All posts by The Trauma Pro

Best of AAST 2022 #1: The Trauma-Specific Frailty Index (TSFI)

Let’s start with the paper that is kicking off the 81st Annual Meeting for the AAST. Everyone recognizes that many of our elderly patients don’t do well after trauma. Unfortunately, elderly is a very imprecise term. According to the TRISS method for predicting mortality it begins at age 55. But we have all seen many patients younger than that who appear much older physiologically. And a few older ones who are in excellent condition.

How can we determine who is frail and thus more likely to develop complications or even die after injury? The trauma group at the University of Arizona – Tucson published their original paper on a 50-variable frailty index in 2014 in order to address this issue. Unfortunately, 50 variables were found to be very unwieldy, which vastly decreased its usability.

They immediately decided to strip it down to the most significant 15 variables, and named it the Trauma-Specific Frailty Index. This tool simply predicted whether the patient would have a favorable discharge (home), or an unfavorable one (skilled nursing facility or death). The TSFI was very good at this, and was far better than using age alone.

The authors rolled the TFSI out to the AAST multi-institutional study group. A total of 17 Level I and II trauma centers participated in a three-year prospective, observational study. All patients with age > 65 had their TFSI calculated. They were stratified into three groups, including non-frail, pre-frail, and frail. The outcomes studied were expanded and included mortality, complications, discharge status, and 3 month status for readmission, falls, complications, and death.

Here are the factoids:

  • A total of 1,321 patients were enrolled across all centers with a mean age of 77 and median ISS 9
  • A third each were classified as non-frail, pre-frail, and frail
  • The overall study group had a 5% mortality, 14% complication rate, and 42% unfavorable discharge rate
  • Frail patients had a higher complication rate vs the pre- and non-frail groups (21% vs 14% vs10%) which was significant
  • They also had a higher mortality rate (7% vs 3% vs 4%) with p=0.048 although significant on multivariate analysis
  • Overall, 16% were readmitted within 3 months and 2% died. This was not stratified in the abstract by frailty group.

The authors claim that the TFSI is an independent predictor of worse outcomes, and that it is practical and effective and should be used in the management of geriatric trauma patients.

Comments: I find the concept of the abstract very interesting. I think most of us can identify the obviously frail patients when we see them. The TFSI promises more objective identification  using 15 variables. For reference, here they are:

  • Comorbidities
    • Cancer history
    • Coronary heart disease
    • Dementia
  • Daily activities
    • Help with grooming
    • Help with managing money
    • Help doing housework
    • Help toileting
    • Help walking
  • Health attitude
    • Feel less useful
    • Feel sad
    • Feel effort to do everything
    • Falls
    • Feel lonely
  • Sexual function
  • Serum albumin

The authors showed that all of the outcomes were significantly and negatively associated with the patient’s frailty index. The analysis appears reasonable, and the numbers are both statistically and clinically significant. 

But the big question now is, how do we use the results? The 15-variable version is reasonably workable. Is it any better than the trauma professional walking into a room and doing a good eyeball test? The study did not look at that. Either way, what can we do when we identify the truly frail patient? What can we alter in the hospital care that might make a difference? Right now, options are limited. Much of what led to the patient’s frailty is water under the bridge due to possibly decades of lifestyle choice or pre-existing disease.

I think that the next step in this train of thought is to start applying specific interventions in patients identified as frail or better yet, pre-frail. Here are my questions for the authors and presenter:

  1. What’s next? You’ve shown that you have a numerical tool that identifies patients who may have a less than desirable outcome. If we implement this, what can we do to try to reduce those undesirable outcomes?

This was thought provoking work, and I am looking forward to the full presentation!

Reference: PROSPECTIVE VALIDATION AND APPLICATION OF THE TRAUMA SPECIFIC FRAILTY INDEX: RESULTS OF AN AAST MULTI-INSTITUTIONAL OBSERVATIONAL TRIAL. AAST 2022 Plenary Paper 1.

It’s AAST Month, 2022!

As many of you are aware, the 81st Annual Meeting of the American Association for the Surgery of Trauma is taking place later this month. Keeping to tradition, I will be analyzing select abstracts that caught my interest over the coming weeks.

As in the past, I’ll analyze what’s available in the short abstract format and provide a bit of background about why it might be important. I will then examine the design and methods and review the results.

Finally, I will provide my own analysis, as well as questions for the authors and presenter that they might encounter at the meeting. In addition to sharing all of this with you, my readers, I always send a message to the authors so they can personally check out the post.

I will get started with an analysis of Oral Paper #1, a multi-center trial using the Trauma Specific Frailty Index.

Fat Embolism Syndrome And Orthopedic Surgery

Regardless of the exact mechanism for the development of fat embolism syndrome, in trauma it most commonly occurs when the medullary (bone marrow) cavity of a long bone is violated. This occurs first when the bone is fractured, and again when it is instrumented for fixation. The initial shower of emboli cannot be prevented. However, ongoing emboli can be reduced with early fixation. This can be in the form of a good splint, or surgical external or internal fixation.

One type of internal fixation, intramedullary (IM) nailing, has been associated with embolism and FES for some time. This technique was introduced 80 years ago and has been refined significantly since. Here is a picture of a femur with an IM nail.

The nail is inserted proximally near the greater trochanter. The marrow cavity is first reamed to make insertion of the nail easier. This causes a number of changes in the physiology of and pressures within the marrow cavity. Pressure increases during the initial reaming, and hits a peak when the reamer enters the distal fragment. Once complete, there are no further increases as the nail is inserted. However, these pressure changes alter medullary blood flow and allow emboli to enter the venous system.

Reaming is actually beneficial in several ways. It simplifies and shortens the surgical procedure. And in animal models there is evidence that bone debris from the reaming process collects at the fracture site, creating an autograft that may improve healing.

A surgical group in Ireland has been using a novel technique for lavaging the marrow cavity during fixation for several years. Once the bone is entered proximally, a cut piece of suction tubing is inserted into the end of the bone. Suction is then applied for 2-3 minutes. The procedure continues, including reaming, then the suction procedure is repeated. Unfortunately, FES is uncommon, so it is difficult to judge whether their technique really works. The authors believe it is safe, but recommend formal studies to prove efficacy.

Use of an additional venting hole between the trochanters has also been studied in a small randomized trial. This allows for drainage of marrow during the reaming process, reducing any pressure rise. The number of embolic events detected using transesophageal echo was significantly reduced in the vented group (20% vs 85% of patients).

Next, prevention and treatment of fat embolism syndrome.

References:

  1. A Simple and Easy Intramedullary Lavage Method to Prevent Embolism During and After Reamed Long Bone Nailing. Cureus 9(8):e1609, Aug 2017.
  2. Relevance of the drainage along the linea aspera for the reduction of fat embolism during cemented total hip arthroplasty. A prospective, randomized clinical trial. Arch Ortho Trauma Surg 119:146, 1999

Diagnosis Of Fat Embolism Syndrome

A number of scoring systems have been developed to identify FES (Gurd’s and Wilson’s criteria, Schonfeld’s criteria, Lindeque’s criteria to name a few). Unfortunately, none of these are helpful. They were developed in the 1980s as part of the authors’ studies on the use of  steroids for treatment, and no one else has taken the time to study their sensitivity and specificity.

Diagnosis of FES is primarily clinical. It relies upon recognition of the principal findings on physical exam, and exclusion of more common conditions that may mimic it.

Here is a template for diagnosing FES:

Is your patient at risk? The vast majority of these patients will have fractures. One, or especially two or more long bone fractures (mostly the femur) are usually present. Other fractures that add risk are those involving the pelvis or bones that contain marrow, such as the ribs and sternum. Patients who have just undergone fracture repair are also at risk and will be discussed in the next section. Finally, patients who have had intraosseous lines placed are also at risk, regardless of the type of infusate.

What signs or symptoms have developed? Skin changes are very suggestive of FES if your patient is at risk. However, rashes are common manifestations of contact allergies, drug reactions, infectious diseases, and many other conditions. If those are ruled out, then the presence of risk factors plus a rash is sufficient to make the diagnosis.

Mental status changes are more difficult to pin on FES, even though it is a more common initial presentation than the rash. Since this is a trauma patient, you must rule out delayed manifestations of head trauma. Urgent CT of the head is required to do so. And typically, there will be no specific findings that point to FES. It is always a diagnosis of exclusion.

Pulmonary dysfunction requires a search for the usual suspects. A good physical examination of the chest coupled with a chest x-ray will help identify pneumothorax, hemothorax, or pneumonia. A chest CT may be indicated if pulmonary embolism is suspected.

Once other more common clinical problems have been eliminated, you are left with the diagnosis of FES. There are no specific lab tests to draw, and more invasive studies are neither helpful nor indicated. Fat embolism syndrome is a diagnosis of exclusion.

Next, the relationship of fat embolism and orthopedic surgery.

Clinical Manifestations Of Fat Embolism Syndrome

There are three organ systems that are classically involved in FES: pulmonary, CNS, and skin. Manifestations generally begin between 24 and 72 hours after injury. In rare cases, symptoms can begin within 12 hours. In my experience, these tend to be the ones that become the most severe and are frequently life-threatening.

Pulmonary (95% of cases): This is the most common manifestation of FES, and may occur without other signs and symptoms. Nearly all patients develop some degree of hypoxia. Progressive tachypnea and mild tachycardia may provide the first clinical clue if oxygen saturation is not being monitored.

Chest x-ray is usually unremarkable early on. And once the syndrome has developed, it is generally not helpful. CT scan is useful for defining the extent of pulmonary injury, but lags the clinical picture by several days. Findings are non-specific, usually consisting of small, ground-glass opacities in the periphery.

In the example above, the opacities are very small and difficult to see.

But they’re a little more obvious here!

Other CT findings include small pulmonary nodules in the upper lobes or along peripheral pulmonary vessels. These are thought to be areas of obstruction caused by the emboli. Nonspecific pleural effusions may be seen, and bronchial thickening has also been described. Rarely, fat globules may be seen in the lower extremity veins or IVC, and should immediately raise suspicion for developing FES even before symptoms develop.

CNS (60% of cases): If they occur, CNS changes generally crop up after the pulmonary manifestations begin. Generally, they start as mild confusion, but can progress to decreasing level of consciousness and even coma. Focal neurologic deficits are occasionally seen, and seizures can occur.

The actual mechanism behind this appears to be very similar to the skin changes which will be described in the next section. Emboli occur in vessels predominantly in the white matter of the brain. This leads to petechial hemorrhages, which are likely due to the inflammatory mechanisms previously described.

Note the numerous dark petechiae visible in the white matter in this specimen.

Retinal exam can also show evidence of fat embolism. Fat globules may actually be seen in the retinal vessels early.

Note the fat globules at the 9:30 and 2:00 positions to the optic nerve in the image above.

Skin (33% of cases): The most recognizable sign of FES is the petechial skin rash. This rash usually involves the torso, and axillary petechiae are very common. It can spread to involve the head and neck, and occasionally the extremities. Subconjunctival hemorrhages are sometimes seen. The rash tends to be transient and usually lasts only a few days. Here is an example of the classic petechial rash.

Other findings: Fat globules may be found in the urine in patients with FES. However, they are commonly present in patients with long bone fractures, so their presence is not helpful or predictive. Nonspecific findings such as fever, leukocytosis, anemia, and thrombocytosis are also relatively common. In severe cases, cardiac dysfunction, hypotension, and peripheral hypoperfusion can occur. I have personally seen necrosis of fingers and toes from a very severe case.

Unfortunately, the “classic” triad of mental status changes, skin rash, and pulmonary insufficiency are seen in only a small minority of patients. Typically, only one or two signs and symptoms appear at the same time, making diagnosis a bit challenging.

In the next post, making the diagnosis of fat embolism syndrome.