Tag Archives: TBI

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.

Abstracts, Head

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

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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.

Practice guidelines

Best Practices For TBI Patients On Oral Anticoagulants: Part 4

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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.

Practice guidelines

Best Practices For TBI Patients On Oral Anticoagulants: Part 3

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My last post covered coagulation tests for oral anticoagulants and antiplatelet agents, as well as target levels of reversal. Today, I’ll share more of the Austrian consensus paper on actual reversal of anticoagulants. I’ll also add a little commentary to some of the answers.

This is a lengthy section in the paper, so I’ll split it into antiplatelet agents today, the vitamin K antagonists tomorrow, and the direct oral anticoagulants (DOACs) after that.

Q1. Should desmopressin (DDAVP) be administered to reverse the effect of platelet inhibitors?

Answer: No recommendation. (My answer: no)

DDAVP accelerates platelet adhesion. Very few papers have looked at using DDAVP in patients with platelet inhibition, and those that did had low numbers of subjects. The only positive study showed a reduction in hematoma of only 0.5 cc (in hemorrhagic stroke patients, by the way, not trauma). This is not clinically significant. It is likely that the nonfunctional platelets do not really respond to DDAVP, so this drug is not very useful.

Q2. Should TXA be used in patients receiving platelet inhibitors?

Answer: No recommendation. (My answer: no)

There are few, if any, studies that address this. A CRASH-2 subset with TBI showed no significant difference in intracranial hematoma size after TXA. Only one very small (80 patient) study showed a decreased total hematoma after TXA administration (2cc vs 4cc). I’m not sure how clinically significant this is. CRASH-3 did not address it. Overall there is too little data to make a decision regarding this one. It’s value, if any, is very subtle.

Q3. Should platelet concentrate be administered to reverse the effect of platelet inhibitors?

Answer: No

There are no studies that have shown any clear benefit to giving units of platelets to these patients. And a meta-analysis showed no survival benefit. Giving platelets sounds like a good idea, but remember that the drug that poisoned the patient’s platelets is still circulating. It can and does poison the new platelets as well. So adding more platelets that are destined to stop functioning doesn’t seem like a good idea.

In my next post, I’ll dig into the recommendations for reversing Vitamin K antagonists (warfarin).

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.

Practice guidelines

Best Practices For TBI Patients On Oral Anticoagulants: Part 2

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In my previous post, I reviewed recommendations from an Austrian consensus panel addressing patients with TBI on anticoagulants of various types. In this one, I’ll share their statements on coagulation tests and target levels for reversal of the different agents.

Q1. Are platelet function tests capable of detecting and/or ruling out the presence of a platelet inhibitor?

Answer: The three commonly used tests (PFA, Multiplate, and VerifyNow) can detect or rule out the presence of these drugs.

They can also determine whether the amount of platelet inhibition is within therapeutic range for the drug. But they cannot predict if someone with high inhibition will actually bleed, or if a patient with low inhibition will not. And knowing that they have a platelet inhibitor on board probably doesn’t help much because there is not much we can do to reverse them (see next post).

Q2. What is the goal INR after reversing Vitamin K antagonists?

Answer: The INR target value should be < 1.5

This recommendation is not supported by great data. We know that as INR rises above 2, the odds of bleeding in TBI increases by 2.6x. But we don’t now exactly how low it needs to be to ensure no more bleeding occurs. And this probably depends on what is actually bleeding. A subarachnoid hemorrhage probably wouldn’t bleed much at any reasonable INR. A subdural (torn bridging veins) is more likely to at lower INR values. And an epidural (middle meningeal artery laceration) remains at high risk at any INR.

Using related literature, the goal INR is all over the place. So choose a number somewhere around 1.5 and use it. And remember, 4-factor prothrombin complex concentrate (PCC) can bring the INR down below that level, but plasma cannot (see my post What’s The INR Of FFP?)

Q3. Should I use standard coagulation tests (PT, PTT) to detect or rule out direct oral anticoulants (DOACs)

Answer: No

Standard assays like PT and PTT are unreliable with these drugs.

Q4. What test can be used to rule out the direct thrombin inhibitor dabigatran?

Answer: A negative thrombin time (TT) rules out any residual dabigatran anticoagulation.

Of course, this assumes that you know the patient is taking it!

Q5. What test should be used to rule out Factor Xa inhibitors?

Answer: Measuring anti-Factor Xa levels can rule these agents out if calibrated to low molecular weight heparin or the particular -xaban in use.

The major problem is that this is a very specialized test and is not available at all hospitals or at all hours. And it takes some time to run. So the practical answer is really “none.”

In my next post, I’ll review the panel’s recommendations for actual reversal of the various anticoagulant medications.

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.