Tag Archives: TBI

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. 

Is Intubation For Low GCS Necessary? Dangerous?

More dogma? I was taught that as the Glasgow Coma Scale (GCS) score drops toward 8, the higher the consideration of intubating the patient. And that a GCS 8 was pretty much an absolute indication for inserting the endotracheal tube. The rationale was that the more obtunded the patient was, the less able they were to protect their airway.

Even ATLS, our trauma textbooks, and practice guidelines from the likes of EAST recommend intubation for GCS 8 and less.

Having said that, I know many of you have been in a situation where you have a patient with GCS 8 or so, and they are lying there breathing peacefully with good oxygenation and ventilation. Do you really need to put in that tube? And we also tend to be very forgiving with obtunded children, avoiding premature intubation there as well.

Intubation is not a benign procedure. There is the potential for mayhem during the process, ICU admission will be required, and a host of ventilator and sedation-related complications are possible once the patient arrives there.

The trauma group at LAC + USC decided to look into this. They performed a five-year retrospective study of data from the TQIP database. A subset of patients was selected with isolated blunt head injury and GCS 7-8 who did not require immediate operation upon arrival. They were divided into intubation and non-intubation groups, and these were further subdivided into intubation within an hour of arrival, intubation after an hour, and never intubated groups.

Here are the factoids:

  • A total of 2,727 patients were studied; about two thirds were intubated within an hour, a quarter were never intubated, and the remaining 9% were intubated after the first hour
  • Immediately intubated patients were significantly younger and had fewer comorbidities
  • Mortality was 19% in the immediate intubation group vs 27% in the delayed group vs 11% in the never intubated group
  • Complications were significantly higher after immediate intubation, particularly DVT and ventilator associated pneumonia (VAP)
  • Regression analysis indicated that immediate intubation was independently associated with mortality compared to late or never intubated patients
  • Using additional regression testing, the authors concluded that the following two subsets of patients would benefit most from early intubation:
    • Younger patients (age < 45) with head AIS 5
    • Patients age <65 with head AIS 5

The authors recommend that “future research focus on more adequate parameters to identify patients requiring immediate intubation and should avoid an isolated fixed GCS threshold.”

Bottom line: This is a difficult paper to understand (at least for me). It looks like the authors are saying we should avoid immediate intubation of severe TBI patients with depressed GCS to reduce mortality and complications.

But you need to read the whole paper closely to really get it. First, let’s look at those mortality figures. The mortality in the three groups was:

  • intubated < 1 hour after arrival – 18.7% (from n = 1,866)
  • intubated > 1 hour after arrival – 27.4% (from n = 223)
  • never intubated – 11.4% (from n = 638)
  • If you combine the last two lines you get the mortality in the non-immediate intubations = 15.5% (from n = 861)

The authors then claim that the mortality for immediate intubation is greater than non-immediate intubation (the other two groups). This may be somewhat misleading, because the delayed intubation group actually has a higher mortality than the immediate group (27%)! This fact is covered up by combining delayed intubation with the never intubated group, bringing the number down to 15.5%!! Why shouldn’t you say that intubating the patient at any time is bad, immediate or delayed??

They suggest some criteria to try to focus in on the patients who really need intubation: younger patients (age < 45 or < 65) with head AIS 5 and GCS 7. Unfortunately, you can’t determine which patients have an AIS 5 in their head without a head CT, which may push them into the higher mortality delayed intubation group.

Remember, this type of study can only show an association, not cause and effect. The authors suggest that early intubation results in more deaths and complications. My suspicion is that patients with severe TBI don’t do poorly because they were intubated. I believe that they were intubated because the clinicians feared that they would do poorly. Unfortunately, this is information that can only be gleaned from a prospective study, not a retrospective database review.  And no amount of statistical manipulation or regression analysis can make up for this shortcoming.

This is yet another one of those studies that ends by concluding that a better study should be done. That would be okay if this one actually provided a hint that the endeavor would be worthwhile. But it doesn’t. I didn’t really learn anything from it, unfortunately.

So I still heartily recommend using your existing training, guidelines, and judgement to intubate these patients early and safely!

Reference: Isolated traumatic brain injury: Routine intubation for GCS 7 or 8 may be harmful! J Trauma, publish ahead of print, DOI: 10.1097/TA.0000000000003123, Feb 16, 2021.

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.

Best Of AAST #4: TBI and Antiplatelet / Antithrombotic Agents

More and more people are taking antiplatelet or antithrombotic agents for a variety of medical conditions. One of the dreaded side effects of these medications is undesirable bleeding, particularly after injury. This is especially true if the bleeding occurs inside the skull after any kind of head trauma.

Which agents, if any, lead to worse outcomes? The literature has been a bit inconsistent over the past 10 years. A group from HCA Healthcare reviewed the trauma registries from 90 hospitals, which I presume are in the HCA system. They included patients patients who suffered a ground level fall and were 65 years or older. They excluded those who had a significant injury to regions other than the head.

Here are the factoids:

  • Over, 33,000 patient records were reviewed, with an average age of 81
  • Nearly half were on single or multiple anti-thrombotic therapy (!)
  • The proportion of patients sustaining a “TBI” was roughly the same (21%) whether they were not on anti-thrombotic therapy or not
  • Apixaban and rivaroxiban were associated with lower rates of “TBI” (13-16%)
  • Clopidogrel was associated with a higher “TBI” rate (23%)
  • Patients requiring brain surgery  were more common in patients taking aspirin plus clopidogrel (2.9%) vs all the others (2%) and this was statistically significant
  • None of the treatment regimens were associated with higher mortality (roughly 2-3%)

The authors conclude that anti-thrombotic use in the elderly who suffer a ground level fall are not at risk for increased mortality and that they may have negligible impact on management.

My comments: The one thing that makes this abstract difficult to read is their use of the term TBI, which is why I put it in quotes above. I think that the authors are conflating this acronym with intracranial hemorrhage. It’s a bit confusing, because I think of TBI as a term that means the head was struck and either left a physical mark (bump on the outside or blood on the inside) or there was known or suspected loss of consciousness. They are apparently using  it to describe intracranial bleeding seen on CT.

And because this is a registry study, many of the patient-specific outcome details cannot be analyzed. Mortality and operative rates are very crude outcomes. What about some of the softer ones? Although the average GCS was stated to be 14.5, it would be interesting to know how many of these patients were able to return to their previous living situation, and how many were significantly impaired even though they didn’t die or need an operation.

Here are my questions for the presenter and authors:

  • How do you define a TBI in this study? Could it be just a concussion? Does it require some type of blood in the head? Assuming that there are lots of TBIs that occur without intracranial bleeding, including such patients in your analyses will skew the data toward lower incidence and will dilute out the patients with hemorrhage.
  • What was the length of your study? If it includes data that is older than six years or so, it may under-represent the use of some of the direct oral anticoagulant drugs (DOACs).
  • Are half of your elderly falls patients really on anti-thrombotic therapy? This is a shocking number, and seems to be high in my experience. Since your study was distributed across a large number of hospitals, it brings up the question of whether so many of our elders really need this medication.
  • Do you have any sense for how your various subgroups fared in terms of their discharge disposition? You conclude that the use of anti-thrombotic agents isn’t so bad, really. At least when it comes to needing brain surgery or dying. But are there other cognitive issues that are common that might encourage trauma professionals to continue to look at these drugs with a wary eye?

This is important work, and I am anticipating a great discussion after your presentation.

Reference: Antiplatelet and antiplatelet agents, alone and in combination, have minimal impact on traumatic brain injury (TBI) incidence, need for surgery, and mortality in ground level falls (GLFs): a multi-institutional analysis of 33,710 patients. AAST 2020 Oral Abstract # 7.

Best Practices For TBI Patients On Oral Anticoagulants: Part 4

In my last post, I started reviewing the anticoagulant reversal section of the Austrian consensus statement on TBI patients taking anticoagulants. Due to its length, I covered only anti-platelet agents. Today I’ll discuss their findings on reversing  Vitamin K antagonists.

Q1. Should Vitamin K antagonists (VKAs) be reversed in case of hemorrhagic TBI?

Answer: That’s simple. Yes!

Q2. Should Vitamin K be administered to reverse the effects of VKAs?

Answer: Yes, as an adjunct to other reversal agents. The usual dose is 5-10mg IV.

Adjuncts must always be used, because Vitamin K only enables the liver to produce factors II, VII, IX, and X. This is not an immediate process, and may take up to 24 hours for the INR to fall to reasonable levels. Additional treatment is needed to raise these factor levels quickly.

Q3. Should prothrombin complex concentrate (PCC) and/or plasma be used for reversal of VKAs?

Answer: Four-factor PCC is the treatment of choice, and is preferred over plasma. 

Reversal of VKAs with plasma requires administration of large volumes, and each unit is given over one to two hours. This results in a slower correction when compared to PCC, which occurs in less than 30 minutes. And many elderly patients with comorbidities cannot tolerate the colloid volume administered with multiple units of plasma. Multiple studies have shown that patients treated with PCC achieve their target INR significantly faster and have less hematoma progression than those treated with plasma.

Q4. Should recombinant activated factor VII (rFVIIa) be used for reversal of VKAs?

Answer: No.

This drug was the darling in trauma care around the turn of the century, but has since fallen into disuse. The few studies available show that there may be INR rebound and more frequent hematoma expansion compared to PCC.

Next post: Recommendations for reversal of DOACs.

Reference: Diagnostic and therapeutic approach in adult patients with traumatic brain injury receiving oral anticoagulant therapy: an Austrian interdisciplinary consensus statement. Crit Care 23:62, 2019.