Category Archives: Head

Who Is At Risk For Blunt Cerebrovascular Injury?

In my last post, I wrote about proper screening for blunt cerebrovascular injury (BCVI). But, as you know, it’s important to screen only when there is a significant risk of the injury being present. Screening using the shotgun approach (screen everyone for everything) yields enough false positive results to present potential danger to your patient.

A variety of authors on this topic have promoted a number of high risk criteria to trigger a screening test. Most make sense, and are related to the anatomy of the vessels in question. The carotid arteries are relatively unprotected, although a bit deep, as they course up the neck. Thus, it is possible to damage them when they suffer a direct and significantly hard blow. Once they enter the skull, they are better protected. However, fractures through key areas of the skull base and face can injure the vessels, even in these protected locations.

The vertebral arteries are deep and relatively protected as they course through the vertebral foramina. However, if the vertebrae are fractured or subluxed, vessel injury can occur.

Finally, and as always, the physical exam is important. If there are unexpected neurologic changes that can’t be explained by other injuries, or there are indications of deep vascular injury, BCVI needs to be considered.

Here is my list of indications to screen for BCVI:

  • Neurologic abnormality not explained by diagnosed injury
  • Arterial epistaxis†
  • Seat belt sign on neck†
  • GCS < 8 (this is the most commonly forgotten one)
  • Petrous bone fracture
  • C‐spine fracture (C1‐C3) or subluxation at any level†
  • Fracture through foramen transversum†
  • LeFort II or III fractures

Bottom line: Be on the lookout for any of the criteria listed above in your trauma patient. If you find one during your initial evaluation, be sure to order a CT angiogram of the neck. And keep an eye out while scanning the head and cervical spine. If any of the other radiographic indications become apparent, add on the CT angiogram at that point.

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What’s The Best Test For Blunt Cerebrovascular Injury?

Blunt injury to the carotids or vertebrals (BCVI) is a little more common than originally thought, affecting about 1% of blunt trauma patients. We have many tools available to help us diagnose the problem: duplex ultrasound, CT angiography (CTA), MR angiography (MRA), and even good old conventional 4 vessel angiography.

But which one is “best?” This is a tough question, because there is always some interplay between clinical accuracy and cost. The surgical group at the Medical College of Wisconsin – Milwaukee did a nice job teasing some answers from existing literature on the topic. The authors tried to take a comprehensive look at costs, including money spent to prevent stroke, the cost of complications of therapy, and the overall cost to society if the patient suffers a stroke.

Here are the factoids:

  • For patients at risk for BCVI, the stroke rate is 11% without screening, 6% with duplex ultrasound screening, 4% with MRA, and 1% with either CTA or conventional angiography
  • From a societal standpoint (includes the lifetime costs of stroke for the patient), CTA is the most cost effective at $3,727 per patient
  • From the hospital standpoint (does not include lifetime cost), no screening is the most cost effective, but has the highest stroke rate (11%)
  • CTA prevents the most strokes, and costs about $10,000 per patient while decreasing societal costs by about $32,000 per patient screened

Bottom line: The “best” test for patients at risk for blunt cerebrovascular injury is the CT angiogram. It minimzes the stroke rate, and provides information on all four vessels supplying the brain, which is probably why the duplex ultrasound has a higher miss rate (can’t see the vertebrals or into the skull). But how do you decide who is at risk for this problem? Tune in to the next post!

Reference: Screening for Blunt Cerebrovascular Injuries is Cost-Effective. J Trauma 70(5):1051-1057, 2011.

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Everything You Wanted To Know About: Cranial Bone Flaps

Patients with severe TBI frequently undergo surgical procedures to remove clot or decompress the brain. Most of the time, they undergo a craniotomy, in which a bone flap is raised temporarily and then replaced at the end of the procedure.

But in decompressive surgery, the bone flap cannot be replaced because doing so may increase intracranial pressure. What to do with it?

There are four options:

  1. The piece of bone can buried in the subcutaneous tissue of the abdominal wall. The advantage is that it can’t get lost. Cosmetically, it looks odd, but so does having a bone flap missing from the side of your head. And this technique can’t be used as easily if the patient has had prior abdominal surgery.

2. Some centers have buried the flap in the subgaleal tissues of the scalp on the opposite side of the skull. The few papers on this technique demonstrated a low infection rate. The advantage is that only one surgical field is necessary at the time the flap is replaced. However, the cosmetic disadvantage before the flap is replaced is much more pronounced.

3. Most commonly, the flap is frozen and “banked” for later replacement. There are reports of some mineral loss from the flap after replacement, and occasional infection. And occasionally the entire piece is misplaced. Another disadvantage is that if the patient moves away or presents to another hospital for flap replacement, the logistics of transferring a frozen piece of bone are very challenging.

4. Some centers just throw the bone flap away. This necessitates replacing it with some other material like metal or plastic. This tends to be more complicated and expensive, since the replacement needs to be sculpted to fit the existing gap.

So which flap management technique is best? Unfortunately, we don’t know yet, and probably never will. Your neurosurgeons will have their favorite technique, and that will ultimately be the option of choice.

Reference: Bone flap management in neurosurgery. Rev Neuroscience 17(2):133-137, 2009.

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Sports Drinks And Electrolyte Replacement In TBI

Yesterday, I wrote about the (lack of) effectiveness of forcing hypernatremia in the management of TBI. However, we do know that some of our head injured patients have trouble maintaining a normal sodium level, and if it drops quickly or too far, hyponatremia can certainly cause problems. Trauma professionals have a number of tools to help fix this, including salt supplements or tablets, saline infusions, or even hypertonic saline in more difficult cases.

But what about using a sports drink to replace electrolytes? Isn’t that what athletes do? There are quite a few of these sports drinks on the market, and new ones seem to appear every week. Common examples are Gatorade, Powerade, Muscle Milk, Vitamin Water, 10-K Thirst Quencher, and many more. What if your brain injured patients eschews the salt tabs and insists on pounding down sports drinks all day?

Here is a table from an old sports medicine paper that describes the composition of a number of sports drinks from back in the day. Some, like Gatorade, are still around. (Click image to see a bigger, readable version)

Note that the electrolyte results are in mg/250cc, so I will translate to meq/liter for you. Gatorade had the highest sodium concentration at the time, 20meq/L, and one of the lowest potassiums at 3meq/L. The majority of the current day sports drinks have about the same electrolyte composition. Note that they are all a bit hyperosmolar (300+ mOsm), and this is made possible by added carbohydrate from some type of sugar. The carb is usually in the form of sucrose, dextrose, and/or high fructose corn syrup (yum!).

Bottom line: Your typical sports drink is equivalent to D30 in 0.1 normal saline. Not good for your TBI patient when consumed for sodium supplementation. It will actually drive the serum sodium down when consumed in quantity. Make sure your patients steer clear of this stuff until their brain injury is healed and they are running their next marathon.

Reference: The Effectiveness of Commercially Available Sports Drinks. Sports Med 29(3):181-209, 2000.

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Targeted Hypernatremia In Trauma Brain Injury: Does This Work?

Traumatic brain injury (TBI) frightens and confuses most trauma professionals. The brain and its workings are a mystery, and there is very little real science behind a lot of what we do for TBI. One thing that we do know is that intracranial hypertension is bad. And another is that we do have some potent drugs (mannitol, hypertonic saline) to treat it emergently.

So if we can “dry out” the brain tissue on a moment’s notice and drop the ICP a bit with a hit of sodium, doesn’t it stand to reason that elevating the sodium level constantly might keep the brain from becoming edematous in the first place? Many neurosurgeons buy into this, and have developed protocols to maintain serum sodium levels in the mid-140s and higher. But what about the science?

A nice review was published in Neurocritical care which identified the 3 (!) papers that have promoted this practice in humans with TBI. In general, there was a decrease in ICP in the patients in the cited papers. Unfortunately, there were also a number of serious and sometimes fatal complications, including pulmonary edema and renal failure requiring hemodialysis. These complications generally correlated with the degree of hypernatremia induced. Papers were also reviewed that involved patients with other brain injury, not caused by trauma. Results were similar.

Bottom line: There is no good literature support, standard of care, or even consensus opinion for prophylactically inducing hypernatremia in patients with TBI. The little literature there is involves patients with severe TBI and ICP monitors in place. There is nothing written yet that justifies the expense (ICU level care) and patient discomfort (frequent blood draws) of using this therapy in patients with milder brain injury and a reliable physical exam. If you want to try out this relatively untried therapy, do us all a favor and design a nice study to show that the benefits truly outweigh the risks. 

And if you can point me to some supportive literature that I’ve missed, please do so!

Related posts:

References:

  • Induced and sustained hypernatremia for the prevention and treatment of cerebral edema following brain injury. Neurocrit Care 19:222-231, 2013.
  • Continuous hyperosmolar therapy for traumatic brain injury-induced cerebral edema: as good as it gets, or an iatrogenic secondary insult? J Clin Neurosci 20:30-31, 2013.
  • Continuous hypertonic saline therapy and the occurrence of complications in neurocritically ill patients. Crit Care Med 37(4):1433-1441, 2009. -> Letter to the editor Crit Care Med 37(8):2490-2491, 2009.
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