All posts by TheTraumaPro

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.

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.

Best Practices For TBI Patients On Oral Anticoagulants: Part 1

Over the past five years, there has been a tremendous increase in the number of patients presenting to hospitals with traumatic brain injury. The bulk of these injuries occur in the elderly, and a rapidly growing number of them are taking anticoagulants for management of their medical comorbidities. Although there is a growing body of literature addressing this issue, many practical questions remained unanswered. This is due to the lack of randomized controlled studies of the clinical problems involved. And given the ethical issues of obtaining consent for them, there likely never will be.

An interdisciplinary group of Austrian experts was convened last year to consider the most common questions asked about TBI and concomitant anticoagulant use. They reviewed the existing literature from 2007 to 2018 and combined it with their own expertise to construct some initial answers to those questions.

Over the course of my next few posts, I’ll dig into each of the questions and review their suggested answers. And remember, all these Q&A apply to patients with known/suspected TBI with known/suspected oral anticoagulant use.

Let’s start with some diagnosis questions.

Q1. Should head CT be performed in all patients with known or suspected TBI and suspected or known use of anticoagulants?

Answer: All patients with TBI and potential or known use of anticoagulants should undergo an initial screening CT scan of the head.

A number of systems that predict the utility of head CT already exist (e.g. Canadian head CT rules). However, they do not and cannot take into account the various permutations of drugs and other medical conditions that may influence coagulation status. Vitamin K antagonists (VKA) like warfarin have been clearly shown to increase mortality after TBI. Data involving the use of anti-platelet agents or direct oral anticoagulants (DOAC) are a bit less clear.

Q2. Should a repeat head CT scan be repeated in these patients, and if so, when?

Answer: Patients with intracranial hemorrhage on their initial scan should have a repeat within 6-24 hours, based on the location of the bleed.

The natural course of patients who have an identified intracranial hemorrhage is extremely unpredictable. For that reason, a repeat scan is suggested. However, there are no consistent data that would indicate when this should occur. Indications and potential for progression vary by type of bleed (subarachnoid, subdural, epidural, intraparenchymal). Thus, you must work with your neurosurgeons to arrive at a reasonable repeat interval, and it may be different for a high-risk location (epidural) vs one with low risk (subarachnoid).

Q3. Should a patient with an initial head CT that is negative be admitted for neurologic monitoring?

Answer: Patients taking only aspirin with GCS 15 and initially negative head CT may be discharged. All other patients should be admitted for at least 24 hours for neurologic monitoring as follows (q1 hr x 4 hrs, q2 hr x 8 hrs, q4 hr x 12 hrs). Repeat head CT is indicated if there is any deterioration in neurologic exam.

Multiple papers have described the occurrence of delayed intracranial hemorrhage in patients taking oral anticoagulants other than aspirin. Although some bleeds may develop days or weeks after the initial injury, the majority occur during the first 24 hours. Routine repeat head CT in this group of patients with an initially negative scan has not been found to be helpful.

Q4. What about patients with an initially negative head CT who cannot be examined neurologically (intubation, sedation, dementia)?

Answer: Unexaminable patients should undergo a repeat head CT within 6-24 hours based on the underlying risk factors for development of delayed hemorrhage.

There is no real literature on this topic, but this statement makes sense. Each center should pick a reasonable time interval and include it in their own practice guideline.

In my next post, I’ll review the panel’s recommendations on coagulation tests and target levels for reversal of the various classes of anticoagulants.

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.

Does Chest Tube Size Matter? Part 3

So far, I’ve looked at the only two papers in the trauma literature that examine the question of chest tube size for hemothorax. As you may recall, both were woefully underpowered. Finding no difference in a study without enough subjects does not infer that the two interventions have the same results. It simply means that a (much) better study needs to be done.

One of these papers admitted that more work needed to be done, the other did not. And the one that admitted no weaknesses has been quoted by some of the pigtail catheter studies I am reviewing this week as supporting their hypothesis. They are using it as the rationale that even small catheters might work. Hmm, faulty premises?

After reviewing the pigtail for hemothorax literature since the beginning of time, I found exactly two papers that address the issue. And really, it’s just one. The first one published in 2012 was the initial series. The numbers were expanded over the following years by the same authors, and the new data was published in 2017. Of interest, the authors cite their own early paper as supporting the effectiveness of using a pigtail catheter, even though it can’t due to very low numbers Let’s dig in.

This one comes from the group a the University of Arizona in Tucson. They prospectively collected data on pigtail catheter insertions from 2008 to 2014. The outcomes studied included initial drainage output, catheter complications, and failure rate (incomplete drainage requiring another intervention).

Tubes and pigtails were placed by attending physicians or residents. Patient selection was at the discretion of the attending surgeon. The total patient group was analyzed, and then it was split into emergent placement vs non-emergent placement. Here are the factoids:

  • A total of 307 chest tubes and 189 pigtails were placed; pigtail usage increased over the study period
  • Pigtail catheter patients were older overall, especially in the non-emergent group (this was admitted as selection bias in the paper)
  • Initial output was higher in the pigtail group and reached statistical significance in the emergent placement group (500 cc vs 250 cc)
  • Pigtail insertion complications trended higher for all patients and in the non-emergent group, but not in the emergent placement group (??)
  • Failure rates were not different across the groups

The authors state the their study “clearly demonstrates favorable outcomes in pigtail catheter usage.” But does it?

Bottom line: Once again, this is a completely underpowered study. The pigtail results would need to be 2-3 times better than chest tube results to show any statistical significance. But they are not. So being non-inferior doesn’t mean anything with such small numbers. However, if you properly power a study that shows no differences, then they truly are equivalent. But with the work available to date, you can’t just run out and start using pigtails because they are “as good as” chest tubes. 

There were a few statistically significant differences in this study, but again this is clouded by other design problems. The emergent group had significantly more initial output through the pigtails. This is odd from a fluid dynamics point of view. How do you get more of a thick liquid to drain from a tiny tube? 

One potential explanation is the ability to more accurately measure the initial output in the pigtail group. When a chest tube is inserted, there is frequently some blood loss on the bed which is difficult to estimate. But when a pigtail is inserted there is almost never any leakage. It all comes out through the tube. Could the excess pigtail drainage be accounted for by external loss during chest tube placement?

The real bottom line: There are a grand total of three published papers in the past seven years that have tried to deal with tube size in traumatic hemothorax. All of them are completely underpowered and rely on the lack of significant differences to tout that they are equivalent. The real answer is: we don’t know. This is certainly not the quality of data you want to use to change your practice. We don’t know for sure if smaller tubes and pigtails result in more retained hemothoraces or followup procedures. So buyer beware! If you choose to use small tubes or pigtails in your patients, you are in uncharted territory. The first author of the 2012 small tube paper even stated that a larger multi-center is needed. I completely agree! Meanwhile, I’ll stick to big (36 Fr) and bigger (40 Fr) for hemothorax.

Reference: A Prospective Study of 7-Year Experience Using Percutaneous 14-French Pigtail Catheters for Traumatic Hemothorax / Hemopneumothorax at a Level-1 Trauma Center: Size Still Does Not Matter. World J Surg 42(1):107-113, 2012.

Does Chest Tube Size Matter? Part 2

In my last post, I reviewed a large prospective series comparing smaller (28-32 Fr) to larger (36-40 Fr) chest tubes for management of pneumothorax. The authors did not detect any significant difference because the study was underpowered given the incidence of the adverse events examined.

Today, I’ve chosen a more recent paper that attempts to do the same thing. Interestingly, it cites the previous paper as a good example showing no differences! This one is from an emergency medicine group in Fukui, Japan. It is a retrospective review of seven years worth of patients who had a chest tube inserted for hemothorax only.

Here are the factoids:

  • Small bore tubes were 20-22 French, and large bore tubes were 28 French (huh?)
  • The tube selection was made (once again) at the discretion of the attending physician
  • Demographics and injury data from the two groups were equal
  • A total of 124 tubes were placed in 116 patients, 68 small bore and 56 large bore
  • Empyema occurred in 1% in each group
  • Retained hemothorax occurred in 2% of small tube patients and 3% of large tube patients
  • An additional tube was placed in 2% of small tube patients and 7% of large tube patients (p = 0.41)
  • Pain was not evaluated

The authors concluded that “emergent insertion of the small-bore tubes had no difference in efficacy of drainage, complications or need for additional invasive procedures.”

Bottom line: Huh? Once again we have an inferior design (retrospective review) and huge potential for selection bias (no criteria or randomization for tube size). But in this case, the tube sizes are very similar! The difference in diameter between a 20 Fr tube and a 28 Fr one is only 2.5mm! Reason #1 for no apparent differences.

For reason #2, look at the sample size. First of all, this hospital placed only 124 tubes in 7 years. That’s a one tube every three weeks. Is there that little chest trauma, or is a chunk of data missing? This sample size is less than half of that in the previous post, so the statistical power is far weaker. Look at the stats above for additional tube placement. A 3.5x change was not even close to being statistically significant. In fact, this sample size would not show a significant difference for retained hemothorax until one group had nearly 8x the number! No wonder the authors assumed there was no difference. The study was not designed in such a way that it could ever show one!

So throw this study in the trash bin, too. I’ll continue my search for a more convincing “size matters” paper in my next post.

And if you think you’ve got one, send it my way so I can have a look!

Reference: Small tube thoracostomy (20-22 Fr) in emergent management of chest trauma. Injury 48(9):1884-1887, 2017.