Jumat, 14 Juli 2017

osteoporosis interventions

osteoporosis interventions

[ silence ] >> hello and welcome to thespinal cord injury forum. i'm chuck bombardier. i'm a rehabilitationpsychologist here at the university ofwashington and the director of the northwest regionalspinal cord injury model system. we're grateful to the nationalinstitute on disability and rehabilitation researchfor sponsoring our forums. they make all the contentand videotaping possible

by a generous grant wehave received from them. tonight, we're very pleasedto welcome dr. jelena svircev as our speaker talking aboutosteoporosis and fractures in persons with spinalcord injury. dr. svircev is an assistantprofessor at the university of washington in the departmentof rehabilitation medicine and she's one ofthe staff physicians at the spinal cord injuryservice at the department of veterans affairs at thepuget sound health care system.

dr. svircev. >> thank you. thank you sci for inviting mehere to speak with you and share with you some of the things thati learned about osteoporosis and spinal cord injuryand fracture management. i have a few disclosures. one is that i have nofinancial disclosures. the second one, as manyof you who are consumers of spinal cord injuryknow that there are--

there's oftentimes verylittle evidence that we have to support many ofour practices. so when i talk about someof the management principles with osteoporosis andwith fracture management, if you find yourselfthinking, "hey, i had a fracture a while back"or "hey, i had a conversation with my provider aboutosteoporosis that's different than what i'm saying," recognizethe fact that there isn't a lot of literature and that eachrecommendation that's made is

based on the literature thati've gathered, the practices that i've learnedfrom my colleagues and how the individualsthat i work with have chosen to interpret the information. so take with you the informationthat i'm sharing with you and when you go talk withyour provider, you can bring up these different issues thatwe've discussed today but know that each treatment is goingto be customized to you. the last disclosure that i haveis, as dr. bombardier mentioned,

all my clinical time, excuseme, is done at the va. so throughout the talk,if i refer to my guys, it's because most of theindividuals that i work with are guys and that it'snot just showing you disrespect to my guys. we have wonderfulrelationships with the veterans. we do service smallfemale population and i don't mean no disrespectto the females in the audience and certainly thefemale veterans.

but i found myselfsometimes using that language. in the next courseof our discussion, i'm hoping we're going to learnsomething about osteoporosis in the spinal cord-injuredpopulation. we're going to talk abouthow one evaluates, treats, and prevents osteoporosis. are these even possibilities? if an individual fractures, whatare the fracture characteristics and how does one then managea fracture in the setting

of spinal cord injury. mr. k is going tobe joining us today. he is one of my guys. he is a young gentlemanwith a paraplegia. he's in his early 40s and hecame into clinic and said, "all right, doc,i've been injured for a couple of years now. i've heard about thisosteoporosis and bony weakening. i've got two little kids.

my two little kids like toride my leg as they show in this picture sometimes. i'm very active. i work full time. i like to ski. i also have a grandma whojust fell and broke her hip and i'm worried withmy occasional falls, with my transferswhat's going to happen to me 'cause she is goingdownhill quickly and doc,

i need your help tosee if there's a way that i can help managethis a little bit better." i said, "all right, mr. k, we're going to have along conversation now. we're going to startwith the basics." so if we think aboutosteoporosis, we think about bones and wethink about a typical long bone which is the long skinny ones, we think of a coupledifferent parts of the bones.

so we have the ends of thebone, the top, and the bottom, those are the epiphyses. we have the diaphysis andthat's the shaft of the bone and we have the metaphyseswhich is the part where the shaft kindof meets the end. and the area that we wantto focus on when we think about spinal cordinjury is the epiphyses, the ends of the bones. bone itself has acouple different parts.

we have the cortical bone,that's the compact bone. it's the outside of the bone. it makes up about 80percent of the bone. and then we have thetrabecular bone and that's kind of the inner, verymeshy layer of the bone. when we think of abone, you usually think of a solid hard object kindof like a rock and i want to emphasize the fact that boneis not a solid nonliving object. it is a very dynamic structure.

you have a coupledifferent parts of bones. bone is part of an organ so itis made up of different cells. we have the osteoidwhich is the bony matrix. it is a noncellular substance,but then we've got a couple of different cells, theosteoblasts, osteocytes and osteoclasts and theseare all living dynamic, tiny components thathelp support the bone, so it's a living, breathingorgan albeit it operates at a much slower pace thanmany of our other organs.

when we think about osteoporosisnow, osteoporosis is a disease where the mass of the bone, thesubstance of the bone is reduced so that fine bony architecturestarts breaking down, which is characterized by animbalance of the bony formation and the bony resorption,the breaking down of bone. and when we start losingthat fine bony architecture, we find that the bonesbecome more fragile and when the bonesbecome more fragile, an item that's more fragileis more bound to break.

in the next couple pictures, wehave just a schematic of what that breakdown looks like. so on the one side, we'vegot the healthy cortical, the outside of the bone and thetrabecular bone where you see that thickened cortex, thethickened outside layer of the bone and thetrabecular bone on the one side, you got lots more fine mesh. and as one goes to the processof developing osteopenia, first weakening ofbone, and osteoporosis

and severe osteoporosis, yousee that that cortical bone, that outside layer ofbones starts shrinking down and you see that youstart losing some of those fine connectionsin the trabecular bone so it is breaking down. those structures are losingconnections, hence leading to increased risk of fractures. this is another example ofthat-- of the top of the femur. so this is the upper leg boneand we see that the cortex,

the outer layer of the boneinitially is very thick and as one developsosteoporosis, it becomes much thinner, same thing with thatintertrabecular layer. it's nice, finely meshed. and as one developsosteoporosis, those connections arebroken down so you're left with a weaker structure. in order to think about howosteoporosis presents itself

in the spinal cordinjury population, i always find it helpful totake a step back and say, "well, why are we so worriedabout osteoporosis anyway? what about the able-bodiedpopulation." and we hear about it quite oftenin the able-bodied population. why do we hear about it and in what settingdo we hear about it. so many people areaffected by fractures, so 300,000 peopleper year in the us.

hip fractures usuallyhappen in adults who are over the age of 65. about 30 percent of individualswill die within the first year of fracture and there's ahuge amount of functional loss in those individuals whoare living the first year to two years after fracture. so only 40 percent of individuals will regain theirprefracture mobility level, so if they were ambulatingbefore fracture,

they may not be ambulatingafter fracture. only 25 percent of individualswill regain their formal functional status, so ableto take care of themselves and perform their activitiesof daily living to the degree that they were beforetheir fracture. and 71 percent ofindividuals aren't able to live in their prefractureenvironment. so we see that in theable-bodied population, not only is therea huge mortality

after one sustains a fracture, but there's a hugefunctional decline and this is where the big concern lies. we have to ask ourselves though, can we immediatelyextrapolate this and apply it to the sci population andi'm going to keep coming back to this idea throughoutthe talk. so how do we diagnoseosteoporosis? like we said, bone strength isrelated to bone mineral density,

so how much substance is thereand osteoporosis is that break down of the substance. one of the ways that we candiagnose osteoporosis is by doing dual-energyx-ray absorptiometry, which is sometimes forshort called dxa scanning for obvious reasons,they're mouthful otherwise. it's the most common methodto diagnose osteoporosis. it's a measurement ofthe bone mineral density. and the areas that oneusually examines when looking

for osteoporosis is thespine, hip, and forearm and this is another ideathat we're going to come back to when thinking aboutdiagnosing osteoporosis in the sci population. so with a dxa scanner, it's apaddy table with an x-ray tube. there are a couple x-raybeams that are performed and the difference betweenthose two beams are used to calculate a score. and then the scorethat one receives

after having a dxa scanis compared to that of a healthy personin their 20s. so when we think about how doesthe definition of osteoporosis, how does one get that diagnosis? we go to the worldhealth organization. osteopenia, which is theweakening of the bones, is given to an individual whohas a bone mineral density that is-- who has a bonemineral density score, as measured by dxascanning, that is lower

than someone in their 20s. someone has osteoporosis ifthe bone mineral density score that is much lower thansomeone in their 20s. so there are precise numbers. i won't go into those but knowthat it's a significant decrease in bone mineral density compared to an able-bodiedperson in their 20s. so what about osteoporosis in the spinal-cordinjured population?

when do we see it? well, we see it pretty soonafter spinal cord injury so it can be seen on x-rayas early as six weeks after spinal cord injury. most people think that anew steady state is reached about two years after spinalcord injury and in fact, about 80 percent of individuals with chronic spinalcord are going to have either osteopeniaor osteoporosis.

so it's a very common occurrencepost spinal cord injury. this is a simple graph thatdemonstrates what we expect to see in the able-bodied. so the top line, the bluesquares represent what we anticipate to see withbone mineral density in males as they age. the pink line demonstrateswhat we anticipate to see with bone mineral densityin the female population. these are both able-bodied sowe see that there's a high level

of bone mineral density whenan individual is in their 20s and it slowly decreasesover time. women have a lower bone mineraldensity than men and it goes down a little bit more abruptlycome about the age of between 50 and 60 with the onsetof menopause. well, what do we see with thespinal cord-injured population? we're going to compare this--we're going to use our example of the spinal cord injuryindividual as a male who is age 45 atthe time of injury

so they are plugging alongwith the bone mineral density on an able-bodied personuntil their injury, age 45. and within two years, that individual's bone mineraldensity is going to be dropping to a level of abouta 70-year-old woman, so there's that profound drop and it's very significant verysoon after and it leaves us with many questions when wethink about the prevention of osteoporosis andthe treatment

because that treatmentperiod for someone with a spinal cord injuryis going to be much longer than it is for someonewho is 70 or 80 years old. let's take a step back andsay, "ok, well, you know, we kind of have an ideaof why osteoporosis occurs in an able-bodied population,aging, weakening bones, alterations in hormonal levelswith the female population. what about spinal cord injury?" and with the sci population,

everyone always leaves theirhands and says, "it's you, it's because youdon't use your legs." well, yes it is. but as we're learningin spinal cord injury, it's never just one thing. there're always multiple factorsthat play a role in any sort of regulation and maintenanceof balance within the body so we see that disuse is one ofthe causes and we're going to go into that a little bitmore in depth in a moment.

we know that disorderedregulation in the delivery of nutrients through theveins and the arteries of the body can play a role. autonomic dysregulation, so thenervous system and the balance of input and output from thenervous system plays a role, how much? we really don't understand. we're just startingto learn this area. hormonal alterations,metabolic disturbances,

poor nutritional status can allplay a role and we don't know to what degree, that's thepoint where we're just starting to do research on hormonalalterations in sci, let alone hormonal alterationsin sci with osteoporosis so we're just starting togather this information. but the point is, isthat as with everything with spinal cord injury, it'snever just one issue which means that if you find a way to treatone component, it's just going to be a componentof the treatment,

that there are many otherfactors that are going to come into play in the developmentof that one condition. i'd said we're goingto talk about disuse. well, this is disuse. and we know that disuse playsa role in the development of osteoporosis and whydoes it play a role? well, we have this idea thatmechanical loading of the bone, so weight being placedon the bones or activity on the bones is communicatedfrom cell to cell.

so we had said that bonesare a living dynamic organism and when one puts pressureon the bones, that pressure, that sensation of pressureis somehow communicated through little connectionscalled gap junctions and with the use of transmitters and those transmitters will tellthe different types of cells, osteoclast, the bone buildingcells, the osteoblast-- i'm sorry, the osteoclast,the bone-breakdown cells. the osteoblast,

the bone-building cellswill tell the blast to act the clast to break down. if you don't have thatmechanical loading, if there isn't weightbeing put on the bones and muscles actively pulling onthe bones on a consistent basis, that communication and thattrigger of bone building and bone breakingdown is altered, so you don't have thesignals that are going to the bone building cellssaying, keep on building.

and if for whatever reason,you aren't getting that turnoff of the bone breakdown cellsof start breaking down. so one ends up withan imbalance. why this occurs? we just don't know. we're just starting to learn about how those transmittersoperate and the regulation of it. what about neurofactors and whatabout this idea of circulation

and nervous system playinga role on osteoporosis. well, we can think about,we know that individuals with spinal cord injury havealtered circulation at times. we know that the nervoussystem somehow plays a role in nutrient exchangethroughout the body. so if one is not gettingadequate nutrients or altered levels ofnutrients, or altered level of oxygenation throughout thebody, throughout the system, we can expect that this may alsobe happening at the bony level,

that there's some sort ofaltered nutrient exchange at the bony level and thatin addition may be causing-- contributing to theosteoporosis. so all right, we've gotan understanding now of osteoporosis,how it developed, how does it look like,how is it manifested in that spinal cordinjury population. when we see osteoporosisand spinal cord injury, we see it happening belowthe level of injury,

so this is the idea ofthe level of injury, how does that come in. well, osteoporosis alwayshappens below the level of injury. we see an average bonemineral density loss of about 30 to 40 percent. we see trabecular bonebeing more effective than cortical boneso that inside area of the bone is more effective

than the outsidelayer of the bone. and we see a greater losshappening at epiphyses, at the ends of the bone,rather than the diaphysis, the shaft of the bones. so if you think about it, ok,if more of my loss is happening at the epiphyses,that's probably where the fracturesare going to happen and that's in fact what we see. so classically, we seebone loss happening

in the lower extremities, thelower one third of the femur, the top upper bone ofthe leg is affected more than the other parts ofthe femur and the top part of the tibia so the top of the bone just below the kneeis most affected by bone loss. other things thancan affect bone loss in spinal cord injuryis level of injury. so we see that there's increasedbone loss in individuals who have tetraplegias orquadriplegias versus paraplegia,

and that kind of makes sense. so if you've got more boneloss occurring below the level of injury, if youhave a tetraplegia, you've got more bones that canbe affected below the level of injury than compared tosomeone with a paraplegia. we also know that the extentof injury, so the completeness of injury can attribute to morebone loss than an individual with incomplete injury. and when we think about this,

this may also intuitivelymake sense, that someone with an incomplete injurywho has some movement of their legs is going to havesome loading, some movement of the muscle pulling ontheir bones to maintain that bone mineral density thansomeone who has a complete level of injury who may not be doingany weight bearing throughout their lower extremity andmay not have that movement to help facilitate themaintenance of some of that bone mineral density.

all the things that mightaffect bone mineral density but we really don'tknow, we talked about-- i just talked about thatidea of incomplete injury and i suggested that tibiaor muscle pulling on bone may in fact maintain some degreeof bone mineral density. but when you thinkabout spasticity, spasticity is muscle pulling onbone, albeit not voluntary most of the time but isbearable for spasticity. the spasticity actually helpedmaintain bone mineral density

when compared to someonewithout spasticity. we don't know. this is kind of the theoreticalpart and the theorized when it comes to osteoporosisand spinal cord injury. how about duration of injury? so someone who's been injuredfor much longer than someone who is just injured, is theirbone mineral density going to be altered. and there are somesuspicion that it is.

we do believe that thereis some stabilization of bone mineral densityabout two or three years out after injury, but isthere a gradual decline that may happen with years. very well maybe, it kindof seems to make sense. we don't have thesestudies to support that but intuitively,it seems logical. well, that's all fineand good but what about the reallyimportant stuff.

so at the beginning,we have said, "well, why are we gettinghot and bothered about osteoporosis anyway." in able-bodied population,we saw increased mortality, we saw increasedfunctional loss. what about the sci population? is that the same thing we'reseeing with the sci population and these are some questionsthat we're just starting to ask. so that's mr. k. mr. kwas like, "all right doc,

you gave me a good lecturethere, what about questions. i asked about prevention,i asked about treatment. is there something i can do? am i going to diefrom fracture?" i said, "all right, mr. k,we're going to get there." so first question, should webe screening for osteoporosis in the sci population? so why do we screen for thingsanyways, why do we screen for things in theable-bodied population.

we screen for things if we thinkabout breast cancer screening, colon cancer screening,prostate cancer screening. we're trying to identifysilent disease or risk factors and the goal is to sortout those individuals who have the disease but don'tknow it from those individuals who don't have the disease andwe've got to keep in our heads that you should be screening forsomething only if care is going to be changed as aresult of the screening. it doesn't make a whole lot ofsense to screen for something if

and then you're going tosay, "yeah, we got it, but i ain't going to doanything for you differently than i would if i didn't know." so let's think about thelocation of scanning. i had referred to thisa little bit earlier. we usually look at the radius,so that's the end of the arm in the able-bodied population,the lumbar spine, the lower area of the spine or the hip. on the spinal cord injuredpopulation, what did we say?

where does spine-- wheredoes osteoporosis occur? it occurs below thelevel of injury. so does it make senseto diagnose osteoporosis by screening for the radiusin the sci population? probably not. i mean, in fact, insome sci population, the radius may actually havea higher bone mineral density than a little old lady becauseyou guys use your arms to walk, so you do a lot of transfers.

you're always propelling,you're maintaining that bone mineral density. what about the lumbar spine? there is some thoughtthat individuals with spinal cord injury may havemaintained bone mineral density in the lumbar spine 'causeyou are constantly loading it. you're always in uprightposition and putting pressure on it, so that's probably nota great place to screen either. and then we think about the hip.

well, measuring up the hipis pretty hard for a lot of individuals withspinal cord injury. not only is the hip not an area that we classicallysee the biggest loss of bone mineral densityin the sci population, but a lot of factorslimit the ability for us to get a good study ofthe hip, so spasticity, if someone transferson to a table and that constantlyjerking up, you're going

to have a hard timegetting good image. what about contractures, whatabout heterotopic ossification. so we had talked about how adxa scan is measuring the bone mineral density. it's measuring thequantity of bone, the quality of bonein that area. heterotopic ossification, extrabone formation, that's going to mess up your reading. it's going to read a wholebunch of extra bone in that area

that you're trying todiagnose osteoporosis. what if someone hashardware in there? what if they had ahip replacement prior to their spinal cord injury? well, you can't reallyuse that area to measure. and then what about just thepracticalities that someone with a spinal cord injury thati'm sure many of you encounter on a daily basis of you're goingto the doctors, you're now going to go over to radiology.

they are totallynot set up for you to transfer over to the scanner. you may not be able to getinto the room and you have to take a step backand say, "ok, well, why am i doing thisagain in the first place? does this make sense for me? is my care going to be changed? is it going to be improvedwith this bit of information?" but when we got the study,shouldn't we just use it.

this is an issue that'scome up relatively recently in the medical community. so radiation exposureaccount-- from medical imaging, accounts for about half of the radiation exposurein the united states. radiation buildsup within the body and it increases therisk of certain cancers. so whenever an individual isplanning on having a study, they should be able to justifythe study, optimize the number

of images that they'regoing to have and limit. so, individuals whoare getting imaging on a more regularbasis should be aware of that cumulative effectand always take ownership of their own health andwhen they're provider says, we're going to get these filedstudies, you should realize, if i'm age 30 rightnow and i'm going to be getting these studies forevery year, every two years, that's going to be cumulative.

so ask you provider, isthis really necessary because i'm going to end up overmy lifespan having a lot more radiation exposure than someonewho is able-bodied most likely. so should we screenfor osteoporosis at all and mr. k is asking, "all rightdoc, you're giving me a lot of information there, shouldi get my screening done?" many people say no. eighty percent of individuals with spinal cord injury had saidhave osteopenia or osteoporosis

if we know that 80percent of individuals do, is it almost safer to assume that one will haveosteoporosis rather than doing a screening studyjust to confirm something that we had alreadysuspected occurs. there are instanceswhere perhaps doing that imaging would provide somevaluable information but that's where you need to sit downand discuss what are the-- why is one gettingthe imaging done

and with the informationprovided by the imaging, what is one going to dowith that information. so there are instances whereone should have screening done, but as a universalrecommendation, we are at the point where weuniversally recommend screening for osteoporosisin sci population. so that mr. k again, he's like,"all right, i got osteoporosis. what can i do to treat them?" so, we can talk aboutdifferent medication options

or vitamin options. we think about calcium. we can think about vitamin d. wecan talk about bisphosphonates, that's one of the prescriptionmedications that's often time used for the treatmentof osteoporosis in the able-bodiedpopulation and teriparatide which is another medicationused in osteoporosis. so, if you think aboutcalcium in spinal cord injury. we know that immediatelyafter spinal cord injury,

there's a giant boost ofcalcium within the body. the bones are no longer beingused as they were in the past. calcium is excretedfrom the bony system. but after a short periodof spinal cord injury, a new balance is established inthe calcium levels in the body. so, just supplementing withcalcium alone is not going to be able to maintainthat bone mineral density. if one is going to usecalcium supplementations, you can usually useabout a thousand

or 1500 milligrams perday, calcium carbonate or calcium citrate are options. calcium carbonate which is liketums is cheaper, but it needs to be taken with meals. it can interfere with how somemeds are absorbed in the body and there are sideeffects of calcium. so, renal stones, we think about spinal cord injurypopulation oftentimes stone formation, kidney stoneformation can be a challenge.

unsettled stomach,indigestion can be a challenge. constipation. constipation with scipopulation certainly common. and once again theabsorption of some meds. so, even what a seeminglybenign medication can cause some challenges and the use of the medication is once againsomething you should discuss with your provider particularlywhen it comes to dosing. what about vitamin d?

this is certainly somethingthat we hear about a lot in the seattle areaand the [inaudible]. there are small studiesthat have been done in the sci populationlooking at vitamin d and vitamin d deficiency. so we know anywherefrom one third to nearly a hundred percent, 96 percent of individuals haveeither vitamin d deficiency or insufficiency, sodefinitely low or pretty low.

why is this? well, sometimes thatplays a role. there's just inadequate intakeand limited sun exposure. so, not only livingin seattle is going to challenge your sun exposure. but individuals with spinal cordinjury perhaps are not accessing and getting out of theirhomes and exposing themselves to the sunlight as much. so some do recommendsupplementation

with vitamin d on a daily basis. one of the forms of vitamind that's recommended is cholecalciferol and it'sjust generally preferred over another form of vitamind called ergocalciferol. safe limits are usuallyabout 400 to 800 internationalunits per day. there's one study,that's the one that i said with the 2000 internationalunits of oral vitamin d and that just suggest thata higher supplementation

of vitamin d may besafe in individuals with spinal cord injurywho are very deficient in vitamin d levels to get themto a normal level and then come down with the moretypical levels of vitamin d supplementation. but we have to remember that vitamin d supplementation,again, is not benign. it is not without its problems. there's a potential toxiceffect of vitamin d consumption

and once again, discussany supplementation with your provider tomake sure that the doses that you're takingare safe for you. what about bisphosphonates. these are the -onate medication,so alendronate, risedronate, ibandronate, zoledronic acid,some of the more common names, fosamax, actonel, boniva. so these are the sally fieldmedications she's always too [inaudible] about herimproved life on boniva.

what we know aboutthese medications is that they stronglyinhibit bone resorption. so they stop the bonefrom breaking down. but we don't have great studiesagain in the sci population to support their use overa long period of time. so we see that onestudy suggested that taking etidronate,one of the oral forms of these medications in the acute spinal cordinjury didn't show much effect

on bone loss. another study suggested thatanother medication, alendronate, in this population dailyincrease bone mineral bone density. some showed-- while it decreasebone mineral density a little bit, some showed it increasesit a little bit over 24 months. who knows what happened after24 months when the study ended. but we got to remember one otherthing is that very recently, we have published literaturein the able-bodied population

that demonstrated thatatypical femur fracture, so not the usual femurfractures that are seen in the able-bodiedpopulation, have been reported to occur more oftenin individuals who are on bisphosphonates. so they were gettingthese odd fractures that were occurring whilebeing on a treatment medication for osteoporosis toprevent fractures. when we think about thismedication being used

for the able-bodiedpopulation, the conclusion was, in that population, we don'tknow how long an individual should be using bisphosphonates. well, what aboutspinal cord injury? so, we said thatfractures very often happen in the able-bodiedpopulation and individuals who are 65 years or older. what if i'm working with someonelike mr. k, he's in his 40s, how long should ibe recommending him

to use bisphosphonates. how long is he going to beat risk for osteoporosis? well, here's theanticipated life span. it's good in 20, 30 years,maybe 40 years we're getting with the spinal cordinjury population. and i can't tell himif this medication in the long run is safe. another medication,teriparatide. so, this is a synthetic hormone.

no studies in the spinalcord injury population. we know that in thepostmenopausal population, able-bodied population,it increases spine and hip bone mineral density and it decreasesfractures in these areas. what are these areas ofconcern in the sci population? so, once again, we can't alwaystake the information that's offered in the able-bodiedpopulation and directly apply it to the sci population andsay they're all the same

and we should betreating them the same. so we have mr. k,again, "it's fine. i don't even liketaking medications. i'm going to minimize them. what else can i do?" so what are the othertreatment options? what about standing? so, many individuals seek outthe use of standing frames. with the standingframe, are we providing

that mechanical loading that mayhelp decrease the bone mineral density loss thatoccurs in individuals with spinal cord injuries? got a number of small studies. unfortunately, theyaren't always consistent. some look at them in the acutepopulation, some look at them in the chronic population. some have complete injuries,some have incomplete injuries. one study suggested that doingstanding or using a treadmill

for walking for five weeksmaintain one's bone mineral density in the acute spinalcord injury population. another study lookedat individuals with chronic spinal cord injuryanywhere from 1 to 26 years and they showed thatthere was no difference in the dxa scanning intheir bone mineral density when compared withtheir ambulatory status. and this isn't to say thatwe're crossing out use of standing frame completely.

there are other benefitsof using a standing frame, so some people feel thatit helps with spasticity, it helps maintainrange of motion. there's certainly apsychological benefit for many individuals ofusing a standing frame, but can we justify the useof a standing frame solely for the idea that itmaintains bone mineral density, not really. what about fes?

so, fes is functionalelectrical stimulation. it's applying electrodesto the legs to produce muscle contractionand we have this idea of bone loading or pullingof the muscle to the bone and that helping to maintainbone mineral density? in this area, there's a lot of research that'scurrently occurring, but many small studies. so, the studies areanywhere from 2 to 38 people.

once again, they're notconsistent in the population of individuals withspinal cord injury that they've chosen to select. so they are varyingdegrees of injuries. they are varyinglevels of injury and various timeframesafter injury. and what they're findingis that perhaps the effect of functional electricalstimulation on bone is site specific.

so, is the end of the femur,actually the area that we want to stop those fracturesfrom occurring, does it maintain thebone mineral density in that location betterthan the top of the tibia, the area just below the kneecap? perhaps? some studies suggest that there is somemaintained bone mineral density with this equipment. but when we say ok, we'vemaintained bone mineral density,

what does that really mean? is a 7 percent increase in bonemineral density significant? so, if i'm going fromreally, really weak bones to just really weak bones,have i really made a difference if i fall from mychair and fracture. one has got to weighthose things out. so, as i said, we don'thave consistent evidence to support the use of functionalelectrical stimulation. some studies suggest that thebone mineral density is kind

of maintained afteryou stop functional electrical stimulation. other studies say thateverything is fine and good while you're doing it, but once you discontinueits use, bone mineral density will goright back to where it's at. we don't know what the frequency of maintenance functionalelectrical stimulation is if there is such a thing.

and we don't know if thatincreased bone mineral density really translates todecrease fractures and that's what we're tryingto prevent in the end. the last technique thatwe'll briefly discuss is low intensity vibration. so, this is the transmission oflow magnitude mechanical signals which are delivered byan oscillating platform. it's a thing that kind oflooks like a big scale, a big bathroom scale that[inaudible] and why this helps?

not quite clear. but we do know that it doesmaintain bone mineral density in animals and somehuman studies. no studies have been publishedyet in the sci population but a number of centers areactively looking at this. some of the challengesare though is that one needs specificadaptation to stand. so, using this oscillatingplatform, the shaking platform, one needs to put theirfull body weight on it.

so, now you've got this platformand you got a standing frame and for someone who hasn'tstood, are you going to run into challenges withorthostatic hypotension, or the drops of blood pressure. how are you going to dothis on a daily basis? ok. so, standing frame, riskof fracture and bearing weight, haven't done that in 30 years. lots of little pieces thatwe saw that will figure out. is it going to besufficient to just sit

and have a platformbelow your feet and do that for a coupleof hours a day? just looking at that right now. so preliminary studiesin progress, more to come in a couple of yearswhen i come back again. so, we have to take a step backand say, ok, what about cost? it's something that wedon't like talking about but we're all talkingabout healthcare cost. so, we think of some ofthe treatment options

that we've come up with. so medications, expensivemedications, many, many years because that risk of developing a diseaseis not going to go away, we think about a standingframe, where we think about functionalelectrical stimulation. so, therapy or caregivertime couldn't put a price on that but generally high. what about a standing frame?

it's about 2,000 dollars. functional electricalstimulation 20,000 dollars. i use the calculationwith our va discount. we could say about 6,000 dollarsper year for medications, about 2,000 dollarsfor a standing frame, 30 years of treatment if we saythe individual was between 40 or 45 years at thetime of their injury. so 200,000 plus dollarsto prevent osteoporosis, our goal is to preventone fracture,

is that worth our investment? and we're going to take a back--a step back and think about one of our-- what wereour first questions, mortality, functional abilities? have we answered that yet? and we haven't yetanswered that. so, do we have a wayto prevent osteoporosis right now, we don't haveany therapeutic intervention that prevents osteoporosis inindividuals who don't ambulate

and we have to ask ourselves. if or when we findtreatments that slow bone loss, are they cost effective? so, is it worth the riskand worth the inconvenience, worth the price of multipleexpensive medications for life? hours of standing frame, hoursof electrical stimulation, how does that affectthe quality of life? so we need to define what isour optimal fracture treatment if one then sustainsthe fracture?

what are the expectedoutcomes after fracture and think about cost as well. so, what can we do toprevent osteoporosis right now and this is kind ofbasic information that we'd give to anyone. consume a healthy diet,quit smoking, limit alcohol, limit caffeine, stayphysically active, stay mentally active,and avoid falls. so, if someone is anambulator, are you ambulating

with the safest device? if someone uses a wheelchair, is the chair properlypositioned for you? are you performing yourtransfers in a safe manner? are you using proper techniques? are the assistivedevices that you're using for the transfers safeand well maintained? are you in an environmentthat allows you to be as safe as possible to minimizeyour falls?

and that's all finding good,but life happens, people fall. and when you do fall, attimes you can fracture. so, how do we nowmanage a fracture in an individual whohas osteoporosis? so, we do know thatfractures happen. so they happen in about a 2to 4 percent annual incidence. an individual who is fracturedat one site is at risk for fracturing atthat site again. so, a broken bone, even whenit's healed will never be

as strong as that intact bone. we talked about those areasthat are at greatest risk for fracture so that end of thefemur, the end of the upper bone of the leg and the top of thetibia, that bone right above-- right below the kneecap are atgreatest risk for fracturing. and we know that very littleforce very often is required to fracture. so, someone who falls from theirwheelchair during a fracture or falls from theirshower commode chair

in the process of bathing. some individuals turn in bedor do range of motion in bed and hear a snap, crack, or popand know that they fractured. we've had individualscome into clinic and say, "doc, my leg is swollen. i have no clue why." and you take a look andyou're like, "oh, my. that leg is in afunny position." and sure enough, theperson is fractured

and they can't give you a goodstory for why they fractured. so, why do we care? individual doesn't walk. why is this important? we know that deformityin a limb can lead to medical complications. so, if an individualhas a fracture, how is that fracturealtered the way they sit, are they placingthemselves at risk

for pressure ulcer development? if that individualhas a fracture that hasn't been well addressed,is that fracture going to heal in an altered position? is that altered position somehowgoing to contribute to how that limb interfaceswith their equipment? are they going to develop wounds and unfortunately endup with bone loss? or is there neuropathic going tobe increased such to the part--

such to the degreethat their quality of life is going to be limited? additionally, if a limb, despitethe fact that it may not be used in the traditionalable-bodied sense, if that individual has a limbthat is in an altered position, is it going to affectthe way they operate in their environment. so, are they going to havefunctional consequences as a result of thataltered healing of the bone?

is it going to change theway their body interfaces with their environmentor with their equipment? and is that change then going tolimit their ability to do some of the things thatthey want to do. so, here's an example of a guythat we worked with at the va who has a higherlevel tetraplegia. he uses a power wheelchairfor his mobility. he fractured the end ofhis legs, so his ankle, and the leg healed inthis pointed toe position.

when you think about whilehe doesn't use his legs, why does this the matter? well, this matters hugely. so, in this individual's case, you can see that his heelis hitting the bottom of his footplate placing himat risk for skin breakdown. additionally, his foot is nowsticking out about 6 inches in front of his footplate which now gives him a 6-inchlonger turning radius.

is he going to be ableto access his environment with his foot stickingout as well? so, this made a hugedifference in how he-- not only his medicalstatus, but he moves about in his environment. so, when you think about fracture management,what are your goals? well, we've got short-termgoals, we've got long-term goals.

short-term goals isthat we want to maximize that individual's functionalabilities while the fracture is healing. we're going to try tominimize the complications. we're going to make surethat any sort of adjustments in equipment that need to bedone are done and we'll try to minimize caregiver cost. the long-term goal, wewant to minimize deformity, maintain prefracture functionalabilities, and once again,

modify any equipmentif necessary. so when you think about howcan we manage fractures? we got surgery, wegot not surgery. so, basic surgical principle. you want to achieveunion of the bone, have the bone come together inthe most anatomic way possible and maintain functionof that limb. we've got reasons forwhy surgeons do surgery. they'll do surgery in abone that's displaced,

so one that is greatlyseparated. they'll do one-- isthey'll perform surgery in an unstable fracture. if it-- they willoften do surgery if it's a femoral neckfracture so that's an upper part of the upper-- it's anarea of the hip bone. and they'll do surgery in abone that has healed incorrectly in the past where othertreatments have failed. in cases where the surgeonsmay be a bit more hesitant

to do surgery. so, osteoporotic bone,that's too fragile to allow for a good surgical fixation, active infectionor osteomyelitis. when you think about, ok, someone with a spinal cordinjury comes in with a fracture, you're going to haveosteoporosis, well, yeah, contraindication for surgery. individuals with spinalcord injury oftentimes have

active infection. so do they have a bony infectionsuch as a bad pressure ulcer and have now fractured? you'll be doing surgery in aninstance of active infection, well, a lot of surgeonswill say no. so individuals with spinalcord injury at a setup of-- will be challenging to managefor the surgeons as well and these are ideas thatyou need to oftentimes bring up when a surgeonapproaches you and says, "yes,

automatically surgeryis the way to go." so, when we think about different conservativeways of healing fractures. we can heal it withdifferent types of splints so something very simplelike a pillow splint. we have casts, we haveoff-the-shelf support so ones that are used in the able-bodiedpopulation sometimes are applied to individuals withspinal cord injury and sometimes you havebig custom-fit devices

that can be fabricated. but the thing that we haveto remember when trying to manage these fracturesconservatively is that folks with spinal cord injury, thebodies sometimes don't fit some of those conservativeoptions very well. so you got to think about yourrange of motion in that limb, you got to think abouthow spasticity is going to play a role if you're tryingto put a limb and maintain it to be stable in order toallow for some healing.

and we got to think about howthe muscle is patterned along the bone and does thatdevice fit for the muscle? and we got a couple ofpictures of that coming up. so, here's an example. what's wrong with this brace? this is one of thoseoff-the-shelf ones. it's a long skinny tube. if we look at the top, wesee the guy's knee popping out of the top of it because hehas a knee flexion contracture.

so, if we're trying to stabilizethis leg, try to avoid it from moving, this cylindricalthing is not providing any support for thisleg that is flexed. so, this is perhaps abetter option for him, something that accommodates that individual'sbaseline range of motion. what about this one? well, it looks ok. you know, it got a lot of straps

and it can accommodatethis person's leg. well, oftentimes, individuals with spinal cordinjury have atrophy, so shrinking of the muscle. if your leg is thatskinny and you put it into a device that'svery big, are you going to be providing muchsupport for it? so, these are things thatindividuals need to bring up with if they do encountera provider who says, "oh,

we're just going toput this brace on." you're going to say,"you know what, my body don't bodyfit that brace. it's not going to work for me." another thing you got to think about when you're managingfractures is how is that individual going toget around with that type of treatment in place? so, is there a leg now ina fully extended position,

supposedly for eight weeks andyou use a manual wheelchair, you usually flex down and youdon't have an elevating leg rest, well how are you going tokeep your leg up for eight weeks and try to get around andlive during this entire time? what about skin andimpaired skin sensation? so, is that device going toallow one to check their skin to make sure that they don'thave those further complications of skin breakdown? how easy is it toget on and off,

once again to do skin checks,once again for those individuals who have impaired hand function? are they going tobe able to remove that brace in an easy way? how's that brace going tointeract with their equipment? what about caregiveravailability and what about their ability tocontinue with their life in the setting offracture healing? we have an individual at theva who fractured his leg,

worked full time, very oftendrove from location to location. he was put in a splintthat put his leg out in a completelyextended position so he can get nowhere near hisdriving-- his steering wheel. things that you got to think about when providingtreatment to an individual. so we have mr. k again. [inaudible], that'sthe way he decided to go with my information.

so, my goal with thisis not to overwhelm one with the different types ofinterventions that can be done which is a pattern of howdifferent considerations-- how we consider differentcomponents of his care when choosing the devicethat was best for him. so, his leg was kind ofrotated out a little bit as we've see in thefirst picture. we were able to make a customdevice that brought it in more in alignment and allowed himto maintain his regular chair,

but we put an elevatingleg rest on it. he healed in a good position and even during thefracture healing period, he was able to continueto maintain care of his toddlers at the time. so we can think about what arethat pros and cons of surgery versus conservative care. well, we know thatsurgery is fast. we go in, get itstabilized, be done with in,

you can start rangeof motion quite early. oftentimes, there'sless shortening or deformity 'cause you'rekind of forcing it in to that one position, but itdoes have its disadvantages. standard surgical risks, there'salways a risk of surgery. there's always a risk ofgoing under anesthesia. individuals with spinal cordinjuries have neurogenic skin, that idea that skin doesn't healas well or heals differently that it does in theable-bodied population

so you're now putting anincision into the skin, is that incisiongoing to heal as well? we are putting at timeshardware into bone that isn't the bestquality, so that means that that hardware hasthe potential of loosening and one has the risk of havingto undergo additional surgeries because of hardware failureor infections that can occur. what about conservative? we like to think,"oh, it's the best."

well, it's not invasivewhich is good and the direct cost is less. certainly, treating witha splint or treating with a brace is lessexpensive than surgery, but it certainly a lot slower and one can have skin breakdowneven in the best of braces. so, there are pros and cons ofboth and one needs to weigh them when discussing withtheir provider. so, we got to take a stepback again and say, well,

why are we doing this again? you know, what was thebig picture things, what were the reallyimportant things? it was the mortality andthe functional questions that we are most worried about. we saw once again,able-bodied population fracture. if you're older, highrisk of mortality, functional changeswere very significant. well, one of theareas of my interest

and of my research isthese questions exactly. so when thinking aboutmanagement of fractures and individuals with spinalcord injury, should we be going with surgery, should we be goingwith conservative treatment? and how do those optionsweigh in to this idea of increased mortality,complications like wounds, blood clots, whether or notthe bone decides to heal, so malunion, connectionof the bone, length of hospital stay,discharge location.

discharge locationoften is a reflection of functional abilities andhealthcare cost in general. so i'm currently ina collaborative study with a colleague of mine atthe va as well as providers in illinois, tennessee,and north carolina, looking at the vadatabase that we have so we are studyingmale veterans. we have just over a thousandfracture cases and we match them to individuals without fracturesand we looked at mortality

in the five years outfollowing fracture and we saw that there was nodifference in survival time for those individuals whohad fractures compared to those individuals whodidn't have fractures. so this idea of, ok, we'vegot to prevent osteoporosis because if we get osteoporosisand then we fracture, we're going to die sooner,well, it's not looking like this might be the casefor the sci population. i'm going to say, ok, so perhapsthere isn't this increased risk

of mortality in sci population. what about functional status? if i fracture aftermy spinal cord injury, am i going to be able totake care of myself as well as i was able to and participatein the things that i wanted to as well as i didbefore my fracture. so we've looked at this aswell both on a larger scale in this study as on a smallerscale of just are population of veterans here atthe va in seattle.

so we saw that manyindividuals, nearly 70 percent of individuals, required somesort of equipment changes, certainly in the short term. we saw that in the short term, so on the first yearfollowing fracture, short-- there was about a 50 percentchance of functional changes. so individuals who fracture thefirst year oftentimes needed increased resistancewith mobility or activities of daily living.

they've got a longbrace on their leg and they've got a tetraplegia. are they able to donand doff that brace? are they going to be ableto dress themselves as well as they did during thatperiod of fracture healing, very often, not as well. but we saw that thisdecreased functional ability, this decreased-- excuse me, functional decline wasreally sustained over the--

beyond one year of injury. so that first year, veryoften people weren't able to maintain their activities ofdaily living, but beyond a year, they were now able to and thisanswers our second question. we've got mortality,well, we don't think that mortality is different with the spinal cord-injuredpopulation, but what about functionalabilities? well, a year out from fracture,individuals are doing pretty ok.

รข  so what can we say? well, we know that ourgoal with management of lower limb fracturesin the sci population is to feel the fracture ideally with minimal riskof complications. we know that shortening,angulation, rotational deformitiesare not acceptable because they very oftenplace an individual at risk

for medical complication andfunctional complications. got to consider the reality ofthe brace, does it work for you in your lifestyle and we'vealso got to remember to take that next step andassess all equipment. so knowing that not only isthe brace going to interface with the body, but the bodyis then going to interface with the chair, with the otherequipment that's available in the environment andabove and beyond everything, we want to maintain thatprefracture functional status

and this is whereyou come along. you should always realizethat you know the best about your body and howyour body interfaces with the different equipmentand look to your environment. so if you are choosingto discuss osteoporosis with your providers, ifyou sustain a fracture and you find yourself in theemergency room or talking with an orthopedic surgeon, ortalking with your rehab doc, you have to realize that youhave to advocate for yourself.

you're often willing to beteaching those providers about the different intricaciesof spinal cord injury and remember that your providersare always a team of providers. so the relationshipthat you have with the orthopedic surgeon,you have to maintain that and sometimes remind him, "oh, we've got to get thept involved" or, "oh, we've got the ot involved" or"please send to me my rehab doc so we can work with thespasticity after my fracture."

so we know that osteoporosisis very often expected we see the patternof injury is unique, but it oftentimes happens, usually happens belowthe level of injury. we know that there are manyfactors, not just as used that plays a role in thedevelopment of osteoporosis and decrease of bone marrowdensity in the sci population. we don't quite know howeffective the medications are in treating osteoporosisand we know

that there isn't one singlething that's going to help in treating osteoporosisin this population. when we think about theconsequences of osteoporosis, we know that lower extremityfractures are not infrequent. historically, we favoredconservative management over surgical management,but things might be changing and there certainly aremany avenues for research when looking into this. so i want to acknowledge dr.susan ott for this presentation.

she has contributed to a wealthof knowledge in this community. she is a geriatrician hereat the university who focuses on osteoporosis research. i also want to acknowledge mymentor, my colleague, my boss, dr. stephen burns at the vawho's also been my partner and crime for research in thisarea and our collaborators at the different vacenters across the us. [ applause ] and so the question iswhy is the mortality

in the able-bodied population sohigh after they break their hip? multifactorial. so lots of differentreasons for it. there're-- some individualsspeculate that the individuals that fall and fracture are anyways in unhealthier population. so if one is at riskfor falling, do you-- are there other medicalcomplications or other medical diseases thatyou're experiencing that led to that fracturein the first place.

so heart disease, lungdisease, general disability that contributed to the fall andthen contributed to the fracture and constellation of thosethings lead to the death. the other thing interestinglythat may also contribute that applies to the spinal cordinjury population is we talked about in the able-bodiedpopulation how oftentimes the discharge home locationor their-- where they're going to beliving postfracture is different than where they're livingprefracture and sometimes what

that comes down tois very simply bowel and bladder management. so someone who didn't,for example, use a foley catheter beforetheir fracture suddenly has a foley catheter in place, areanyway of lower health status than they were priorto injury, are they now at increased risk of infection. so it's kind of anindirect, wasn't doing great, i fall and fractured, i nowhave a number of other things

that are being done to methat are increasing my risk for infection and then i endup dying because of that. is the functional abilitiesand functional status altered because i was really active, ifell and fractured, i can't move as much because i'mnot moving as much. i'm not breathing as well. i'm setting myself upat risk for pneumonia, do i actually get a pneumonia? is it direct causefrom the fracture?

well no, but constellationof conditions. so the question is,what is the-- what are the top threereasons for fractures. i'm assuming the spinalcord injury population. falls, falls, falls. most of the falls arerelated to transverse. oftentimes, there isn'tgreat information on it but from why we've collected,we see that most of the times, the falls are related totransverse, very often related

to bathroom transverse,someone [inaudible] in the wet slippery skin factor. i would say thoseare the top two and then the others are justkind of a conglomeration of running in offractures as the result of altered equipment interfaceand that's a fancy term of saying i was in my chairand i caught my toe in the door and twisted my ankle andfractured and in some instances, the fall-- or the fractures areresult of high impact injury.

so just because you havea spinal cord injury, it doesn't mean you can't getinto a car accident or be hit by a car while crossingthe street. but i would say, falls,falls, falls, ramming the leg into a door or the sideof a wall and then some of the more unusual instances.

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