Category Archives: Practice guidelines

In The Next Trauma MedEd Newsletter: Practice Guidelines

The November issue of the Trauma MedEd newsletter will be sent out soon! It’s chock full of tips and tricks dealing with trauma practice guidelines

This issue is being released over the weekend. If you are already a subscriber, you will receive it automatically. If not and you sign up any time before then, you will receive it, too. Otherwise, you’ll have to wait until it goes out to the general public a week or two later. Click this link right away to sign up now and/or download back issues.

In this issue, get some tips on:

  • The Value Of Practice Guidelines
  • Guidelines vs Protocols
  • Developing Your Own Protocols/Guidelines
  • Anatomy Of A Guideline
  • How To Monitor Your Guidelines
  • Sample Guidelines

As always, this month’s issue will go to all of my subscribers first. If you are not yet one of them, click this link right away to sign up now and/or download back issues.

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New EAST Practice Guideline: Spleen Vaccines After Angioembolization

I am trying to figure out how I missed it! The Eastern Association for the Surgery of Trauma (EAST) snuck a new practice management guideline into the Injury journal last fall. And it desperately tries to answer a question that has been hanging around for several years. Do we vaccinate spleen injury patients who undergo angioembolization or not?

I’ve been pondering this for some time and have reached my own conclusion based on some very old literature. Decades ago, we figured out that removing the spleen significantly affects immune function. Splenectomy patients are known to be more susceptible to encapsulated bacteria like Neisseria meningiditis, Streptococcus pneumoniae, and Haemophilus influenzae. Most trauma centers routinely vaccinate these patients before they are discharged home.

With the more recent emphasis on splenic salvage and nonoperative management of injury to this organ, angioembolization has become commonplace. This technique can be done in two ways: proximal and distal. Proximal embolization blocks the splenic artery, so there is no further blood flow to the spleen through it. Distal embolization (selective or super-selective) strives to block flow to very specific areas of the organ.

Do we need to give the vaccines if we cut off blood flow to pieces of the spleen or the main splenic artery? Based on my appreciation of very old splenectomy and partial splenectomy papers, it looked like we should in some cases. One report showed that splenic protection from encapsulated bacteria required about 50% of the spleen to be present and perfused by the splenic artery. This caveat stems from a time when we would perform a trauma splenectomy, dice the spleen up on the back table, and then implant a bunch of spleen cubes into the mesentery to try to provide some immune protection. Turns out that the pieces lived but didn’t do a damn thing.

My practice, then, has been to look at the fluoro images and estimate how much of the spleen was left. I would order the vaccines if a main splenic artery embolization (proximal) was performed. If a distal embolization were performed, I would eyeball the amount of devascularized spleen and give the vaccines if it looked like more than half was dark. Not very precise, I know.

But what would EAST say? They tried to perform a systematic review and meta-analysis of studies that compared outcomes in splenectomy vs. angioembolization patients. Unfortunately, there isn’t a lot of research material out there. So they settled on looking at papers that analyzed immune function, typically using B-cells, T-cells, and antibodies. The authors performed two comparisons: angioembolization vs. splenectomy and angioembolization vs. control.

Angioembolization vs. Splenectomy

These papers compared embolization patients who may or may not have spleen function to splenectomy patients who definitely have none. Embolization patients had fewer infectious complications during their hospital stay and better immune function using the indirect methods noted above. Unfortunately, the data quality was poor, with a significant risk of bias. There was no stratification of proximal vs. distal embolization. Nevertheless, this suggests that, at least overall, the embolization patients retained immune function.

Angioembolization vs. Controls

What about comparing embolization patients to spleen-injured patients who did not undergo any procedure? They should have normal function. Again, the quality of the very few papers available was low. But overall, there was no difference in immune function between the groups.

Bottom line: The EAST review team conditionally recommended against routine spleen vaccines after angioembolization for spleen injury. They concluded that immune function was maintained, so it should not be necessary.

What, you ask, about patients with proximal splenic embolization? The reality is that this only stops inflow from the splenic artery, and only for a few days or weeks. It may slowly resume over time. And it does nothing to the inflow from the short gastric arteries. Apparently, this is enough to provide immune protection against infection.

Whether this is actually true is open to debate. We have no idea if the numbers of T- and B-cells seen and the antibody titers are actually enough to avoid overwhelming post-splenectomy sepsis. And unfortunately, this condition is so rare that we will never accumulate enough cases to make a definitive statement.

But for now, it is probably okay to forgo the vaccines in patients undergoing angioembolization. Besides, the differing guidelines on which vaccines to use, when to give them, and when to schedule boosters were getting way out of hand! Please keep it simple!

Reference: Vaccination after spleen embolization: a practice management guideline from the Eastern Association for the Surgery of Trauma. Injury 53:3569-3574, 2022.

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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.

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Best Practices For TBI Patients On Oral Anticoagulants: Part 3

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.

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Best Practices For TBI Patients On Oral Anticoagulants: Part 2

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.

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