Douglas W. Lundy, MD, MBA, FACS, FAOA, discussed the future of orthopaedic trauma with William T. Obremskey, MD, FAOA, Director of Orthopaedic Trauma at Vanderbilt University Medical Center. Dr. Obremskey shares his vision for the future of orthopaedic trauma surgery, focusing on reducing complications through advanced technologies and improved practices.
Perhaps most thought-provoking is Dr. Obremskey's perspective that some of the most impactful advances may not come from fancy technology at all—but from addressing underlying patient factors like smoking cessation and blood sugar control that dramatically affect healing outcomes. The future of trauma care involves both cutting-edge science and fundamental public health initiatives working in tandem.
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Episode Transcript
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Speaker 2 (00:23):
Welcome to the AOA Future in Orthopedic Surgery
podcast series.
This AOA podcast series willfocus on the future in
orthopedic surgery and theimpact on leaders in our
profession.
These podcasts will focus onthe vast spectrum of change that
will occur as the futurereveals itself.
We will consider changes asthey occur in the domains of
(00:44):
culture, employment, technology,scope of practice, compensation
and other areas.
My name is Doug Lundy, host ofthis podcast series.
(01:06):
Joining us today is Dr BillAbramski is the Director of the
Division of Orthopedic Traumaand the Fellowship Director for
Orthopedic Trauma Research atVanderbilt University Medical
Center in Nashville, Tennessee.
Bill also serves as a leadinvestigator for the Major
Extremity Trauma ResearchConsortium, also known as METRIC
, which is a large clinicalresearch network aimed at
defining treatment guidelinesfor injuries throughout the
world and specifically combatinjuries.
(01:26):
Dr Obremski did his doctor ofmedicine at Duke University and
then also did his master ofpublic health at the University
of North Carolina.
At Chapel Hill he did hisresidency at the University of
Washington Medical Center, thenhis fellowship at the AO
Research Institute in Davos,Switzerland.
Not only after that, he alsodid his management in healthcare
(01:50):
master's degree at VanderbiltUniversity, where he's currently
, of course, on faculty.
So, Dr Abramski, my friend,welcome to the podcast series,
sir.
Speaker 3 (02:00):
Doug, thank you.
It's a pleasure and an honor tobe here.
Speaker 2 (02:04):
Thank you, bill.
Thank you very much.
We appreciate you being on and,as I was saying before, so I've
known Bill for quite a while.
In full disclosure, I did mytrauma fellowship at Vanderbilt
University and Bill and I haveoverlapped in many places over
our careers.
But Bill and I were also on thequestion writing task force for
the American board oforthopedic surgery and it became
(02:26):
very clear to me that I didn'tknow anybody who knew the
orthopedic literature he'sembarrassed me saying this, but
I'm going to say it anywaybetter than Bill did, and so I
don't think there's anybody Iwould rather talk to about the
future in orthopedic trauma thanyou, sir.
So when we look at where ourspecialty in orthopedic trauma
than you, sir.
(02:46):
So when we look at where ourspecialty in orthopedic trauma
surgery is headed over the next10, 15, 20, whatever you feel
comfortable, going out to years,where do you see us heading in
the future within the UnitedStates and North America about
trauma surgery?
Speaker 3 (03:01):
Sure, I think our advances will be more in
identifying and preventingcomplications, in that it's
truly amazing that the humanbody heals the vast majority of
times, sometimes in spite of us,and in orthopedic trauma we
have maybe one of the highestcomplication rates in general if
(03:25):
you look at infection andnon-union compared to any other
specialty.
The total joint doctors are upin arms about an infection rate
of 0.5% and there's been moreliterature on that and ACLs and
stiffness, the number of NIHgrants go into those things.
But we truly, in 2024, haveinfection rates of 20% to 30% in
(03:49):
some pretty common injuriesopen tibia fractures and peel on
some plateaus, and non-unionrates of you know, even in one
of the most common surgeries of,you know, clavicle fractures of
still 5%.
So I think a lot of our futurewill be hopefully decreasing the
complications and maybe helpingus predict who is at risk for
(04:13):
those complications and evensignificant complications like
DVT or infection as well frombiomarkers.
So I think that's the generalarea we will be heading to try
to decrease some of thoseproblems, and I guess I could
talk about some of the specificsof those.
Speaker 2 (04:32):
So I know that you've been involved in some pretty
extensively high levelcollaborative research on
preventing and diagnosinginfection and orthopedic trauma.
Can you tell us briefly aboutwhat your consortium has been
working on and what thatconsortium is?
Speaker 3 (04:50):
Sure, I have worked with the well.
I think it probably came fromworking on the OTA
evidence-based medicinecommittee and when I was lucky
enough to chair that for thetask force and then the
committee for a total of about10 years.
But we did some work oninfection prevention with open
fractures and developing someguidelines.
And somewhat because of thatwork the AO group was looking to
(05:13):
incorporate more of acollaborative and international
group of people and asked me to,as the OTA representative from
the Evidence-Based MedicineCommittee, to participate on a
group, the AO Anti-InfectionTask Force as it was called at
the time, and that group lookedat the literature and tried to
develop a consensusevidence-based medicine
(05:35):
guidelines and consensusrecommendations with several
members of the OTA and then theAO as well as several
international groups from aroundthe world to participate in
that.
And I think we tried to lookvery critically at the world's
literature to try to makemanagement or treatment
decisions for prevention andmanagement.
(05:56):
And also around the same timethe Parvizi group had expanded
their infection prevention toall specialties and we had a
summer meeting in there and Ihelped lead that group and one
of my goals was to try to makeall these consistent so there
weren't conflicting guidelinesacross different specialties.
Speaker 2 (06:17):
So some people could accuse us of being knuckle
draggers, because in many ways,I think we probably are, because
I know many orthopedic traumasurgeons who are still using the
antibiotics that still onAnderson recommended in 1976 for
crying out loud.
So what are your thoughts interms of what should we be doing
(06:38):
currently to reduce infectionin 2024?
And you talked about biomarkersand other forms of technology.
Can you tell us what's beenbeing worked on that's going to
propel us into the future?
Speaker 3 (06:50):
Sure, looking at infection prevention, maybe open
fractures are a reasonablemodel for that and, as you said,
we are still in 2024, not ahundred percent sure what the
right dose and duration ofantibiotics are to prevent.
The metric group has a proposalin to try to work on this in a
(07:11):
large-scale fashion.
But the current recommendationsso far for type 1 and type 2
and possibly even type 3 openfracture is that you need a
first-generation cephalosporinprimarily and that for those
that are at higher risk forgram-negative, which are type 3A
contaminated fractures and or3B, that we increase the
(07:34):
spectrum to have gram-negativecoverage.
And historically those wereoften gentamicin.
I think both of those theguidelines and the Parvizi
infection ICM guidelines bothcaution people on using
gentamicin in that we don'talways know people's renal
function when they hit the doorand that that can potentially
(07:57):
cause some renal ornephrotoxicity and so.
But some gram negative coveragehas indicated the exact type.
Whether it's genomycin orfluoroquinolone or tobramycin is
not completely clear or whetheryou just need a
third-generation cephalosporin,septazidime or some type of
broader coverage for those.
There's a little bit of datathat indicates that type 3
(08:20):
contaminated fractures.
That extension beyond 24 hoursis helpful, up to 72 hours.
Speaker 2 (08:28):
So tell us about these biomarkers you were
discussing and what technologyis being used in the future to
reduce infection rates.
Speaker 3 (08:36):
Yeah.
So I'm not sure that thebiomarkers will help us reduce
them initially, but there doesseem to be some evidence from
micro RNA and that the those whoare at risk for non-union and
infection is evident very earlyin their serum.
One thing Vanderbilt is veryyou know, I guess, lucky to have
(08:57):
is that we have been gatheringpatient serum for 15 years and
there's hundreds of thousands ofpatients that are in a database
and I am working with the AOInstitute to attempt to look at
people who have and have not hadnon-unions or infections and
look at the early microRNA thatare present when they are early
(09:21):
postoperatively to see if someof those hypotheses or what
micro RNA you know may helppredict those who are going to
have a non-union or be at riskfor infection.
It may not be 100% but it mightraise our you know, level of
concern or earlier interventionin those at risk.
Speaker 2 (09:41):
What about implants?
You could obviously we can coatimplants with bone healing
chemicals versus antibiotics,versus both.
How do you see the implantsbeing changed that will help
mitigate our two, you couldargue.
Our two biggest complicationson the fracture side are
non-unions and infections.
Of course, we have the wholeDVT thing to deal with as well,
(10:03):
but how do you see the implantshelping with that?
Speaker 3 (10:07):
How do you see the implants helping with that?
Yeah, so there's only onecoated implant on the market
currently is a genomycin coatednail and been released about 10
years in Europe, but there'ssurprisingly little data on that
.
Does it really decreaseinfection rate?
I think there have been othernails that have been
electrically charged to see ifthat electrical charge tries to
(10:30):
decrease infection rate.
And a nail like that is alsoavailable internationally, but
not in the US, with a goldpalladium coating which creates
a charge, electrical charge thatmay help repel bacteria to
prevent them from sticking tothe implant.
And Christina was right 60years ago.
(10:51):
You know it's all about therace for the surface.
And how do you prevent that?
With a local antibiotic, withthe centering or some sort of
modulation of the surface of theimplant to make it more
amenable for eukaryotic cells asopposed to prokaryotic cells.
So I think all those things maydevelop over time either
(11:13):
antibiotic coating or electricalcoating or some sort of a
sintering of the implant to makeit more amenable, to prevent or
to make it more unlikely thatbacteria prokaryotes will adhere
to the implants.
The other thing that in termsof infection is not just the
implants but maybe local use.
(11:35):
You know the metric group hasdone the Banco trial looking at
use of local antibiotics, andhave the infection rate of gram
positive from 7% to 3% with useof vancomycin in use in pylons
and plateau fractures.
The problem is it's still 3%and it didn't affect the gram
negatives and powder goes awayfairly quickly.
(11:59):
And I think there will be othersubstances such as hydrogels
and or a macromolecule polymerthat often has a combination of
PDLA, lipid and then drug ofsome sort that can be applied
and protect the race for thesurface longer, and that how
long that is exactly?
But it's probably in the threeto seven day range.
(12:21):
And if you look at when cellsmigrate onto implants and so we
can have some substance likethat that can be put in the
wound at the time or in thecanal at the time of implant
fixation, a bone fixation withimplants that they can help
protect the implants, that thatwill probably be the next phase.
I think eventually we willprobably have implants that are
(12:44):
made of peak or some substancelike that that will eventually
dissolve or slowly dissolve andeliminate.
You know what no surgeon looksgood doing the hardware removal
phenomena.
That's right.
It's one of the most commonprocedures for orthopedic
surgeons applying for theirboards and it's a huge
healthcare cost for hardwareremoval.
(13:06):
And I in clinic this morning Isigned up two you know people
who they're tired of theirolecranon plate or tired of
their screws on their anteriormedial tibia from a nail and,
and some people just want theirhardware out.
And if we have slowlydissolvable plates or nails that
modulate and change their, youknow, change their elasticity as
(13:27):
they dissolve and that that mayhelp, you know, eliminate that
complication of you know, changetheir elasticity as they
dissolve and that may help, youknow, eliminate that
complication of, you know,hardware removal.
Whether you've got acomplication expectation, it may
be a, you know, purely parsingyour words, but it's a huge
healthcare cost and a risk cost.
You know there's nothing youcan't make worse than an
operation.
Speaker 2 (13:46):
Right.
How about non-unions, both froma implant standpoint, in terms
of improving our implants?
Speaker 3 (13:55):
the freshness to heal better and also the biologics.
Yeah, I hope one thing we can dois educate people to stop
things or control do a betterjob of controlling things that
put them at risk for non-unions,such as their hemoglobin A1C,
or stopping smoking and helptheir own biology.
I do think that we willeventually have either coating
(14:19):
on the implant but it's probablymore appropriate to have it at
the fracture site a implantableand biologics that occur in the
right sequence.
You know, right now we haveBMP2, you know which recombinant
BMP2, which is just a foghorn,a huge super physiologic blast,
(14:41):
and what you need is a symphonyof, you know, bmp7 and BMP2.
And then you know PDGF and somesort of up and down regulation
at the fracture site, and wewill probably figure that out
someday and have some sort ofcoating or implant or goes in
like toothpaste and sets up likeconcrete and provides
(15:02):
additional stimulation but alsohas, you know, the correct
biologic transformation andrelease of bone healing
substances in the right sequenceand the right dose.
Speaker 2 (15:16):
Very interesting, very, very good.
So what about deep veinthrombosis and pulmonary emboli?
You and I treat injuries thatset folks up for those, yeah,
proximal femurs, pelvis.
We've probably way over-treatedpeople.
Speaker 3 (15:28):
We've probably way over-treated people.
We have probably wayover-treated some people and way
under-treated some people.
And you know, I think we wereboth part of this large 12,000
patient prospector randomizedtrial of multi-trauma patients
looking at aspirin versusLovenox and I think what we all
knew and the total joint docsknew before is that lovinox
causes bleeding in some peopleand it can be a problem and
(15:52):
increase their risk ofreoperation and infection
because of the blood that's inthe in the area of the injury
and bacteria like blood.
Ever heard of blood auger?
That's what they grow it on.
So it's a huge risk forpatients having, you know,
excess bleeding at a fracture,at a fracture site or injury
site.
And there are probably peoplewho are clotters that may clot
(16:17):
no matter what you do.
And there are those who arenon-clotters and this is also
where I think the biologic,genetic makeup or understanding
those who are really at risk forclotting and you probably only
need to prophylax those who arereally at low risk for clotting
for a very short period of timeuntil they are up and mobile and
then those who may need it fora much longer time and need one
(16:41):
or two substances that maybehelp prevent their coagulation
cascade at a couple points.
Right now we have found thatplatelets blocking platelets
which are the beginning of aclot with aspirin is as good in
terms of DVT prophylaxis,preventing PEs, preventing DVTs,
preventing all-cause death asLovenox has been.
(17:04):
That we have been done and weare beginning to make that
transition.
That was a New England Journalarticle.
I think we can probably be evenmore specific, more patient
specific, based on their genepool.
We just haven't figured outwhat that gene pool is, but I
envision the day where you comein, you're a multi-trauma, we
(17:25):
draw your gene pool.
Come in, you're multi-trauma,they.
We draw your gene pool, we runit through the, through the, the
match.
Speaker 2 (17:32):
We, we know that you're at a 10 or 20 or a 50
risk for dvd prophylaxis andthat you will respond to
platelet blockers or cascadeblockers or both, depending upon
your risk profile that's funnyseeing that I'm looking at that
vanderbilt health sign behindyou as you're doing this and I
always my youngest, my oldestson was born while we were at
(17:53):
Vanderbilt and I always thoughtthat someday he's going to look
at what I do and go well, blesshis heart.
Dad thought he was doing theright thing, but we all know
it's this thing now.
But things are going to changeso dramatically between the time
that and you have.
You have a daughter who's aphysician, don't you?
Speaker 3 (18:08):
dramatically between the time that and you have, you
have a daughter who's aphysician, don't you?
I have a son and a daughterthat are both smart like their
mother, and pediatricians.
Speaker 2 (18:19):
Ah, okay, all right, let's step out of the clinical.
We'll directly clinical run fora minute and start looking at
some of the healthcare practiceand stuff like that.
Like everything else in theworld, orthopedic trauma surgery
is heading into the outpatientarena.
Where do you see that headed?
Speaker 3 (18:31):
I mean that's a train that's already headed that way
and you know our entiredepartment is planning on moving
offsite and having an offsite.
You know 24-hour surgery andASC and that'll probably just
continue, except formulti-trauma.
You know complex spine, complexjoints, tumor cases and that's
(18:53):
probably better.
I think every time it's beenstudied that it's done more
efficiently with greater patientsatisfaction, with lower
complication rates in thoseoutpatient or you know systems
where that's what they do atthat surgery center is they do
pylons, they do plateaus, we do.
(19:14):
You know outpatient fracturefixation and you can increase
productivity.
The patients drive up, they getin their car, they drive away.
I mean every day today inclinic, every patient.
I apologized for the parking,the transport.
You know we're underconstruction and it's just
impossible and they walk, theywalk, they walk farther to come
see me than I probably do fromour parking lot to the clinic
(19:37):
and but that's that's just partof it.
I think can you do it safelywith patients and our we think
we'll rely on our anesthesiateam to identify those patients
that can safely have outpatientor 24-hour surgery in a
different setting than a mainhospital.
Speaker 2 (19:54):
You kind of tapped around the edge of it, but I
found regional blocks,especially with the bupivacaine
sorry, the liposomal bupivacaineto really help out.
Have you stepped into that part?
Speaker 3 (20:05):
Oh, yeah, I like to say I am the greatest utilizer
of the block team in the entirehospital.
I just, I mean it, we'vestudied it works right, you know
, I mean, some people hate toget stuck with the, you know,
stuck with the needle before andI think it takes communication
and we have developed a protocolwith our anesthesia team that
(20:26):
you know.
These are the things that youcan block and we want you to
block them and please block thempre-op and if there's any
questions, or we put in a notesaying you know, we need to
check the radial nerve post-op.
So don't, you know, don't blockit before.
But blocks, you know, decreasesanesthetic intra-op.
Decreases delirium post-op.
Decreases narcotics post-op.
(20:47):
Improves patient satisfaction.
What's the problem?
Right, I?
Uh, and yeah, you have to havea system so they're not delaying
your time by 30 to 40 minutesby doing that.
But I, I think we will continueto use different blocks.
You kidding me when, when youand I were in training, you gave
everybody intramuscular demerol, right, you know, we kept total
knees in the hospital for fivedays, immobilized their knee and
(21:10):
gave them Demerol for three orfour days and zonked them.
And you know, now you'regetting non-union operation as
an outpatient.
So yeah, we will continue tomake advancements in regional
block.
And not just that, but multimodal medication.
And you know, now we use multi.
(21:32):
You knowontin, tramadol,toradol, you know a variety of
medicines and we know they workbetter together and the ota
wrote some great clinicalpractice guidelines for that.
And it's not just themedications.
And you know joe shoe.
Joe shoe has been great atpromoting multi-therapy.
You know, using aromatherapy orsound therapy, electrical, you
know 10 unit therapy.
There are lots of differentmodalities that just work.
(21:53):
Every time we've studied themin prospective randomized trial.
They work better thanmonotherapy.
And just given and I was guilty, I gave everybody Oxycontin,
you know, and we create a lot ofaddicts based on false data and
we were guilty, so we got, sowe were part of the problem.
We need to be part of thesolution and read our literature
and change our practices to tryto decrease the problems which
(22:16):
we have created and with betterpain control with patients.
Speaker 2 (22:21):
Now, how many orthopedic surgeons do y'all
make every year?
Were there in Nashville Four orfive.
I know it was five when.
Speaker 3 (22:27):
I was.
Our residency program has five,just going to six last year.
Speaker 2 (22:31):
I think there was four when I was there, I can't
remember, I was only there formy fellowship.
But so y'all are making five ayear.
You're fixing to make six ayear.
Those are very expensive peopleto make orthopedic surgeons.
You and I both know that.
So in the future, let's, let'scrown you as a secretary of
(22:51):
health and human services.
Okay, so now you're doing that.
How do you see the scope ofpractice in terms of developing
what the nation needs in thefuture for orthopedic trauma
surgeons?
Are orthopedic trauma surgeonsdoing all the fresh work?
Do we have other people doingthe ankles and the other stuff
like that and we are doing thehigh energy stuff?
(23:11):
What's the best utilization, aswe go forward, for the
workforce?
Speaker 3 (23:15):
Yeah, I don't know the answer to this.
I do know that, in general, 90%of fractures are cared for in
this country by non-fellowshiptrauma trained individuals, by
non-fellowship trauma trainedindividuals, and so we cannot we
being the Orthopedic TraumaAssociation generate enough
(23:36):
orthopedic surgeons to do allthe fracture work Right, and so
routine fracture care has got tocontinue to be part of the
general orthopedic knowledge, sothat ankles, wrists, hips, you
know, femoral neck fractures,can all be cared for by people
who are well-trained in generalorthopedics.
(23:57):
That that should probablymaintain, and so and they can
stay close to their home forcare and to just help make sure
that people continue to becompetent and patients could get
care with that, and so I don'tthink that will or should change
.
I mean to continue to provideexcellent educational
opportunity to help them withthe fine points, to identify,
(24:18):
maybe, what's not routine and totransfer patient, transfer care
that they're not comfortablewith.
And I do see, though, thatcomplex fracture work is
expanding into the level twos.
You know, when you and I do see, though, that complex fracture
work is expanding into the leveltwos, you know, when you and I
were training, it was almost alllevel ones.
Everything got shipped there.
The reality is that you know wehave been fortunate enough to
train enough orthopedic traumasurgeons that now the primary
(24:41):
place that our graduates aregoing on the fellowship
committee are going to level twocenters.
Personally, I think that's agood thing, I think they're, and
I think it's good for patients,it's probably good for local
orthopedic surgeons and andhopefully it's good for the our
trainees that are going thereand they're a resource in their
(25:01):
community that can do the harderfractures or those that you
know that maybe need a littlemore experience.
And and also so that theeverybody, the total joint
surgeon or the sports surgeondon't feel compelled to start
that tibia nail at seven o'clockat night after their you know
(25:22):
their last elective case wentand you know they're tired, the
team's tired.
I mean, even at Vanderbilt weare one of the busiest trauma
centers in the world.
It's got to be really bad forme to be there doing it after
7pm, because I am not much goodby myself and and and when I say
give me a what's it and I get awho's it in my hand and and
(25:46):
they are.
They look at me and say I don'tknow what you're talking about.
I mean, even at a busy placelike ours, our personnel are
just not skilled enough and andthere are many things you just
need the A game team and youknow we have been fortunate to
go through that transition tomake trauma more semi-elective.
I mean sure there's things thatwe're going to have to get up
middle of middle of the nightand do Dirty, dirty compartment
(26:08):
syndrome, bad infections,bleeding to death but the
routine stuff I can and hopeshould be semi-elective and that
systems will have OR capacityand personnel trained available
in terms of x-ray techs, scrubtechs, first assistants, to make
(26:32):
it a much more sustainable lifeand career.
I feel fortunate we've beenable to build that at Vanderbilt
and you've been our guestspeaker and you've seen our
system and I tell our fellowswhen they leave that you're
going to miss us a little bit,the faculty.
You're really going to miss ourtechs, our cast techs, our
system that we've built aroundit with APPs to help us run a
(26:55):
fairly efficient high volumesystem.
Speaker 2 (26:58):
I barely recognized that.
I was there 98 to 99.
And when I was up there it waslike, wow, this place has
exploded and it was great when Iwas there and it's unbelievable
now.
Trauma.
Now, obviously you and I arehighly biased on this, so I can
hear everybody rolling theireyes and that's okay.
But trauma is the number onekiller of Americans between the
(27:21):
age of six months and 45 yearsof age, and so our disease
process that we treat iscrippling the American economy,
the North American economy, theworld economy.
When I work in Africa, itcauses a massive amount of
problems there for the economicdriving force of the societies
(27:42):
that people are injured in.
So, as you and I also know, asignificant amount of funding is
directed toward cancer, cardiacdisease, hiv you name it as
opposed to what you and I alsobelieve is something that, if
more money and attention wasapplied to it, we could really
make societal changes for adisease process that massively
(28:06):
affects a significant amount ofthe economic driver and the of
important workforce folks in ourcountry.
Once again, your secretary ofhhs, how do you fix this?
Heck, I'll make you presidentus.
How do you fix this problem?
What?
What do you think in the future.
What's the right thing to do totry to mitigate this?
(28:29):
This?
However, you want to financetrauma care, trauma prevention,
whatever.
Speaker 3 (28:35):
Yeah, so you know, I was a undergraduate econ major
and, as you said, I did abusiness degree a while ago, and
so in my view it's it's aboutvalue and and what's the cost
per quality adjusted life yearand that's cost per quality in
(28:56):
the econ world and I hope we getto the point where that society
at least looks at where you'regoing to put your investment.
I mean, the amount of need isinfinite in terms of problems of
the human condition and everygovernment you know needs to put
resources towards what I wouldhope would be those where they
(29:20):
get the greatest bang for theirbuck.
And for I don't know 20 years Ihave been saying you know,
bring it in terms of orthopedicsin general or particularly
orthopedic trauma.
You know, right now totaljoints get all the credit for
having one of the lowest youknow costs per quality.
But the reality is that I wouldsay, compare that to a femur
(29:41):
fracture.
All right, you know.
I mean the average age of aperson with a total joint is 60
something.
Average patient with femurfracture is 40 something, this
40 year old.
If they don't get this done,60% don't go back to work.
This is why Switzerlandinvested in femoral nailing and
why the Swiss government fundedthe AO Research Institute in the
(30:06):
50s 60s, because they realizedthey had a workforce and they
had a universal coverage and sopeople would go back to work.
And so the cost just think ofthe cost per quality of those
two things Total joints are moreexpensive than a femoral nail.
Their patients don't live aslong, they're not working
anymore, they're not payingtaxes, assuming they're retired
(30:28):
and this 40-year-old's gotanother 20 to 30 years of work
life in them.
And so if you want to run thateconomic analysis, bring it.
And so in a world where valuematters and maybe worlds or
governments have to makedecisions, I would hope that you
and I, or our specialties,could make that argument that
(30:49):
this is worth investing in inpreventing disability death.
You know the deaths come frommotor vehicle collisions and
that's maybe.
You know we the rare, ourpatients don't usually die.
They do occasionally they getinfection at around or you know.
But the prevention comes on thecar manufacturers on the
(31:10):
driving on.
You know, preventing drinkingand driving and drinking and
motor scootering in Nashville,taxpaying people to requiring
government assisted often, andinvesting in those people to
prevent disability, to returnthem to the working force, I
(31:35):
think could be the ROI on that.
I mean, you're the business guy, you've been the leader of huge
groups and chairman of thedepartment and you understand
ROI.
If you're going to put yourwhere's your, where are you
going to put your investment?
Your return on investment wouldbe much greater in that
population of people who aregoing to return to work to avoid
(31:58):
complications of infection,non-union DVT or death or
amputation.
You prevent those four thingsor amputation.
You prevent those four thingsand you have greatly improved
the quality of life with afairly low cost per quality
adjusted life year.
Speaker 2 (32:16):
That's funny.
You were saying something Ithought.
We did a tour of the Porschemuseum in Stuttgart and there
was a little plaque that if youweren't looking you'd miss it.
But they said that deaths frommotor vehicle collisions have
decreased substantially and ofcourse they patted themselves on
their back for their vehicularsafety.
But they did acknowledge thattrauma care had improved
dramatically over that time.
But thinking out of the box Ithink you touched on this, I
(32:39):
know you touched on this earlierand I think this may be the
disruptive way of looking at it.
Tell me what you think of this.
In many ways, if we want toreally reduce the complications
of fractures, many thingsoutside of the things that you
and I focus on on a daily basisspecifically eradicating smoking
(32:59):
and doing something to helpwith these horrible HbA1c's that
we see all the time wouldmaterially probably do more than
many other things we do.
Unlike the joint surgeons, wedon't have the opportunity many
times to tee our patients up.
We do in a non-union setting,but prior to that we don't.
It's kind of interesting tothink that maybe in trauma
(33:20):
surgery, if we could hit a magicwand and get rid of smoking and
get rid of crazy HPA1Cs.
We may do more to affect theoutcome of our care than almost
anything else.
What do you think of that?
Speaker 3 (33:33):
Oh, I know, we know that's true, you know
orthopedics and the consequencesare public health diseases and
crises.
And you know, I think it'spretty common knowledge that
smoking increases non-unioninfection rate.
What's not really been known isthat hyperglycemia,
perioperatively is also raisesinfection rates.
(33:54):
And and I mean we have lookedat this retrospectively,
prospectively, in isolatedorthopedic and in multi-trauma
patients and published it.
All the above and every timethat the odds ratio of infection
with hyperglycemia innon-diabetic patients raises the
(34:14):
risk about three times equal toan open fracture of having a
perioperative infection, afracture-related infection.
So this perioperativehyperglycemia is huge, even in
the non-diabetics.
So in the diabetics it's evengreater.
And you're 100 right.
That's where those who are atrisk is, where we ought to put
(34:38):
as much or as as of our effortas we can it's almost funny that
the best thing made me to comeout is none of the cool sexy
technology driven stuff.
Speaker 2 (34:46):
Have it's.
Just quit smoking and get yourdiabetes under control and we,
materially, would do more yeahyeah.
Speaker 3 (34:53):
And the chronic inflammatory state of obesity is
a problem as well for fracturehealing and the hormonal
imbalance of that.
That's more of a data-freeopinion, but I think that it's
true.
Speaker 2 (35:05):
Funny that that would be the thing that would really
help the most.
So where do you see the futureas it relies or relates to the
management and or the preventionof fracture-related infection?
Speaker 3 (35:16):
Yeah, we talked a little bit about prevention in
terms of the patient-codedimplants or local antibiotics.
But one thing that is feasibleand I think in almost every
systems is the fix and flapphilosophy which the Oxford
group in Europe has reallypromoted.
And I think they're right.
And I think Paul Tornettarecently put together a four 400
(35:37):
plus tibia fractures and thegreatest predictor was doing the
fixation with doing the flapcoverage within 48 hours of
definitive fixation.
And we have a patient like thatthis week that came in he's got
a 3B tibia.
My partner did IND damagecontrol plate, did another
debridement yesterday and thenI'm going to do a debridement
(35:58):
and put a nail in it tomorrowand then on Friday morning the
patient is scheduled for theirfree flap and to try to minimize
that time from a systemstandpoint in trading off who's
taking care of the patient andthen providing definitive
coverage, you know to try todecrease the time to race to the
surface and get that patientcovered is within 48 hours.
(36:19):
So that's one thing we'retrying to do for prevention, the
management future.
I think we've come a long waybut we still have so far to go
and I think part of it is thisonce bacteria become established
.
They're really hard to get ridof.
I just it's like a worthyadversary.
And you know, I was a Duke guy.
(36:41):
I spent undergrad med school atDuke and I sort of think of his
Duke Carolina basketball gamesand Coach K and in 40 years he
was 50-50.
He only won half the games.
That's just a great rivalry,and in our fight with bacteria
we won't always win but weshould do better.
And because, you know, staff inparticular goes up the
(37:02):
canaliculi of our bonetrabeculae, they form micro
abscesses, they form biofilm,become senescent and in none of
those I mean even our whiteblood cells can't get up into
the canoleculi.
They can't get in the microabscess, nor can they get in the
biofilm.
And so we have got to developsome ways to try to help
(37:25):
eradicate infection once it'sestablished.
And I think some of those onthe bacteria and also in the
bone and some of those ways thatI think that we might make
progress in the future, becauseour recurrence is embarrassingly
high.
When we look at infectednon-unions, the management of
those, we fail one out of fiveabout the reality is when you
(37:49):
look at large series, it's abouta 20% failure rate, and so we
need to do better in that.
And so what are the things wecan do in the face of infection
to help eradicate the bacteria?
Even if you remove the implant,you still have trouble with the
bacteria there.
But I think there will besolutions that are biobusting
(38:11):
biobusters that can reallypenetrate the mechanism and what
holds biofilm together andcause it to dissolve, and that
may help us eradicate thebiofilm in some ways.
Other things that can removebiofilm from implants that are
in place and maybe you don'twant to do.
(38:32):
You get an infection at threeweeks from a bicon or plateau
that you smoosh together.
Do you really want to take allthat hardware out?
You know we've proven that youcan treat them to union.
You know, with just debridementand antibiotics 80% of the time
, but you're still not winning20% of the time.
And so when something thatmight improve that is using
(38:53):
electrical current and I see aspotentially electrifying the
implants and that that beingeffective at sloughing off or
killing the bacteria that are inthe biofilm and and I think
that may be something that willhelp us Other solutions that may
sit for a while.
(39:13):
You know there's all this inthe total joint of Experian or
dilute betadine and more in theprevention world, but I think
that some of that will translateinto the infection management
world to try to help with thesemicro abscesses, these bacteria
up the canaliculi that need tosit for a while before the
bacteria can be killed fromthose areas.
(39:37):
And the other thing that I thinkwe will develop is the use of
phages.
Phages are the natural hunterkillers of bacteria.
They were all the rage of theforties, fifties until
penicillin got invented and thenall that phage data and just
sort of went away.
But now with multi-drugresistance returning that phage
(39:59):
therapy in terms of ability tomaintain an implant, because
phages are so small that theycome in and they can go into the
biofilm, they can go up thecanaliculi and they can even
penetrate a micro abscess andthen they go in, they attach
themselves to bacteria and thenthey enter the bacteria, they
(40:22):
take over the mechanism of thebacteria and then they make
morphages and then they disrupt,that cell dies and they go away
and they look for more and theyhunt and kill and then they go
away when all the bacteria aredead.
What a great natural hunterkiller of bacteria to use that
in combination with either totaljoints or implants.
We want to keep in place.
(40:43):
The standard mechanisms of doingthat, I think, are challenging
and we don't know those yet, butI see phages as in our
armamentarium in the future.
Until then, I think we will getmore use of local antibiotics
as well, which can sit in highdose locally where there may not
be great blood flow because ofa perfascial disease or the
(41:05):
damage to that area, but eitherwith right now one of the best
carriers is calcium sulfate, andI use far more than I ever used
to because it all dissolves andit just takes several weeks,
but it can be effective in themanagement of a chronic
infection in terms of lettinghigh dose local that doesn't
have has very little systemiceffects on patients or kidneys.
(41:27):
And so that combination oflocal antibiotics with either a
hydrogel or a calcium sulfate,having bio busters some, or
electricity to eliminate orsolutions to eliminate the
biologic biofilm, are some ofthe things that we can.
We can do in the future to tryto help maintain hardware and do
(41:52):
it better than we are in termsof allowing, you know, fractures
to heal without having to takeit out.
And then the other trend whichis coming is the PO antibiotics.
I've been on that train for 30years, you know we have finished
our metric study on acute FRAwhere it's represented, at the
OTA a couple of years ago andthat has been submitted to JAMA
(42:12):
surgery and hopefully it'll comeback positive accepted.
But we're in the middle ofenrolling patients in PO versus
IV antibiotics in infectednon-unions and I expect the data
will be the same.
There's some data out of Europethat says it is the same
already.
So those were.
I think we're going in terms ofmanagement of acute and of of
infections associated withfractures with or without a non
(42:35):
union.
Speaker 2 (42:36):
Wow, this has been an absolute pleasure talking with
my friend and colleague, dr BillLabrowski, who is
well-recognized as aninternational leader in
orthopedic trauma surgery, onthe future in orthopedic trauma.
Dr Abramski, sir, thank you forbeing on the podcast.
Speaker 3 (42:51):
Doug, my honor and pleasure.
It's been an honor to be yourfriend and colleague and I look
forward to following in yourfootsteps as the president of
the Orthopedic TraumaAssociation.
Speaker 2 (43:00):
You're very generous, sir.
Thank you and I look forward toseeing you in Montreal and, for
the rest of y'all, stay tunedfor more in this series on the
future in orthopedic surgery, onthis AOA podcast channel.
Thank you.
Welcome to the AOA Future in Orthopedic Surgery
podcast series.
This AOA podcast series willfocus on the future in
orthopedic surgery and theimpact on leaders in our
profession.
These podcasts will focus onthe vast spectrum of change that
will occur as the futurereveals itself.
We will consider changes asthey occur in the domains of
(00:44):
culture, employment, technology,scope of practice, compensation
and other areas.
My name is Doug Lundy, host ofthis podcast series.
(01:06):
Joining us today is Dr BillAbramski is the Director of the
Division of Orthopedic Traumaand the Fellowship Director for
Orthopedic Trauma Research atVanderbilt University Medical
Center in Nashville, Tennessee.
Bill also serves as a leadinvestigator for the Major
Extremity Trauma ResearchConsortium, also known as METRIC
, which is a large clinicalresearch network aimed at
defining treatment guidelinesfor injuries throughout the
world and specifically combatinjuries.
(01:26):
Dr Obremski did his doctor ofmedicine at Duke University and
then also did his master ofpublic health at the University
of North Carolina.
At Chapel Hill he did hisresidency at the University of
Washington Medical Center, thenhis fellowship at the AO
Research Institute in Davos,Switzerland.
Not only after that, he alsodid his management in healthcare
(01:50):
master's degree at VanderbiltUniversity, where he's currently
, of course, on faculty.
So, Dr Abramski, my friend,welcome to the podcast series,
sir.
Speaker 3 (02:00):
Doug, thank you.
It's a pleasure and an honor tobe here.
Speaker 2 (02:04):
Thank you, bill.
Thank you very much.
We appreciate you being on and,as I was saying before, so I've
known Bill for quite a while.
In full disclosure, I did mytrauma fellowship at Vanderbilt
University and Bill and I haveoverlapped in many places over
our careers.
But Bill and I were also on thequestion writing task force for
the American board oforthopedic surgery and it became
(02:26):
very clear to me that I didn'tknow anybody who knew the
orthopedic literature he'sembarrassed me saying this, but
I'm going to say it anywaybetter than Bill did, and so I
don't think there's anybody Iwould rather talk to about the
future in orthopedic trauma thanyou, sir.
So when we look at where ourspecialty in orthopedic trauma
than you, sir.
(02:46):
So when we look at where ourspecialty in orthopedic trauma
surgery is headed over the next10, 15, 20, whatever you feel
comfortable, going out to years,where do you see us heading in
the future within the UnitedStates and North America about
trauma surgery?
Speaker 3 (03:01):
Sure, I think our advances will be more in
identifying and preventingcomplications, in that it's
truly amazing that the humanbody heals the vast majority of
times, sometimes in spite of us,and in orthopedic trauma we
have maybe one of the highestcomplication rates in general if
(03:25):
you look at infection andnon-union compared to any other
specialty.
The total joint doctors are upin arms about an infection rate
of 0.5% and there's been moreliterature on that and ACLs and
stiffness, the number of NIHgrants go into those things.
But we truly, in 2024, haveinfection rates of 20% to 30% in
(03:49):
some pretty common injuriesopen tibia fractures and peel on
some plateaus, and non-unionrates of you know, even in one
of the most common surgeries of,you know, clavicle fractures of
still 5%.
So I think a lot of our futurewill be hopefully decreasing the
complications and maybe helpingus predict who is at risk for
(04:13):
those complications and evensignificant complications like
DVT or infection as well frombiomarkers.
So I think that's the generalarea we will be heading to try
to decrease some of thoseproblems, and I guess I could
talk about some of the specificsof those.
Speaker 2 (04:32):
So I know that you've been involved in some pretty
extensively high levelcollaborative research on
preventing and diagnosinginfection and orthopedic trauma.
Can you tell us briefly aboutwhat your consortium has been
working on and what thatconsortium is?
Speaker 3 (04:50):
Sure, I have worked with the well.
I think it probably came fromworking on the OTA
evidence-based medicinecommittee and when I was lucky
enough to chair that for thetask force and then the
committee for a total of about10 years.
But we did some work oninfection prevention with open
fractures and developing someguidelines.
And somewhat because of thatwork the AO group was looking to
(05:13):
incorporate more of acollaborative and international
group of people and asked me to,as the OTA representative from
the Evidence-Based MedicineCommittee, to participate on a
group, the AO Anti-InfectionTask Force as it was called at
the time, and that group lookedat the literature and tried to
develop a consensusevidence-based medicine
(05:35):
guidelines and consensusrecommendations with several
members of the OTA and then theAO as well as several
international groups from aroundthe world to participate in
that.
And I think we tried to lookvery critically at the world's
literature to try to makemanagement or treatment
decisions for prevention andmanagement.
(05:56):
And also around the same timethe Parvizi group had expanded
their infection prevention toall specialties and we had a
summer meeting in there and Ihelped lead that group and one
of my goals was to try to makeall these consistent so there
weren't conflicting guidelinesacross different specialties.
Speaker 2 (06:17):
So some people could accuse us of being knuckle
draggers, because in many ways,I think we probably are, because
I know many orthopedic traumasurgeons who are still using the
antibiotics that still onAnderson recommended in 1976 for
crying out loud.
So what are your thoughts interms of what should we be doing
(06:38):
currently to reduce infectionin 2024?
And you talked about biomarkersand other forms of technology.
Can you tell us what's beenbeing worked on that's going to
propel us into the future?
Speaker 3 (06:50):
Sure, looking at infection prevention, maybe open
fractures are a reasonablemodel for that and, as you said,
we are still in 2024, not ahundred percent sure what the
right dose and duration ofantibiotics are to prevent.
The metric group has a proposalin to try to work on this in a
(07:11):
large-scale fashion.
But the current recommendationsso far for type 1 and type 2
and possibly even type 3 openfracture is that you need a
first-generation cephalosporinprimarily and that for those
that are at higher risk forgram-negative, which are type 3A
contaminated fractures and or3B, that we increase the
(07:34):
spectrum to have gram-negativecoverage.
And historically those wereoften gentamicin.
I think both of those theguidelines and the Parvizi
infection ICM guidelines bothcaution people on using
gentamicin in that we don'talways know people's renal
function when they hit the doorand that that can potentially
(07:57):
cause some renal ornephrotoxicity and so.
But some gram negative coveragehas indicated the exact type.
Whether it's genomycin orfluoroquinolone or tobramycin is
not completely clear or whetheryou just need a
third-generation cephalosporin,septazidime or some type of
broader coverage for those.
There's a little bit of datathat indicates that type 3
(08:20):
contaminated fractures.
That extension beyond 24 hoursis helpful, up to 72 hours.
Speaker 2 (08:28):
So tell us about these biomarkers you were
discussing and what technologyis being used in the future to
reduce infection rates.
Speaker 3 (08:36):
Yeah.
So I'm not sure that thebiomarkers will help us reduce
them initially, but there doesseem to be some evidence from
micro RNA and that the those whoare at risk for non-union and
infection is evident very earlyin their serum.
One thing Vanderbilt is veryyou know, I guess, lucky to have
(08:57):
is that we have been gatheringpatient serum for 15 years and
there's hundreds of thousands ofpatients that are in a database
and I am working with the AOInstitute to attempt to look at
people who have and have not hadnon-unions or infections and
look at the early microRNA thatare present when they are early
(09:21):
postoperatively to see if someof those hypotheses or what
micro RNA you know may helppredict those who are going to
have a non-union or be at riskfor infection.
It may not be 100% but it mightraise our you know, level of
concern or earlier interventionin those at risk.
Speaker 2 (09:41):
What about implants?
You could obviously we can coatimplants with bone healing
chemicals versus antibiotics,versus both.
How do you see the implantsbeing changed that will help
mitigate our two, you couldargue.
Our two biggest complicationson the fracture side are
non-unions and infections.
Of course, we have the wholeDVT thing to deal with as well,
(10:03):
but how do you see the implantshelping with that?
Speaker 3 (10:07):
How do you see the implants helping with that?
Yeah, so there's only onecoated implant on the market
currently is a genomycin coatednail and been released about 10
years in Europe, but there'ssurprisingly little data on that
.
Does it really decreaseinfection rate?
I think there have been othernails that have been
electrically charged to see ifthat electrical charge tries to
(10:30):
decrease infection rate.
And a nail like that is alsoavailable internationally, but
not in the US, with a goldpalladium coating which creates
a charge, electrical charge thatmay help repel bacteria to
prevent them from sticking tothe implant.
And Christina was right 60years ago.
(10:51):
You know it's all about therace for the surface.
And how do you prevent that?
With a local antibiotic, withthe centering or some sort of
modulation of the surface of theimplant to make it more
amenable for eukaryotic cells asopposed to prokaryotic cells.
So I think all those things maydevelop over time either
(11:13):
antibiotic coating or electricalcoating or some sort of a
sintering of the implant to makeit more amenable, to prevent or
to make it more unlikely thatbacteria prokaryotes will adhere
to the implants.
The other thing that in termsof infection is not just the
implants but maybe local use.
(11:35):
You know the metric group hasdone the Banco trial looking at
use of local antibiotics, andhave the infection rate of gram
positive from 7% to 3% with useof vancomycin in use in pylons
and plateau fractures.
The problem is it's still 3%and it didn't affect the gram
negatives and powder goes awayfairly quickly.
(11:59):
And I think there will be othersubstances such as hydrogels
and or a macromolecule polymerthat often has a combination of
PDLA, lipid and then drug ofsome sort that can be applied
and protect the race for thesurface longer, and that how
long that is exactly?
But it's probably in the threeto seven day range.
(12:21):
And if you look at when cellsmigrate onto implants and so we
can have some substance likethat that can be put in the
wound at the time or in thecanal at the time of implant
fixation, a bone fixation withimplants that they can help
protect the implants, that thatwill probably be the next phase.
I think eventually we willprobably have implants that are
(12:44):
made of peak or some substancelike that that will eventually
dissolve or slowly dissolve andeliminate.
You know what no surgeon looksgood doing the hardware removal
phenomena.
That's right.
It's one of the most commonprocedures for orthopedic
surgeons applying for theirboards and it's a huge
healthcare cost for hardwareremoval.
(13:06):
And I in clinic this morning Isigned up two you know people
who they're tired of theirolecranon plate or tired of
their screws on their anteriormedial tibia from a nail and,
and some people just want theirhardware out.
And if we have slowlydissolvable plates or nails that
modulate and change their, youknow, change their elasticity as
(13:27):
they dissolve and that that mayhelp, you know, eliminate that
complication of you know, changetheir elasticity as they
dissolve and that may help, youknow, eliminate that
complication of, you know,hardware removal.
Whether you've got acomplication expectation, it may
be a, you know, purely parsingyour words, but it's a huge
healthcare cost and a risk cost.
You know there's nothing youcan't make worse than an
operation.
Speaker 2 (13:46):
Right.
How about non-unions, both froma implant standpoint, in terms
of improving our implants?
Speaker 3 (13:55):
the freshness to heal better and also the biologics.
Yeah, I hope one thing we can dois educate people to stop
things or control do a betterjob of controlling things that
put them at risk for non-unions,such as their hemoglobin A1C,
or stopping smoking and helptheir own biology.
I do think that we willeventually have either coating
(14:19):
on the implant but it's probablymore appropriate to have it at
the fracture site a implantableand biologics that occur in the
right sequence.
You know, right now we haveBMP2, you know which recombinant
BMP2, which is just a foghorn,a huge super physiologic blast,
(14:41):
and what you need is a symphonyof, you know, bmp7 and BMP2.
And then you know PDGF and somesort of up and down regulation
at the fracture site, and wewill probably figure that out
someday and have some sort ofcoating or implant or goes in
like toothpaste and sets up likeconcrete and provides
(15:02):
additional stimulation but alsohas, you know, the correct
biologic transformation andrelease of bone healing
substances in the right sequenceand the right dose.
Speaker 2 (15:16):
Very interesting, very, very good.
So what about deep veinthrombosis and pulmonary emboli?
You and I treat injuries thatset folks up for those, yeah,
proximal femurs, pelvis.
We've probably way over-treatedpeople.
Speaker 3 (15:28):
We've probably way over-treated people.
We have probably wayover-treated some people and way
under-treated some people.
And you know, I think we wereboth part of this large 12,000
patient prospector randomizedtrial of multi-trauma patients
looking at aspirin versusLovenox and I think what we all
knew and the total joint docsknew before is that lovinox
causes bleeding in some peopleand it can be a problem and
(15:52):
increase their risk ofreoperation and infection
because of the blood that's inthe in the area of the injury
and bacteria like blood.
Ever heard of blood auger?
That's what they grow it on.
So it's a huge risk forpatients having, you know,
excess bleeding at a fracture,at a fracture site or injury
site.
And there are probably peoplewho are clotters that may clot
(16:17):
no matter what you do.
And there are those who arenon-clotters and this is also
where I think the biologic,genetic makeup or understanding
those who are really at risk forclotting and you probably only
need to prophylax those who arereally at low risk for clotting
for a very short period of timeuntil they are up and mobile and
then those who may need it fora much longer time and need one
(16:41):
or two substances that maybehelp prevent their coagulation
cascade at a couple points.
Right now we have found thatplatelets blocking platelets
which are the beginning of aclot with aspirin is as good in
terms of DVT prophylaxis,preventing PEs, preventing DVTs,
preventing all-cause death asLovenox has been.
(17:04):
That we have been done and weare beginning to make that
transition.
That was a New England Journalarticle.
I think we can probably be evenmore specific, more patient
specific, based on their genepool.
We just haven't figured outwhat that gene pool is, but I
envision the day where you comein, you're a multi-trauma, we
(17:25):
draw your gene pool.
Come in, you're multi-trauma,they.
We draw your gene pool, we runit through the, through the, the
match.
Speaker 2 (17:32):
We, we know that you're at a 10 or 20 or a 50
risk for dvd prophylaxis andthat you will respond to
platelet blockers or cascadeblockers or both, depending upon
your risk profile that's funnyseeing that I'm looking at that
vanderbilt health sign behindyou as you're doing this and I
always my youngest, my oldestson was born while we were at
(17:53):
Vanderbilt and I always thoughtthat someday he's going to look
at what I do and go well, blesshis heart.
Dad thought he was doing theright thing, but we all know
it's this thing now.
But things are going to changeso dramatically between the time
that and you have.
You have a daughter who's aphysician, don't you?
Speaker 3 (18:08):
dramatically between the time that and you have, you
have a daughter who's aphysician, don't you?
I have a son and a daughterthat are both smart like their
mother, and pediatricians.
Speaker 2 (18:19):
Ah, okay, all right, let's step out of the clinical.
We'll directly clinical run fora minute and start looking at
some of the healthcare practiceand stuff like that.
Like everything else in theworld, orthopedic trauma surgery
is heading into the outpatientarena.
Where do you see that headed?
Speaker 3 (18:31):
I mean that's a train that's already headed that way
and you know our entiredepartment is planning on moving
offsite and having an offsite.
You know 24-hour surgery andASC and that'll probably just
continue, except formulti-trauma.
You know complex spine, complexjoints, tumor cases and that's
(18:53):
probably better.
I think every time it's beenstudied that it's done more
efficiently with greater patientsatisfaction, with lower
complication rates in thoseoutpatient or you know systems
where that's what they do atthat surgery center is they do
pylons, they do plateaus, we do.
(19:14):
You know outpatient fracturefixation and you can increase
productivity.
The patients drive up, they getin their car, they drive away.
I mean every day today inclinic, every patient.
I apologized for the parking,the transport.
You know we're underconstruction and it's just
impossible and they walk, theywalk, they walk farther to come
see me than I probably do fromour parking lot to the clinic
(19:37):
and but that's that's just partof it.
I think can you do it safelywith patients and our we think
we'll rely on our anesthesiateam to identify those patients
that can safely have outpatientor 24-hour surgery in a
different setting than a mainhospital.
Speaker 2 (19:54):
You kind of tapped around the edge of it, but I
found regional blocks,especially with the bupivacaine
sorry, the liposomal bupivacaineto really help out.
Have you stepped into that part?
Speaker 3 (20:05):
Oh, yeah, I like to say I am the greatest utilizer
of the block team in the entirehospital.
I just, I mean it, we'vestudied it works right, you know
, I mean, some people hate toget stuck with the, you know,
stuck with the needle before andI think it takes communication
and we have developed a protocolwith our anesthesia team that
(20:26):
you know.
These are the things that youcan block and we want you to
block them and please block thempre-op and if there's any
questions, or we put in a notesaying you know, we need to
check the radial nerve post-op.
So don't, you know, don't blockit before.
But blocks, you know, decreasesanesthetic intra-op.
Decreases delirium post-op.
Decreases narcotics post-op.
(20:47):
Improves patient satisfaction.
What's the problem?
Right, I?
Uh, and yeah, you have to havea system so they're not delaying
your time by 30 to 40 minutesby doing that.
But I, I think we will continueto use different blocks.
You kidding me when, when youand I were in training, you gave
everybody intramuscular demerol, right, you know, we kept total
knees in the hospital for fivedays, immobilized their knee and
(21:10):
gave them Demerol for three orfour days and zonked them.
And you know, now you'regetting non-union operation as
an outpatient.
So yeah, we will continue tomake advancements in regional
block.
And not just that, but multimodal medication.
And you know, now we use multi.
(21:32):
You knowontin, tramadol,toradol, you know a variety of
medicines and we know they workbetter together and the ota
wrote some great clinicalpractice guidelines for that.
And it's not just themedications.
And you know joe shoe.
Joe shoe has been great atpromoting multi-therapy.
You know, using aromatherapy orsound therapy, electrical, you
know 10 unit therapy.
There are lots of differentmodalities that just work.
(21:53):
Every time we've studied themin prospective randomized trial.
They work better thanmonotherapy.
And just given and I was guilty, I gave everybody Oxycontin,
you know, and we create a lot ofaddicts based on false data and
we were guilty, so we got, sowe were part of the problem.
We need to be part of thesolution and read our literature
and change our practices to tryto decrease the problems which
(22:16):
we have created and with betterpain control with patients.
Speaker 2 (22:21):
Now, how many orthopedic surgeons do y'all
make every year?
Were there in Nashville Four orfive.
I know it was five when.
Speaker 3 (22:27):
I was.
Our residency program has five,just going to six last year.
Speaker 2 (22:31):
I think there was four when I was there, I can't
remember, I was only there formy fellowship.
But so y'all are making five ayear.
You're fixing to make six ayear.
Those are very expensive peopleto make orthopedic surgeons.
You and I both know that.
So in the future, let's, let'scrown you as a secretary of
(22:51):
health and human services.
Okay, so now you're doing that.
How do you see the scope ofpractice in terms of developing
what the nation needs in thefuture for orthopedic trauma
surgeons?
Are orthopedic trauma surgeonsdoing all the fresh work?
Do we have other people doingthe ankles and the other stuff
like that and we are doing thehigh energy stuff?
(23:11):
What's the best utilization, aswe go forward, for the
workforce?
Speaker 3 (23:15):
Yeah, I don't know the answer to this.
I do know that, in general, 90%of fractures are cared for in
this country by non-fellowshiptrauma trained individuals, by
non-fellowship trauma trainedindividuals, and so we cannot we
being the Orthopedic TraumaAssociation generate enough
(23:36):
orthopedic surgeons to do allthe fracture work Right, and so
routine fracture care has got tocontinue to be part of the
general orthopedic knowledge, sothat ankles, wrists, hips, you
know, femoral neck fractures,can all be cared for by people
who are well-trained in generalorthopedics.
(23:57):
That that should probablymaintain, and so and they can
stay close to their home forcare and to just help make sure
that people continue to becompetent and patients could get
care with that, and so I don'tthink that will or should change
.
I mean to continue to provideexcellent educational
opportunity to help them withthe fine points, to identify,
(24:18):
maybe, what's not routine and totransfer patient, transfer care
that they're not comfortablewith.
And I do see, though, thatcomplex fracture work is
expanding into the level twos.
You know, when you and I do see, though, that complex fracture
work is expanding into the leveltwos, you know, when you and I
were training, it was almost alllevel ones.
Everything got shipped there.
The reality is that you know wehave been fortunate enough to
train enough orthopedic traumasurgeons that now the primary
(24:41):
place that our graduates aregoing on the fellowship
committee are going to level twocenters.
Personally, I think that's agood thing, I think they're, and
I think it's good for patients,it's probably good for local
orthopedic surgeons and andhopefully it's good for the our
trainees that are going thereand they're a resource in their
(25:01):
community that can do the harderfractures or those that you
know that maybe need a littlemore experience.
And and also so that theeverybody, the total joint
surgeon or the sports surgeondon't feel compelled to start
that tibia nail at seven o'clockat night after their you know
(25:22):
their last elective case wentand you know they're tired, the
team's tired.
I mean, even at Vanderbilt weare one of the busiest trauma
centers in the world.
It's got to be really bad forme to be there doing it after
7pm, because I am not much goodby myself and and and when I say
give me a what's it and I get awho's it in my hand and and
(25:46):
they are.
They look at me and say I don'tknow what you're talking about.
I mean, even at a busy placelike ours, our personnel are
just not skilled enough and andthere are many things you just
need the A game team and youknow we have been fortunate to
go through that transition tomake trauma more semi-elective.
I mean sure there's things thatwe're going to have to get up
middle of middle of the nightand do Dirty, dirty compartment
(26:08):
syndrome, bad infections,bleeding to death but the
routine stuff I can and hopeshould be semi-elective and that
systems will have OR capacityand personnel trained available
in terms of x-ray techs, scrubtechs, first assistants, to make
(26:32):
it a much more sustainable lifeand career.
I feel fortunate we've beenable to build that at Vanderbilt
and you've been our guestspeaker and you've seen our
system and I tell our fellowswhen they leave that you're
going to miss us a little bit,the faculty.
You're really going to miss ourtechs, our cast techs, our
system that we've built aroundit with APPs to help us run a
(26:55):
fairly efficient high volumesystem.
Speaker 2 (26:58):
I barely recognized that.
I was there 98 to 99.
And when I was up there it waslike, wow, this place has
exploded and it was great when Iwas there and it's unbelievable
now.
Trauma.
Now, obviously you and I arehighly biased on this, so I can
hear everybody rolling theireyes and that's okay.
But trauma is the number onekiller of Americans between the
(27:21):
age of six months and 45 yearsof age, and so our disease
process that we treat iscrippling the American economy,
the North American economy, theworld economy.
When I work in Africa, itcauses a massive amount of
problems there for the economicdriving force of the societies
(27:42):
that people are injured in.
So, as you and I also know, asignificant amount of funding is
directed toward cancer, cardiacdisease, hiv you name it as
opposed to what you and I alsobelieve is something that, if
more money and attention wasapplied to it, we could really
make societal changes for adisease process that massively
(28:06):
affects a significant amount ofthe economic driver and the of
important workforce folks in ourcountry.
Once again, your secretary ofhhs, how do you fix this?
Heck, I'll make you presidentus.
How do you fix this problem?
What?
What do you think in the future.
What's the right thing to do totry to mitigate this?
(28:29):
This?
However, you want to financetrauma care, trauma prevention,
whatever.
Speaker 3 (28:35):
Yeah, so you know, I was a undergraduate econ major
and, as you said, I did abusiness degree a while ago, and
so in my view it's it's aboutvalue and and what's the cost
per quality adjusted life yearand that's cost per quality in
(28:56):
the econ world and I hope we getto the point where that society
at least looks at where you'regoing to put your investment.
I mean, the amount of need isinfinite in terms of problems of
the human condition and everygovernment you know needs to put
resources towards what I wouldhope would be those where they
(29:20):
get the greatest bang for theirbuck.
And for I don't know 20 years Ihave been saying you know,
bring it in terms of orthopedicsin general or particularly
orthopedic trauma.
You know, right now totaljoints get all the credit for
having one of the lowest youknow costs per quality.
But the reality is that I wouldsay, compare that to a femur
(29:41):
fracture.
All right, you know.
I mean the average age of aperson with a total joint is 60
something.
Average patient with femurfracture is 40 something, this
40 year old.
If they don't get this done,60% don't go back to work.
This is why Switzerlandinvested in femoral nailing and
why the Swiss government fundedthe AO Research Institute in the
(30:06):
50s 60s, because they realizedthey had a workforce and they
had a universal coverage and sopeople would go back to work.
And so the cost just think ofthe cost per quality of those
two things Total joints are moreexpensive than a femoral nail.
Their patients don't live aslong, they're not working
anymore, they're not payingtaxes, assuming they're retired
(30:28):
and this 40-year-old's gotanother 20 to 30 years of work
life in them.
And so if you want to run thateconomic analysis, bring it.
And so in a world where valuematters and maybe worlds or
governments have to makedecisions, I would hope that you
and I, or our specialties,could make that argument that
(30:49):
this is worth investing in inpreventing disability death.
You know the deaths come frommotor vehicle collisions and
that's maybe.
You know we the rare, ourpatients don't usually die.
They do occasionally they getinfection at around or you know.
But the prevention comes on thecar manufacturers on the
(31:10):
driving on.
You know, preventing drinkingand driving and drinking and
motor scootering in Nashville,taxpaying people to requiring
government assisted often, andinvesting in those people to
prevent disability, to returnthem to the working force, I
(31:35):
think could be the ROI on that.
I mean, you're the business guy, you've been the leader of huge
groups and chairman of thedepartment and you understand
ROI.
If you're going to put yourwhere's your, where are you
going to put your investment?
Your return on investment wouldbe much greater in that
population of people who aregoing to return to work to avoid
(31:58):
complications of infection,non-union DVT or death or
amputation.
You prevent those four thingsor amputation.
You prevent those four thingsand you have greatly improved
the quality of life with afairly low cost per quality
adjusted life year.
Speaker 2 (32:16):
That's funny.
You were saying something Ithought.
We did a tour of the Porschemuseum in Stuttgart and there
was a little plaque that if youweren't looking you'd miss it.
But they said that deaths frommotor vehicle collisions have
decreased substantially and ofcourse they patted themselves on
their back for their vehicularsafety.
But they did acknowledge thattrauma care had improved
dramatically over that time.
But thinking out of the box Ithink you touched on this, I
(32:39):
know you touched on this earlierand I think this may be the
disruptive way of looking at it.
Tell me what you think of this.
In many ways, if we want toreally reduce the complications
of fractures, many thingsoutside of the things that you
and I focus on on a daily basisspecifically eradicating smoking
(32:59):
and doing something to helpwith these horrible HbA1c's that
we see all the time wouldmaterially probably do more than
many other things we do.
Unlike the joint surgeons, wedon't have the opportunity many
times to tee our patients up.
We do in a non-union setting,but prior to that we don't.
It's kind of interesting tothink that maybe in trauma
(33:20):
surgery, if we could hit a magicwand and get rid of smoking and
get rid of crazy HPA1Cs.
We may do more to affect theoutcome of our care than almost
anything else.
What do you think of that?
Speaker 3 (33:33):
Oh, I know, we know that's true, you know
orthopedics and the consequencesare public health diseases and
crises.
And you know, I think it'spretty common knowledge that
smoking increases non-unioninfection rate.
What's not really been known isthat hyperglycemia,
perioperatively is also raisesinfection rates.
(33:54):
And and I mean we have lookedat this retrospectively,
prospectively, in isolatedorthopedic and in multi-trauma
patients and published it.
All the above and every timethat the odds ratio of infection
with hyperglycemia innon-diabetic patients raises the
(34:14):
risk about three times equal toan open fracture of having a
perioperative infection, afracture-related infection.
So this perioperativehyperglycemia is huge, even in
the non-diabetics.
So in the diabetics it's evengreater.
And you're 100 right.
That's where those who are atrisk is, where we ought to put
(34:38):
as much or as as of our effortas we can it's almost funny that
the best thing made me to comeout is none of the cool sexy
technology driven stuff.
Speaker 2 (34:46):
Have it's.
Just quit smoking and get yourdiabetes under control and we,
materially, would do more yeahyeah.
Speaker 3 (34:53):
And the chronic inflammatory state of obesity is
a problem as well for fracturehealing and the hormonal
imbalance of that.
That's more of a data-freeopinion, but I think that it's
true.
Speaker 2 (35:05):
Funny that that would be the thing that would really
help the most.
So where do you see the futureas it relies or relates to the
management and or the preventionof fracture-related infection?
Speaker 3 (35:16):
Yeah, we talked a little bit about prevention in
terms of the patient-codedimplants or local antibiotics.
But one thing that is feasibleand I think in almost every
systems is the fix and flapphilosophy which the Oxford
group in Europe has reallypromoted.
And I think they're right.
And I think Paul Tornettarecently put together a four 400
(35:37):
plus tibia fractures and thegreatest predictor was doing the
fixation with doing the flapcoverage within 48 hours of
definitive fixation.
And we have a patient like thatthis week that came in he's got
a 3B tibia.
My partner did IND damagecontrol plate, did another
debridement yesterday and thenI'm going to do a debridement
(35:58):
and put a nail in it tomorrowand then on Friday morning the
patient is scheduled for theirfree flap and to try to minimize
that time from a systemstandpoint in trading off who's
taking care of the patient andthen providing definitive
coverage, you know to try todecrease the time to race to the
surface and get that patientcovered is within 48 hours.
(36:19):
So that's one thing we'retrying to do for prevention, the
management future.
I think we've come a long waybut we still have so far to go
and I think part of it is thisonce bacteria become established
.
They're really hard to get ridof.
I just it's like a worthyadversary.
And you know, I was a Duke guy.
(36:41):
I spent undergrad med school atDuke and I sort of think of his
Duke Carolina basketball gamesand Coach K and in 40 years he
was 50-50.
He only won half the games.
That's just a great rivalry,and in our fight with bacteria
we won't always win but weshould do better.
And because, you know, staff inparticular goes up the
(37:02):
canaliculi of our bonetrabeculae, they form micro
abscesses, they form biofilm,become senescent and in none of
those I mean even our whiteblood cells can't get up into
the canoleculi.
They can't get in the microabscess, nor can they get in the
biofilm.
And so we have got to developsome ways to try to help
(37:25):
eradicate infection once it'sestablished.
And I think some of those onthe bacteria and also in the
bone and some of those ways thatI think that we might make
progress in the future, becauseour recurrence is embarrassingly
high.
When we look at infectednon-unions, the management of
those, we fail one out of fiveabout the reality is when you
(37:49):
look at large series, it's abouta 20% failure rate, and so we
need to do better in that.
And so what are the things wecan do in the face of infection
to help eradicate the bacteria?
Even if you remove the implant,you still have trouble with the
bacteria there.
But I think there will besolutions that are biobusting
(38:11):
biobusters that can reallypenetrate the mechanism and what
holds biofilm together andcause it to dissolve, and that
may help us eradicate thebiofilm in some ways.
Other things that can removebiofilm from implants that are
in place and maybe you don'twant to do.
(38:32):
You get an infection at threeweeks from a bicon or plateau
that you smoosh together.
Do you really want to take allthat hardware out?
You know we've proven that youcan treat them to union.
You know, with just debridementand antibiotics 80% of the time
, but you're still not winning20% of the time.
And so when something thatmight improve that is using
(38:53):
electrical current and I see aspotentially electrifying the
implants and that that beingeffective at sloughing off or
killing the bacteria that are inthe biofilm and and I think
that may be something that willhelp us Other solutions that may
sit for a while.
(39:13):
You know there's all this inthe total joint of Experian or
dilute betadine and more in theprevention world, but I think
that some of that will translateinto the infection management
world to try to help with thesemicro abscesses, these bacteria
up the canaliculi that need tosit for a while before the
bacteria can be killed fromthose areas.
(39:37):
And the other thing that I thinkwe will develop is the use of
phages.
Phages are the natural hunterkillers of bacteria.
They were all the rage of theforties, fifties until
penicillin got invented and thenall that phage data and just
sort of went away.
But now with multi-drugresistance returning that phage
(39:59):
therapy in terms of ability tomaintain an implant, because
phages are so small that theycome in and they can go into the
biofilm, they can go up thecanaliculi and they can even
penetrate a micro abscess andthen they go in, they attach
themselves to bacteria and thenthey enter the bacteria, they
(40:22):
take over the mechanism of thebacteria and then they make
morphages and then they disrupt,that cell dies and they go away
and they look for more and theyhunt and kill and then they go
away when all the bacteria aredead.
What a great natural hunterkiller of bacteria to use that
in combination with either totaljoints or implants.
We want to keep in place.
(40:43):
The standard mechanisms of doingthat, I think, are challenging
and we don't know those yet, butI see phages as in our
armamentarium in the future.
Until then, I think we will getmore use of local antibiotics
as well, which can sit in highdose locally where there may not
be great blood flow because ofa perfascial disease or the
(41:05):
damage to that area, but eitherwith right now one of the best
carriers is calcium sulfate, andI use far more than I ever used
to because it all dissolves andit just takes several weeks,
but it can be effective in themanagement of a chronic
infection in terms of lettinghigh dose local that doesn't
have has very little systemiceffects on patients or kidneys.
(41:27):
And so that combination oflocal antibiotics with either a
hydrogel or a calcium sulfate,having bio busters some, or
electricity to eliminate orsolutions to eliminate the
biologic biofilm, are some ofthe things that we can.
We can do in the future to tryto help maintain hardware and do
(41:52):
it better than we are in termsof allowing, you know, fractures
to heal without having to takeit out.
And then the other trend whichis coming is the PO antibiotics.
I've been on that train for 30years, you know we have finished
our metric study on acute FRAwhere it's represented, at the
OTA a couple of years ago andthat has been submitted to JAMA
(42:12):
surgery and hopefully it'll comeback positive accepted.
But we're in the middle ofenrolling patients in PO versus
IV antibiotics in infectednon-unions and I expect the data
will be the same.
There's some data out of Europethat says it is the same
already.
So those were.
I think we're going in terms ofmanagement of acute and of of
infections associated withfractures with or without a non
(42:35):
union.
Speaker 2 (42:36):
Wow, this has been an absolute pleasure talking with
my friend and colleague, dr BillLabrowski, who is
well-recognized as aninternational leader in
orthopedic trauma surgery, onthe future in orthopedic trauma.
Dr Abramski, sir, thank you forbeing on the podcast.
Speaker 3 (42:51):
Doug, my honor and pleasure.
It's been an honor to be yourfriend and colleague and I look
forward to following in yourfootsteps as the president of
the Orthopedic TraumaAssociation.
Speaker 2 (43:00):
You're very generous, sir.
Thank you and I look forward toseeing you in Montreal and, for
the rest of y'all, stay tunedfor more in this series on the
future in orthopedic surgery, onthis AOA podcast channel.
Thank you.
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