Category Archives: Complications

Best Of AAST 2022 #11: Trauma And The Gut Microbiome

You know I don’t usually write about animal studies. I’m going to break that rule today to review an abstract that addresses what I think is an under-appreciated contributor to outcomes in trauma. The gut microbiome describes the collection of all genomes from microorganisms found in a particular environment. These genomes include bacteria, viruses, and fungi and can be found on all external surfaces of humans.

And I use the term “external” loosely. It includes the areas of the human body that are obviously exposed to the environment, but also areas where our body is wrapped around yet still separate from the it, such as the aerodigestive tract and vagina.

We are beginning to recognize the importance of the micro-organisms that inhabit these areas. They aid in digestion, fine tune the immune system, and synthesize proteins, amino acids, and vitamins that are essential to our health to name a few key tasks.

Many things can disrupt the microbiome including disease, diet, stress, and antibiotics. Previous work has shown that the microbiome changes throughout the hospital stay after trauma. Beneficial species tend to die out, and the ratio of pathologic vs beneficial species tilts toward the dark side.

The group from the University of Florida studied the effects of trauma and chronic stress in a group of rats to study the impact on the gut microbiome. One group of rats was subjected to a polytrauma model including pulmonary contusion, shock, cecectomy, and femur fractures. Another received the polytrauma treatment plus two hours of restraint stress daily. These groups were compared to an untreated control group. Gut flora were measured at baseline and on days 3 and 7.

Here are the factoids:

  • As expected, the microbiomes were similar across all groups at baseline
  • Polytrauma caused a significant change in bacterial diversity at both days 3 and 7 with both Bacteroides and Enterococcus prevalent
  • Polytrauma plus stress also depleted “good bacteria” and was associated with a switch to predominantly Enterococcus colonization

The authors suggested that the observed transitions to a pathologic microbiome may influence outcomes after severe trauma and critical illness.

Bottom line: I wanted to highlight this simple study because it relates to a similar topic that is exploding in the clinical nutrition field. The gut microbiome is being recognized as a key element of our overall health. However, it is very sensitive to external events and can be “knocked out of whack” by stress, trauma, bad diet, and even a single dose of antibiotics. Its derangement is recognized as a major factor in the development of C Difficile colitis.

This simple little rat study confirms that major trauma and stress negatively impact the animals’ microbiome. It did not examine outcomes, so no associations can be made here. Any such associations would not be directly applicable to humans, anyway. But it should serve to stimulate some thought and additional human studies to continue investigation in this field.

I have been struck by how we mistreat the gut microbiome in hospitalized patients through my own clinical observations over the years. A short course of antibiotics has been shown to severely impact the diversity of gut flora within days, and may require a year or more to recover back to baseline.

Extended fasting exhausts the food supply for the bacteria which may lead to the use of the gut lining for food, creating additional pathology. The composition of the nutritional supplements used in hospital are formulated from cheap ingredients which have been shown to disrupt the microbiome. Then add on trauma and chronic stress. It’s a terrible combination, yet we see it every day in hospitalized patients!

I predict that we will learn to pay more attention to all our various microbiomes in the future. A more thorough understanding may allow us to reduce complications (think C Diff) and might help us recognize some subtle factors that are contributing to overall mortality. 

Here are my comments and questions for the authors / presenters:

  1. The audience will not be familiar with the microbiome diversity measures described in the abstract. Please take a little time to explain it, what is normal, and what happens when it changes.
  2. Were there any obvious outcome correlations observed that were not reported?
  3. Where do you go from here? Any plans for human studies on this topic?

As you can see, I find this area fascinating and believe that it is an underappreciated source of outcome variability in the patients we take care of. Figuring this out will help us tweak and optimize our overall patient care.

Reference: MULTICOMPARTMENTAL TRAUMATIC INJURY AND THE MICROBIOME: SHIFT TO A PATHOBIOME. Plenary paper #54, AAST 2022.

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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.

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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
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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.

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Fat Embolism vs Fat Embolism Syndrome

It’s fat embolism week! I’ll cover this uncommon, yet very important clinical condition in my next four posts.

Fat embolism syndrome (FES) is one of those clinical problems that trauma professionals read about during their training, then rarely ever see. Although the clinical manifestations are frequently mild, they can progress rapidly and become life-threatening. Over the next five days, I’ll try to  help you better understand this condition, and provide details on diagnosis and treatment.

Fat embolism syndrome (FES) is a constellation of findings that arise from a single, unified cause: the escape of fat globules into the circulation (fat embolism). The ultimate resting places of those globules determine the specific manifestations of FES seen in clinical practice. When it occurs, it typically becomes apparent 24 to 72 hours after injury.

Simple fat embolism occurs to some degree any time tissues containing fat are manipulated or injured. It has been demonstrated during plastic surgical injections for cosmetic purposes and lipid infusions. It is more frequently seen with orthopedic injuries, especially those involving the femurs and pelvis. And it makes sense that the more fractures that are present, the more likely fat embolism will occur. Embolism is also known to occur when performing orthopedic procedures, particularly those involving the marrow cavity (intramedullary nailing), but has also been reported in total knee and hip procedures.

Fat embolism syndrome has a generally reported incidence of 1 – 10%, although I believe that is on the high side. I see a case every 3 – 4 years in a predominantly blunt, fracture-laden practice. Fat embolism without symptoms occurs much more frequently. A study from 1995 using transesophageal echo found evidence of emboli in 90% of patients with long bone fractures.

But how do these fat globules get into the circulation and produce such chaos? We know that they can be mechanically pushed into small venules when tissues containing fat cells or bone marrow are injured. In bone, there are numerous small venules located throughout that are anchored to it. When the bone is fractured, these venules tear and are held open so yellow (fatty) marrow can be pushed into them.

If enough emboli enter the blood stream, they may accumulate in the end vessels of tissues and block flow. Although this is a simple and appealing explanation, it may not be the full story. If the emboli primarily occur during and after injury, why does it take several days for the full-blown syndrome to develop?

A likely explanation is that the fat globules begin to degrade while in the circulatory system. Breakdown into free fatty acids results in the release of a cascade of cytokines and other mediators. The inflammatory response around the end vessels create the gross pathology that we associate with fat embolism syndrome.

In the next post, clinical manifestations of fat embolism syndrome.

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