. Most of the time, these patients undergo imaging for brain injury and the fracture is found incidentally. Once identified, go back and specifically look for a CSF leak. Clear fluid in the nose is, by definition, CSF. Don’t waste time on a beta-2 transferring (see below).

If a laceration is clearly visible over the fracture, or if a CSF leak was identified, notify your maxillofacial specialist immediately. If more than a little pneumocephalus is present, let your neurosurgeon know. Otherwise, your consults can wait until the next morning.

In general, these patients frequently require surgery for the fracture, either to restore cosmetic contours or to avoid mucocele formation. However, these are seldom needed urgently unless the fracture is an open fracture with contamination or there is a significant CSF leak. If in doubt, though, consult your specialist.

Related posts:

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Antihypertensive Treatment In Acute TBI

Yes, we know high blood pressure can be bad. Over the long term, it can accelerate atherosclerotic heart disease and pound away at the kidneys and brain. And when it is acutely elevated to critical levels, it can lead to stroke.

But is it always bad in trauma? Trauma hurts like hell, so it’s no wonder than many of our patients (not suffering blood loss of course) are hypertensive.  But how often have you seen this scenario occur:

An elderly patient fell from standing, striking her head. She is brought to your ED by ground EMS. She has a GCS of 8 (E1 V3 M4) with a BP of 200/130 and pulse of 56.  This meets your trauma activation criteria and the team assembles to meet the patient.

As you move her onto the bed, one of your colleagues calls out for some nicardipine to control the pressure. Is this a wise move? Remember the First Law of Trauma:

Any anomaly in your trauma patient is due to trauma, no matter how unlikely it may seem.

What else can cause hypertension and bradycardia in your trauma patient? In this case, certainly a subdural or epidural hematoma.

And why is that happening? Because the intracranial pressure is elevated from the space-occupying lesion. Remember the formula for cerebral perfusion pressure (CPP):

CPP = MAP – ICP

Where MAP = mean arterial pressure and ICP = intracranial pressure.  Normally the MAP is around 90 torr and ICP is about 10 torr. Thus, the normal CPP is approximately 80. The range is 60  to well over 100 torr, and flow autoregulation keeps brain perfusion constant over this range.

But let’s say that we are psychic and know the ICP of our patient to be 60 because of a large subdural hematoma. Her current CPP is 150 – 60 or about 90 torr. What happens if we start her on a nicardipine drip or some other antihypertensive medication? We can certainly normalize the blood pressure to 120/80. But now her CPP drops to 90  – 60 = 30 torr!

Congratulations, you have just shut down circulation to her brain!

Bottom line: Think first before calling for antihypertensive medications in patients who may have increased intracranial pressure. You may be sabotaging the only mechanism protecting their brain while you are calling your neurosurgeon for help. Your top priority is to get them to the CT scanner while permitting that pressure. If it turns out that there is no evidence for pathology that would lead to increased ICP, then turn to the antihypertensive agents to help protect against stroke. 

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