IVC Filters: Another Nail In The Coffin?

IVC filter insertion has been one of our tools for preventing pulmonary embolism for decades. Or so we thought. Its popularity has swung back and forth over the years, and has been in the waning stage now quite some time. This pendulum like motion offers an opportunity to study effectiveness when coupled with some of the large datasets that are now available to us.

IVC filters have been used in two ways: prophylactically in patients at high risk for pulmonary embolism (PE) who cannot be anticoagulated for some reason, and therapeutically once a patient has already suffered one. Over the years, guidelines have changed, and have frequently been in conflict. Currently, the American College of Chest Physicians does not recommend IVC filters in trauma patients, while the Eastern Association for the Surgery of Trauma promote their use in certain subsets.

A Pennsylvania group performed a large, retrospective review of three databases, the  Pennsylvania Trauma Outcome Study (462K patients), the National Trauma Data Bank (5.8M patients), and the National Inpatient Sample. All were patients with an emergent trauma-related admission.

Here are the most interesting factoids:

  • About 2% of all patients underwent IVC filter insertion, and 94% were inserted prophylactically
  • About 90% of patients with a prophylactic filter had at least one predictor for PE, which means that the remaining 10% had none (!)
  • Conversely, about 86% of patients who developed a PE had at least one risk factor, meaning that 14% had no recognized risk factors (!!)
  • The use of IVC filters peaked in 2006-2008 at 2-4%, then falling steadily over the following 5-7 years to less than 1%
  • PE rates peaked in 2008, then declined by 30% in the PTOS sample and stayed steady in the NTDB

Bottom line: The use of IVC filters peaked in 2008 and has been in decline since then. But interestingly, the rates of PE and fatal PE have been steady to declining, depending on the data set. Obviously, there are always some shortcomings for studies like this. Remember, IVC filters are intended to prevent fatal PE. It is possible that some fatal PEs were not identified in these databases. Furthermore, it was not possible to obtain any information on the use of chemical prophylaxis in these patients. 

Overall, there has been no increase in PE and fatal PE rates over the time period that IVC filter usage has been decreasing. This suggests that these devices have not had their intended effect. Trauma professionals need to very seriously consider the specific indications in any patient they are considering for insertion. They may not have the protective effect you think.

Related posts:

Reference: Vena Cava Filter Use in Trauma and Rates of Pulmonary Embolism, 2003-2015. JAMA Surg 152(8):724-732, 2017.

The August 2017 Trauma MedEd Newsletter Is Here!

Welcome to the current newsletter. In this one, I’ll be presenting and discussing some of the “Laws of Trauma” that I’ve observed over the years. I think you’ll find them interesting and amusing, and hopefully valuable. As a bonus, I’ll also include a copy of Norm McSwain’s Rules of Patient Care. Enjoy!

To download the current issue, just click here! Or copy this link into your browser: http://bit.ly/TME201708.

The “Egg Timer” Injury

Most patients with major traumatic injuries are handled in a very systematic way by both EMS and trauma centers. We have routines and protocols designed to provide rapid, quality care to these individuals. But over the years, I’ve begun to appreciate the fact that there is a very small subset of these patients who are different.

I term these patients as having an “egg timer injury”. These are patients who have only a certain number of minutes to live. This fact requires us to change the usual way we do things in order to save their lives or limbs. The usual routine may be too slow.

And unfortunately, no one can tell us exactly how many minutes are left on the timer. We only know that it’s ticking. Here are some examples of such  injuries:

  • Pericardial tamponade
  • Penetrating injury to the torso with profound hypotension
  • Orbital compartment syndrome

In each case, speed is of the essence. What can we do to decrease the time to definitive intervention? For prehospital providers, you may need to bypass a closer hospital that might not have the necessary resources at a particular time of day. Once at the hospital, the patient may need to bypass the emergency department and proceed straight to the OR. Or you may need to do a lateral canthotomy yourself, rather than waiting for an ophthalmologist to drive in only to have the patient lose their vision because of the  delay.

Bottom line: Remember that protocols are not necessarily etched in stone. They will cover 99.9% of cases you see. But that remaining 0.1%, the patients with the “egg timer injury”, will require you to think through what you know about the patient at the time, and make decisions about their care that may have a huge outcome on their life or livelihood. And as always, if you find that you must do things differently in the best interest of your patient, be sure to document what you knew and your thought processes thoroughly so you explain and/or justify your decision-making when you are invariably asked.

Syncope Workup in Trauma Patients – Updated With CPG

Syncope accounts for 1-2% of all ED visits, and is a factor in some patients with blunt trauma, especially the elderly. If syncope is suspected, a “syncope workup” is frequently ordered. Just what this consists of is poorly defined. Even less understood is how useful the syncope workup really is.

Researchers at Yale retrospectively looked at their experience doing syncope workups in trauma patients. They were interested in seeing what was typically ordered, if it was clinically useful, and if it impacted length of stay.

A total of 14% of trauma patients had syncope as a possible contributor to their injury. The investigators found that the following tests were typically ordered in these patients:

  • Carotid ultrasound (96%)
  • 2D Echo (96%)
  • Cardiac enzymes (81%)
  • Cardiology consult (23%)
  • Neurology consult (11%)
  • EEG (7%)
  • MRI (6%)

Most of this testing was normal. About 3% of cardiac enzymes were abnormal, as were 5% of carotid imaging and 4% of echocardiograms.

Important! Of the patients who underwent an intervention after workup, 69% could have been identified based on history, physical exam, or EKG and did not depend on any of the other diagnostic tests.

Is it possible to determine a subset of this population that may show a higher yield for this screening? Surgeons at Temple University in Philadelphia found that there was little utility in using carotid duplex studies. They did note that patients with a history of heart disease were more likely to have an abnormal EKG, and that an abnormal EKG predicted an abnormal echo. Overall, only patients with a history of significant cardiac comorbidity, older age, and higher ISS had findings requiring intervention.

Bottom line: Don’t just reflexively order a syncope workup when there is a question of this problem. Think about it first, because the majority of these studies are nonproductive. They are not needed routinely in trauma patients with “syncope” as a contributing factor.  Obtain a good cardiac history, and if indicated, order an EKG and go from there. See the practice guideline proposed by the Temple group below. And be sure to include the patients primary doctor in the loop!

References:

  1. Routine or protocol evaluation of trauma patients with suspected syncope is unnecessary. J Trauma 70(2):428-432, 2011.
  2. Syncope workup: Greater yield in select trauma population. Intl J Surg, accepted for publication June 27, 2017.

Is Fine-Tuning Lovenox Dosage Using Anti-Factor Xa Worthwhile?

Deep venous thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous thromboembolism (VTE), are major concerns in all hospitalized patients. A whole infrastructure has been developed to stratify risk, monitor for the presence of, and provide prophylactic and/or therapeutic drugs for treatment. But if you critically look at the literature from the past 20 years or so, we have not made much progress.

One of the newer additions to our arsenal has been to figure a way to determine the “optimal” dose of enoxaparin. Three options are now available: weight-based dosing, confirmation by thormboelastography (TEG), and anti-factor Xa assay. Let’s look at another paper that focuses on the last item.

Anti-factor Xa levels provide a way to monitor low molecular weight heparin activity. A number of papers published have sought to determine a level that predicts adequate activity. Although they are not of the greatest size or quality, a range of 0.2-0.4 IU/ml seems to be the consensus.

A large number of patients at a busy Level I trauma center were retrospectively studied to see if achieving a peak anti-factor Xa level of at least 0.2 IU/ml would result in less VTE. All patients were started on enoxaparin 30mg SQ bid within 48 hours of admission. Anti-factor Xa was measured 4 hours after the third dose. If the level was less than 0.2 IU/ml, the dose was increased by 10mg per dose. The cycle was repeated until anti-factor Xa was therapeutic.

Here are the factoids:

  •  All patients with a Greenfield Risk Assessment Profile (RAP) of 10 or more (high risk) were included; duplex ultrasound surveillance for lower extremity DVT was performed weekly
  • 194 patients were included, with an average RAP of 9 and ISS of 23 (hurt!)
  • Overall VTE rate was 7.4%, with 10 DVT and 5 PE (!)
  • Median time to diagnosis was 14 days
  • Initial anti-factor Xa levels were therapeutic in only one third of patients, and another 20% reached it after dose increases. 47% never achieved the desired level, even on 60mg bid dosing.
  • There was no difference in DVT, PE, or VTE rates in patients who did vs did not achieve the goal anti-factor Xa level
  • Injury severity and obesity correlated with inability to reach the desired anti-factor Xa level

Bottom line: In this study, achieving or not achieving the goal anti-factor Xa level made no difference whether the patient developed VTE or not. And it was difficult to achieve anyway; only about half ever made it to the desired level. How can this happen?

Well, there are still many things we don’t understand about the genesis of VTE. There are probably genetic factors in every patient that modify their propensity to develop it after trauma. And there are certainly additional mechanisms at play which we do not yet understand. 

For now, we will continue to struggle, adhering to our existing protocols until we can figure out the real reason(s) VTE happens, the best ways to prevent, and the best methods to treat.

Related posts:

Reference: Relation of Antifactor-Xa peak levels and venous thromboembolism after trauma. J Trauma accepted for publication Aug 2, 2017.

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