Tag Archives: TBI

Abstracts

EAST 2019 #8: How To Keep Neurotrauma Patients At Level III Trauma Centers

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Hospitals that do not have neurosurgical coverage are faced with a dilemma when they receive a head-injured patient. Do they automatically transfer to a higher level trauma center, or do they keep the patient? This is especially poignant in rural areas, where transfer times may be lengthy. If a patient doesn’t really have any significant pathology, they are likely to be evaluated at the receiving Level I or II center, then discharged all the way back home. But if they are kept at the initial hospital, there may be a nagging doubt about what happens if…

Five years ago, the group at University of Arizona – Tucson published a simple brain injury classification system that was designed to predict which injuries were likely to progress and need neurosurgical intervention. They called this system BIG for Brain Injury Guidelines. It was created and validated on a group of nearly 4,000 patients over four years, and the results have been promising. Since then, BIG has been validated using small study groups (<405) in pediatric head injury, and at Level I and III trauma centers.

Here’s the guideline:

One of the Quick Shot presentations at next week’s EAST Annual Scientific Assembly is another validation study at a Level III center in Lake Havasu City, Arizona that introduces one small modification to the guidelines. Normally, BIG is calculated after CT of the head is complete. This modification entailed BIG calculation after anticoagulation was reversed. Patients with BIG scores of 1 or two after reversal was complete were kept at the Level III, and were managed by the trauma surgeons. All BIG 3 patients were transferred to a higher level center.

Four years of trauma registry data were analyzed. During the first two years, patients with any positive BIG score were transferred. During the final two years, only patients who scored BIG 3 after reversal were moved.

Here are the factoids:

  • During the pre-BIG period, there were 72 transfers: 36 BIG-1, 23 BIG-2, and 13 BIG-3
  • Once the protocol was in place, there were 119 patients identified, 52 patients with BIG-1 or 2 who were kept and 67 BIG-3 patients who were transferred
  • 13 patients in the post-BIG time frame were excluded
  • None of the BIG-1 or 2 patients required transfer later
  • 39 of the 52 BIG-1 or 2 patients had repeat scans, and none worsened clinically, with an average hospital length of stay of 1.4 days
  • Estimated helicopter transport savings was $1.9M based on an average charge of nearly $50K per flight

The authors concluded that modified BIG could be used to triage neurotrauma patients for transfer, but cautioned that good clinical judgment should also be applied.

Here are some questions for the authors and presenter to consider in advance to help them prepare for audience questions:

  • Are you satisfied that BIG is sufficiently validated? To date, there are only a handful of validation studies and they have relatively small numbers.
  • Why did you choose to modify the score to wait until anticoagulation? Couldn’t this nullify the validation studies?
  • Do you have any practice guidelines in place to ensure consistent care of the patients you now keep at your center? Do they allow you to manage common problems like subarachnoid hemorrhage or intraparenchymal hemorrhage?
  • How did you ensure that your surgeons, hospitalists, and nurses were comfortable managing these neurotrauma patients? Did you have any educational sessions or other training for things like GCS monitoring and neuro exam?
  • How do you reverse anticoagulation, and how long does that usually take? Plasma and prothrombin complex concentrate are commonly used, but with vastly different reversal times. And what do you do about aspirin, clopidogrel, and the novel oral anticoagulants?
  • Why did you exclude 13 patients once you started using BIG?
  • Has your hospital administration provided any numbers regarding increased revenue from this practice? Your hospital is larger (171 beds), but this type of information will be vital for small, critical access hospitals.

This is very interesting work, and highly applicable to rural trauma centers!

References:

  • Successful management of select radiographic intracranial injuries in a rural trauma center without neurosurgeon coverage using a modified brain injury guideline. EAST 2019, Quick Shot Paper #6.
  • The BIG (brain injury guidelines) project: Defining the management of traumatic brain injury by acute care surgeons. J Trauma 76(4):965-969, 2014.
Abstracts

EAST 2019 #1: Predicting Outcome After Brain Injury

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Here’s the first abstract I’ll review from the EAST 2019 Annual Assembly in January.

This one comes to us from the University of Arizona system, and specifically from Tucson. The senior author has an interest in traumatic brain injury (TBI) and geriatric trauma, so it’s not surprising to see this abstract that fuses the two. The aim was to create a new tool to predict mortality in patients who had sustained a TBI.

The authors devised a score, the Brain Trauma Outcome Score (BTOS) using three variables: age, injury severity score (ISS), and presence of blood transfusion. Furthermore, this was used to create a Brain Trauma Outcome Score (BTOS), by dividing the BTOS by the GCS. These equations were developed and tested using data sets from two years worth of TQIP data. I know, lots of acronyms, but stay with me. After generating the equations for GTOS and BTOS from one TQIP dataset and testing against another, both of these systems were checked for discriminatory power by generating receiving operator characteristic curves.

The authors found that the tested BTOS was better at predicting mortality than the tested GTOS. They concluded that “BTOS can accurately predict in-hospital mortality in all TBI patients.” Seems like a pretty bold assertion.

Here are some questions for the authors and presenter to consider in advance to help them prepare for audience questions:

  • Be aware that some typos crept into the final copy. When preparing abstracts, try not to use special characters (i.e. +) as they may not be generic enough for the commercial printing software used to prepare final copy. This is similar to avoiding video or links to YouTube videos in slide sets. I was able to figure out what the question marks really were (I think), but make sure the audience does, too.
  • Why did you even think to create this model? Some new “systems” are just wild guesses, and sometimes it’s even possible to find one that appears to have a significant correlation with reality. What was the rationale that prompted you to combine ISS, age, blood, and GCS? Did your clinical experience suggest this? Papers on related prediction systems? Then what?
  • Is validating your test data using other patients from the same dataset legitimate? Shouldn’t they be very similar since they are in the same 2-years of data? This could make the system less accurate when applied to a very different patient cohort.
  • The GCS range studied was very high and narrow. If I read the abstract correctly, the median was 14-ish with a range from 12-15. These are mostly mild TBIs, so why were they dying anyway? And if the formula for GTOS was derived using predominantly mild TBI data, how can it possibly work well for moderate and severe? And I still worry that patients were dying of problems unrelated to TBI.
  • Make sure you clearly explain your methods to the audience. Some are not well versed in ROC curves, and many will not understand the nuances and potential pitfalls of developing and validating numerical systems like this. It’s easy to lose them, so make sure you are clear and concise in your explanations.
  • How do you see a system like this being used in the future? It’s nice to have some appreciation of the practicality, and an assurance that this isn’t just an academic exercise.

I enjoyed the abstract, and look forward to hearing it in person next month!

Reference: The Brain Trauma Outcome Score (BTOS): Estimating mortality after a traumatic brain injury. EAST 2019, Paper #6.

Head

Everything You Wanted To Know About: Cranial Bone Flaps

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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.

CNS, Head

Sports Drinks And Electrolyte Replacement In TBI

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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.

CNS, Head

Targeted Hypernatremia In Trauma Brain Injury: Does This Work?

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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.