Used to be, motorcyclists were young men riding modest machines. But I’m sure all of you have noticed the changing demographic. Nowadays, they tend to be middle aged (or older!) men, who are losing their hair, growing their waistline, and taking warfarin.
At the same time, I’ve noted more significant injuries from motorcycles, and deadlier outcomes. A recent study has now quantified this and confirmed my impression. Brown University researchers analyzed data in the National Electronic Injury Surveillance System, focusing on the injuries and outcomes of motorcycle crashes over an 8 year period.
Some of the more interesting tidbits:
- Of course, most injured riders were male (86%)
- Injuries occurred most frequently in younger age groups, and least frequently in older age groups
- Odds of having injuries requiring hospitalization doubled in the middle age group (40-59), and tripled in the older age group (60+)
- Similar trends were seen in injury severity as age increased
- The number of injuries in middle aged riders increased 62% from year 1 to year 8
- The number of injuries in older riders increased 247% during the study!
- Injuries in the middle aged and older groups tended to be upper torso and head/neck
Bottom line: Subjective impressions of injury trends in older motorcycle riders are borne out by this study. Why? As we age, we have less reserve, more comorbidities, loss of elasticity and bone density, and a host of other lesser factors. Additionally, older riders can often afford more expensive (“better”?) bikes that may tax their ability to ride safely in unexpected conditions. Trauma professionals need to be aware of these trends and always treat these patients as if they have life-threatening injuries until you can prove otherwise.
Reference: Injury patterns and severity among motorcyclists treated in US emergency departments, 2001–2008: a comparison of younger and older riders. Injury Prevention, ePub Feb 6, 2013.
The February issue of TraumaMedEd is ready to go! This issue deals with trauma prevention.
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I believe that bioprinting (using 3D printers to create organs, skin grafts and other stuff we need) will be the next big thing. Lots of people are working in the field now, and the printed products are getting much more sophisticated.
Tracheas and bladders have already been done. But now, how about an ear? Loss of an ear is very disfiguring and, like other injuries to the head and face, can create a fair amount of psychological trauma. Bioengineers at Weill Cornell Medical College have now printed an ear that is nearly indistinguishable from the ones we are born with.
Bioprinter creating an ear encapsulated in hydrogel.
The technique used here is a little different than others I have described. In this case, a digitized image of the subject’s other ear is used to print a “negative”, actually a mold that can create the new ear. The mold is filled with a collagen mixture (from rat tails!), and then injected with cartilage cells (from cows!). The collagen serves as a structure over which the cartilage can grow.
The whole process is fast. It takes half a day to model the mold, a day to print it, 30 minutes to inject the gel, and the ear is ready 15 minutes later. Obviously, it has no skin so must be implanted under a prepared skin area in the patient. Over a few months, the cartilage grows and replaces the collagen within the ear.
The next step is to use human collagen and cell cultures. Ideally, if the patient can be the source, there should be no chance of future rejection. Expect more advances in this technology creating more ways to rebuild our patients.
Reference: High-Fidelity Tissue Engineering of Patient-Specific Auricles for Reconstruction of Pediatric Microtia and Other Auricular Deformities, PLoS ONE, 2013, DOI: 10.1371/journal.pone.0056506.
If you’ve been reading these posts for any length of time, you may have realized that I regularly write about new (or sometimes not so new) research studies that I believe have some impact on trauma professionals. But if you look closely, you’ll see that the vast majority are human studies. I can only recall 1 or 2 animal studies that I’ve commented on in the past 3+ years.
Why is that? Well, there are several reasons.
First, many of those papers describe low-level biomedical research that is tough for the average person to follow. They use sophisticated measurement and analysis techniques to pick apart a specific biological pathway or process. It almost takes a PhD to understand them.
Next, most of these studies are performing work that only incrementally increases our understanding of what’s going on at that microscopic level. These little bits of progress may ultimately add up to a major advance. But if I find it difficult to provide the big picture view of the importance of one of these minor findings to the average trauma professional, I’m not going to write about it.
Finally, and most importantly, many of these published results will not have any significance to our field. Some interesting, positive finding in an animal model may have been discovered. But why should we believe this will translate to something relevant to humans?
Look at the model of inflammation that’s been used to develop all manner of potential human drugs to block it in critically ill patients. To date, there have been nearly 150 such drugs developed and tested, at great expense. How many have actually worked and been approved for human use? Zero. Why? It turns out that the inflammation model used in mice creates a response that looks the same as what happens to humans. But it’s not. It turns out that completely different, parallel pathways have been studied. So the thousands of papers that picked apart these pathways used to treat mouse inflammation do not really apply to human medicine. Only to veterinary medicine. And mice veterinarians only!
Reference: Genomic responses in mouse models poorly mimic human inflammatory diseases. Proc Nat Acad Sciences, ePub Feb 11, 2013.
Spleen injury grading is not as complicated as people think! The grading system ranges from Grade I (very minor) to Grade V (shattered, devascularized).
There is one nuance that people frequently don’t appreciate: multiple injuries can increase the grade. Technically, multiple injuries advance the maximum grade by one point, up to a maximum of Grade 3. So Grade 1 + Grade 1 = Grade 2, but Grades 2+2 = 3! Weird arithmetic!
The vast majority of injuries are Grades 1 to 3, and they are actually the easiest to grade. I use this simple rule: 1 and 3, 10 and 50.
The first set of numbers indicates the depth of a laceration in centimeters.
- Grade 1 – < 1 cm laceration depth
- Grade 2 – 1-3 cm laceration depth
- Grade 3 – >3 cm laceration depth
The second set of numbers refers to size of a subcapsular hematoma in percent of the total surface area of the spleen. Hint: most of these low grades are determined by laceration depth. Very few actually have sizable subcapsular hematomas. So memorize the 1-3 rule first!
- Grade 1 – <10% subcapsular hematoma
- Grade 2 – 10-50% subcapsular hematoma
- Grade 3 – >50% subcapsular hematoma
Grades 4 and 5 use other criteria, but in general if it looks completely pulped it’s a 5, and if it’s a little less pulped, it’s a 4.
- Grade 4 – hilar injury with >25% devascularization OR contrast blush (active bleeding)
- Grade 5 – shattered spleen, or nearly complete devascularization