Re: Re-Tear after ACL Reconstruction -- Possible causes of ACL-graft failure....

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Re: Re-Tear after ACL Reconstruction -- Possible causes of ACL-graft failure....

Posted By: Michael Frind
Date: Sunday, 31 January 2010, at 1:21 a.m.

In Response To: Re Tear of after Acl Reconstruction (jacquelyn Salisbury)

Dear Jacquelyn,
I am sorry to hear that your nephew tore his grafted ACL.
There are many reasons why a reconstructed ACL can fail. Foremost among these is surgeon error. Determining the exact locations of where the bone tunnels should go is key to successful ACL reconstruction. Sadly, there are still many surgeons out there who simply do not know how to correctly place the bone tunnels. Even a slight error in the drilling of the bone tunnels will result in the graft being forced to stretch abnormally during the knee's range of motion. This can result in the graft stretching out and failing either gradually or abruptly.
Of course, it is always possible to re-tear an ACL (i.e. tear a reconstructed ACL) simply by subjecting it to the injurious types of forcing that can tear the original ACL. Planting and twisting (also known as cutting) is a major cause of ACL tearing, and so it is no surprise that this same mode of forcing can cause grafted ACLs to fail. Many athletes (e.g. soccer players, basketball players) have developed the pernicious habit of planting their entire shoe sole and then pivoting. It takes a lot of effort and practice to learn how to pivot in a knee-friendly fashion (i.e. planting only the front portion of the foot, prior to pivoting). Has your nephew been taught how to pivot properly?
Failure of an ACL graft can also be precipitated by the patient doing too much too soon. This is a major danger, especially given how modern arthroscopic surgery, combined with highly effective pain-management techniques, can result in the patient feeling comfortable doing things such as descending stairs without crutches right after the surgery. While straight-line walking should be fine, pivoting could result in high stresses on the grafted ACL. And, even though the graft might be physically strong and well-anchored, remember that it is dead tissue (it dies because it has no blood supply). It takes several months for that sliver of dead tendon to become invaded by blood vessels, and for living cells to appear in sufficient quantity for the tissue to function as a ligament. And, for proper ligamentization to occur, it is essential that the graft be subjected to gradually increasing stresses (i.e. not too much at first, but not too little later on). This is why adhering to the rehabilitation protocol closely is very important. Too many athletes, eager to return to their favourite sports, work very hard on regaining muscle strength (and yes, muscle strength is helpful in preventing future knee injuries, and yes, the muscles often atrophy as a result of the bloodflow-stanching tourniquet used on the thigh during surgery), but they forget that the ligamentization process cannot be hurried. No amount of muscle strength can compensate for missing ligament functioning.
Remember that because the ACL graft is dead tissue for a period of time after the surgery, it contains no nerve endings. So, excessive stress on that ACL graft would not cause pain to be felt. This places the overly eager athlete in great danger: strong muscles confer a feeling of strength, and the lack of pain from the knee convinces the athlete that the knee is able to handle more than the rehabilitation protocol advises. What is even more frightening is that it is easy to damage an ACL graft at this stage without any apparent warning sign, because the damage might only become apparent much later on, when the athlete returns to knee-demanding activities...and thereupon completely ruptures the grafted ACL, thereby simultaneously damaging other structures in the knee, for example the menisci and the articular-cartilage surfaces (bone-bruising, which itself is a harbinger of osteoarthritis).
The ACL can also be torn by sideways forcing as well as by injurious hyperextension. How did your nephew tear his ACL originally? And, how did he re-tear it? I am thinking of not just the activity he was involved in, but how the knee was actually forced, and whether the injury involved contact or not. (If your nephew was wearing a functional brace, i.e. one with a rigid frame and hinged uprights on each side of the knee, then the injury would be noncontact [i.e. twisting], because the brace would have prevented injury via forced hyperextension or sideways forcing.)
Another possible cause of graft failure is actual rejection of the graft, but this is not an issue with autografts since the tissue is taken from the patient's own body. But it is possible for any type of graft to fail to incorporate, given that the process of ligamentization (i.e. conversion of the graft, which is essentially a sliver of pilfered tendon, into a fully functional living graft) sometimes fails to proceed properly. If the graft simply remains a piece of dead tissue, it will stretch out and fail, and revision reconstruction would then be needed.
Graft failure can also be caused by other factors too. One notable example is any type of biomechanical abnormality, such as bowleggedness (genu varum) or knock-kneedness (genu valgum). Knees that naturally hyperextend grotesquely (i.e. they "go back" very far, to the point that anyone watching cringes when the person locks their knees) can also be at high risk for ACL tearing (or re-tearing), given that the forces on the cruciate ligaments (when called upon to limit extension of the knee) increase exponentially the more the knee extends backwards. (A small amount of hyperextension-type movement is normal, and is essential in enabling the knee to lock when standing.)
The risk of ACL tearing (and also graft failure) can also be increased by poor running technique and other biomechanical aspects. Athletic shoes with too-high or too-low arch supports can engender ankle injuries, which in turn can result in a loss of balance that in turn can result in an ACL injury (particularly during jump landings, such as in basketball or soccer). In other sports, such as alpine skiing, the ankle-immobilizing effect of the ski boot results in devastating ACL tears. (There are engineering-type solutions to this problem, for example encasing the knee with a hinged brace that is also connected to the ski boot, but they are generally not considered practical for prophylactic use. And, they would not be helpful for athletes involved in cutting-type sports.)
Other ACL-injury/reinjury-precipitating factors include neurological abnormalities (e.g. balance problems), weak hamstrings (a problem more common in female athletes), and poor jump-landing technique (i.e. landing with knees inadequately flexed; again, this is more common in female athletes). In fact, many of the ACL-injury-predisposing factors that are seen in female athletes (who have a 2-8-fold higher ACL-injury risk) can also be found in a small subset of the male-athlete population. In other words, just because your nephew is (of course) male does not make him immune to the types of ACL injuries typically associated with females.
Of course, females are unique in that they have a monthly hormonal cycle with its ligament-weakening estrogen spikes. But in this modern world, which is permeated with estrogen-mimicking chemicals (most notably organohalogens such as the highly biopersistent brominated flame retardants widely used in everything from electronics to furniture, and also the extremely dangerous fluorinated non-stick coatings still found on frying pans), it is not surprising that feminization of male humans is starting to appear. So far, this alarming phenomenon has been observed mostly in the context of employees working in factories that produce organohalogen products, but it has also been observed in animals at the top of their food chains. Remember, too, that organohalogens cause myriad problems in the natural world. For example, given that they can affect brain development, what would their effect be on crucial injury-avoidance data processing in the brain? The influence of such xenobiotic chemicals on sports injuries (either directly via the estrogen-mimicking route or indirectly via harm to the brain's motor-learning and movement-related functions, or via some other route) would make for a fascinating research topic at the Master's or Doctorate level, cross-disciplinary between environmental toxicology, organic chemistry, neurology, histology, endocrinology, human physiology, and kinesiology. In fact, this realm would be enough to occupy thousands of graduate students and professors at numerous universities worldwide.
The aforementioned 2-8-fold higher risk of female athletes tearing their ACLs has given rise to training programs targeted at preventing injuries in this group. Now it is clear that these same training programs are extremely valuable for male athletes as well. (Some, such as Cincinnati Sportsmetrics, have been made available to both males and females for many years now. Others, such as Girls Can Jump, are targeted towards females only.) These programs focus on developing correct jump-landing techniques, and they include other exercises useful for reducing ACL injuries. These same exercises also bring the benefit of improved athletic performance. Has your nephew been exposed to such a training program?
The patellar-tendon (PT) autograft, which is what your nephew had, is universally considered to be the gold standard for ACL reconstruction. This is largely due to the fact that it comes with bone plugs at both ends, thus ensuring reliable bone-plug-to-bone-tunnel healing. Fortunately, the quick and reliable incorporation due to the bone plugs at both ends also means that, in comparison to the hamstring (DLSTG) autograft, the PT autograft is relatively unlikely to remain a dead piece of tissue and gradually stretch out. However, like all cruciate-ligament grafts, this graft is vulnerable to failure if incorrectly placed. And, of course, it can be torn in the same types of injury situations as bedevil a natural ACL.
Although a reconstructed ACL can come very close to a natural ACL in terms of biomechanical functioning, there are still significant differences between the two. For example, a natural ACL has a well-defined multi-bundle structure that elegantly mirrors the roles it is called upon to fulfill. In contrast, the typical reconstructed ACL has a simplistic single-strand structure that, while infinitely better than no ACL, technically only replaces part of what the natural ACL does. (Some surgeons are now doing double-bundle ACL grafts. While such grafts do indeed better duplicate the natural ACL's structure and function, the problem is that double-bundle ACL grafting makes much greater demands on the surgeon's skill set. In other words, there is greater opportunity for surgeon error. Given that surgeon error is still the major cause of failure with the standard single-bundle ACL grafts, it could be argued that only a small number of surgeons are ready to tackle the challenge of correctly installing double-bundle ACL grafts. More information on double-bundle ACL grafting can be found in the Knee Library.)
It should be kept in mind that the ACL fulfills multiple biomechanical roles: not only is it responsible to controlling forwards tibial sliding as well as inwards tibial twisting, but it also plays a key role in limiting how far the knee extends (this is a role it shares with the PCL, which is why both cruciate ligaments must be intact for the knee to function normally). Also, in situations where the collateral ligaments (MCL and LCL) are compromised, the ACL helps resist sideways forcing (in conjunction with the PCL).
As well, correct functioning of the ACL is essential to meniscal longevity (and so a missing ACL will result in meniscal deterioration, hence osteoarthritis). Note that each and every giving-way incident of the knee, as well as any time the knee is left ACL-deficient, will bring cumulative, permanent damage (which could be termed "collateral damage") in terms of an increased predisposition to osteoarthritis. This is why it is surprising that the physiotherapist and surgeon apparently did not rigorously test your nephew's knee (i.e. the same manual-manipulation tests as would have been done after the initial injury: Lachmann drawer test, anterior drawer test, pivot-shift test, Macintosh test, dial test, and so on...and all these tests ideally would be done under anesthesia in order to ensure that muscle tenseness cannot mask ligamentous deficiencies), prior to releasing him to return to sports. Simply allowing the athlete with a questionable knee to return to knee-demanding sports "to see how the knee holds up" is inherently very risky because of the collateral damage that invariably occurs in conjunction with an ACL tear/retear.
Evaluation of an ACL-reconstructed knee is not something to be done only at the very end of the long and gruelling rehabilitation period. The knee's progress throughout the rehabilitation stages should be tracked and recorded. Any worrisome signs of graft failure should not be ignored, and should be followed up on meticulously. A graft that has stretched out (or completely failed) at, say, three months post-op will never be useful, and so revision reconstruction should be pursued without further delay. Looking back on your nephew's rehabilitation progress over the past eight months, were there any warning signs during this period? Were there any missed milestones on the rehabilitation timeline? Was there anything that triggered a delay in progress?
It is also important to keep in mind that a natural ACL is filled with tension-sensitive nerve endings, which serve to keep the brain informed as to what is going on inside the ligament. (This process is known as proprioception, and it plays a key role in optimal athletic performance as well as injury avoidance. Proprioceptive feedback occurs automatically in the natural ACL, but neurologically it is similar to the pain-sensation aspect I noted earlier.) Such nerve endings may never regrow in a reconstructed ligament (although there is some reason for hope; more information on this can be found in articles in this forum's Knee Library). This means that, in a person with a torn-and-reconstructed ACL, the brain can be expected to have less information regarding position in space (including movement parameters such as speed and direction) from the affected limb than from the never-injured limb. This means that the brain's movement-related decisions (most of which are done completely automatically, and which involve tensing muscles in a certain sequence with split-second timing precision) are affected. Even small changes in which muscles are tensed when, and by how much, can result in increased stresses on the knee ligaments.
One strategy to compensate for the missing proprioception includes regimens of sports-specific training exercises. Such exercises should have been included in the latter stages of your nephew's physiotherapy program...and he should have been advised to continue with these exercises on his own, after returning to sports. (Of course, now that the ACL has been retorn, all knee-demanding activities should be halted until an orthopedist has examined the knee.) The wearing of devices on the leg, including anything ranging from a simple neoprene sleeve to a high-end functional knee brace, stimulates skin-subsurface nerve endings and can provide a surrogate form of proprioception too. (Articles on this topic can be found in the Knee Library's Functional Knee Bracing section, as well as elsewhere.)
I think the key thing to keep in mind is that modern ACL reconstruction, despite being a tremendously common surgery, is still a technically very demanding pursuit. It makes major demands on the surgeon's skill set, and it requires a surgeon who is diligent, exceedingly careful, caring, thoughtful, analytical, patient, knowledgeable, experienced, and painstakingly thorough. There are many excellent surgeons out there who are highly skilled and highly experienced, and who have very low failure rates. But there are also surgeons who are not so skilled and not so experienced, and these ones might be turning out higher failure rates. It is also important to keep in mind that surgeons are human too. Even the best surgeon can make a mistake. And, even if the surgeon does not make a mistake, it is still possible for the graft to fail to ligamentize.
My advice here is to consult another orthopedist, and to pursue a revision reconstruction as promptly as possible. It is worthwhile to have standard X-rays of the knee taken: these show the bone tunnels, thus providing insight into whether the graft failure was due to surgeon error, patient error, or some other cause. The failure cause (or causes, since multiple factors can contribute to a given failure) should be addressed. For example, incorrectly placed bone tunnels will need to be bone-grafted prior to new tunnels being drilled in the correct location.
After the revision reconstruction and a thorough rehabilitation (with protocol carefully followed), the knee should be tested carefully (as noted above). The sports-specific exercises, including both the knee-injury-preventive and the proprioceptive-regainment exercises, should also be pursued as part of a comprehensive return-to-sports program, but only after the successful ligamentization of the revision-reconstructed ACL graft has been confirmed.
Yours truly,
Michael Frind.
Knee Library http://factotem.org/library

Messages In This Thread

Re Tear of after Acl Reconstruction (views: 339) -- jacquelyn Salisbury -- Saturday, 30 January 2010, at 9:32 a.m.
- Re: Re-Tear after ACL Reconstruction -- Possible causes of ACL-graft failure.... (views: 1123) -- Michael Frind -- Sunday, 31 January 2010, at 1:21 a.m.

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Message: > Dear Jacquelyn, > I am sorry to hear that your nephew tore his grafted ACL. > There are many reasons why a reconstructed ACL can fail. > Foremost among these is surgeon error. Determining the > exact locations of where the bone tunnels should go is key > to successful ACL reconstruction. Sadly, there are still > many surgeons out there who simply do not know how to > correctly place the bone tunnels. Even a slight error in > the drilling of the bone tunnels will result in the graft > being forced to stretch abnormally during the knee's range > of motion. This can result in the graft stretching out and > failing either gradually or abruptly. > Of course, it is always possible to re-tear an ACL (i.e. > tear a reconstructed ACL) simply by subjecting it to the > injurious types of forcing that can tear the original ACL. > Planting and twisting (also known as cutting) is a major > cause of ACL tearing, and so it is no surprise that this > same mode of forcing can cause grafted ACLs to fail. Many > athletes (e.g. soccer players, basketball players) have > developed the pernicious habit of planting their entire > shoe sole and then pivoting. It takes a lot of effort and > practice to learn how to pivot in a knee-friendly fashion > (i.e. planting only the front portion of the foot, prior to > pivoting). Has your nephew been taught how to pivot > properly? > Failure of an ACL graft can also be precipitated by the > patient doing too much too soon. This is a major danger, > especially given how modern arthroscopic surgery, combined > with highly effective pain-management techniques, can > result in the patient feeling comfortable doing things such > as descending stairs without crutches right after the > surgery. While straight-line walking should be fine, > pivoting could result in high stresses on the grafted ACL. > And, even though the graft might be physically strong and > well-anchored, remember that it is dead tissue (it dies > because it has no blood supply). It takes several months > for that sliver of dead tendon to become invaded by blood > vessels, and for living cells to appear in sufficient > quantity for the tissue to function as a ligament. And, for > proper ligamentization to occur, it is essential that the > graft be subjected to gradually increasing stresses (i.e. > not too much at first, but not too little later on). This > is why adhering to the rehabilitation protocol closely is > very important. Too many athletes, eager to return to their > favourite sports, work very hard on regaining muscle > strength (and yes, muscle strength is helpful in preventing > future knee injuries, and yes, the muscles often atrophy as > a result of the bloodflow-stanching tourniquet used on the > thigh during surgery), but they forget that the > ligamentization process cannot be hurried. No amount of > muscle strength can compensate for missing ligament > functioning. > Remember that because the ACL graft is dead tissue for a > period of time after the surgery, it contains no nerve > endings. So, excessive stress on that ACL graft would not > cause pain to be felt. This places the overly eager athlete > in great danger: strong muscles confer a feeling of > strength, and the lack of pain from the knee convinces the > athlete that the knee is able to handle more than the > rehabilitation protocol advises. What is even more > frightening is that it is easy to damage an ACL graft at > this stage without any apparent warning sign, because the > damage might only become apparent much later on, when the > athlete returns to knee-demanding activities...and > thereupon completely ruptures the grafted ACL, thereby > simultaneously damaging other structures in the knee, for > example the menisci and the articular-cartilage surfaces > (bone-bruising, which itself is a harbinger of > osteoarthritis). > The ACL can also be torn by sideways forcing as well as by > injurious hyperextension. How did your nephew tear his ACL > originally? And, how did he re-tear it? I am thinking of > not just the activity he was involved in, but how the knee > was actually forced, and whether the injury involved > contact or not. (If your nephew was wearing a functional > brace, i.e. one with a rigid frame and hinged uprights on > each side of the knee, then the injury would be noncontact > [i.e. twisting], because the brace would have prevented > injury via forced hyperextension or sideways forcing.) > Another possible cause of graft failure is actual rejection > of the graft, but this is not an issue with autografts > since the tissue is taken from the patient's own body. But > it is possible for any type of graft to fail to > incorporate, given that the process of ligamentization > (i.e. conversion of the graft, which is essentially a > sliver of pilfered tendon, into a fully functional living > graft) sometimes fails to proceed properly. If the graft > simply remains a piece of dead tissue, it will stretch out > and fail, and revision reconstruction would then be needed. > Graft failure can also be caused by other factors too. One > notable example is any type of biomechanical abnormality, > such as bowleggedness (genu varum) or knock-kneedness (genu > valgum). Knees that naturally hyperextend grotesquely (i.e. > they "go back" very far, to the point that anyone > watching cringes when the person locks their knees) can > also be at high risk for ACL tearing (or re-tearing), given > that the forces on the cruciate ligaments (when called upon > to limit extension of the knee) increase exponentially the > more the knee extends backwards. (A small amount of > hyperextension-type movement is normal, and is essential in > enabling the knee to lock when standing.) > The risk of ACL tearing (and also graft failure) can also > be increased by poor running technique and other > biomechanical aspects. Athletic shoes with too-high or > too-low arch supports can engender ankle injuries, which in > turn can result in a loss of balance that in turn can > result in an ACL injury (particularly during jump landings, > such as in basketball or soccer). In other sports, such as > alpine skiing, the ankle-immobilizing effect of the ski > boot results in devastating ACL tears. (There are > engineering-type solutions to this problem, for example > encasing the knee with a hinged brace that is also > connected to the ski boot, but they are generally not > considered practical for prophylactic use. And, they would > not be helpful for athletes involved in cutting-type > sports.) > Other ACL-injury/reinjury-precipitating factors include > neurological abnormalities (e.g. balance problems), weak > hamstrings (a problem more common in female athletes), and > poor jump-landing technique (i.e. landing with knees > inadequately flexed; again, this is more common in female > athletes). In fact, many of the ACL-injury-predisposing > factors that are seen in female athletes (who have a > 2-8-fold higher ACL-injury risk) can also be found in a > small subset of the male-athlete population. In other > words, just because your nephew is (of course) male does > not make him immune to the types of ACL injuries typically > associated with females. > Of course, females are unique in that they have a monthly > hormonal cycle with its ligament-weakening estrogen spikes. > But in this modern world, which is permeated with > estrogen-mimicking chemicals (most notably organohalogens > such as the highly biopersistent brominated flame > retardants widely used in everything from electronics to > furniture, and also the extremely dangerous fluorinated > non-stick coatings still found on frying pans), it is not > surprising that feminization of male humans is starting to > appear. So far, this alarming phenomenon has been observed > mostly in the context of employees working in factories > that produce organohalogen products, but it has also been > observed in animals at the top of their food chains. > Remember, too, that organohalogens cause myriad problems in > the natural world. For example, given that they can affect > brain development, what would their effect be on crucial > injury-avoidance data processing in the brain? The > influence of such xenobiotic chemicals on sports injuries > (either directly via the estrogen-mimicking route or > indirectly via harm to the brain's motor-learning and > movement-related functions, or via some other route) would > make for a fascinating research topic at the Master's or > Doctorate level, cross-disciplinary between environmental > toxicology, organic chemistry, neurology, histology, > endocrinology, human physiology, and kinesiology. In fact, > this realm would be enough to occupy thousands of graduate > students and professors at numerous universities worldwide. > The aforementioned 2-8-fold higher risk of female athletes > tearing their ACLs has given rise to training programs > targeted at preventing injuries in this group. Now it is > clear that these same training programs are extremely > valuable for male athletes as well. (Some, such as > Cincinnati Sportsmetrics, have been made available to both > males and females for many years now. Others, such as Girls > Can Jump, are targeted towards females only.) These > programs focus on developing correct jump-landing > techniques, and they include other exercises useful for > reducing ACL injuries. These same exercises also bring the > benefit of improved athletic performance. Has your nephew > been exposed to such a training program? > The patellar-tendon (PT) autograft, which is what your > nephew had, is universally considered to be the gold > standard for ACL reconstruction. This is largely due to the > fact that it comes with bone plugs at both ends, thus > ensuring reliable bone-plug-to-bone-tunnel healing. > Fortunately, the quick and reliable incorporation due to > the bone plugs at both ends also means that, in comparison > to the hamstring (DLSTG) autograft, the PT autograft is > relatively unlikely to remain a dead piece of tissue and > gradually stretch out. However, like all cruciate-ligament > grafts, this graft is vulnerable to failure if incorrectly > placed. And, of course, it can be torn in the same types of > injury situations as bedevil a natural ACL. > Although a reconstructed ACL can come very close to a > natural ACL in terms of biomechanical functioning, there > are still significant differences between the two. For > example, a natural ACL has a well-defined multi-bundle > structure that elegantly mirrors the roles it is called > upon to fulfill. In contrast, the typical reconstructed ACL > has a simplistic single-strand structure that, while > infinitely better than no ACL, technically only replaces > part of what the natural ACL does. (Some surgeons are now > doing double-bundle ACL grafts. While such grafts do indeed > better duplicate the natural ACL's structure and function, > the problem is that double-bundle ACL grafting makes much > greater demands on the surgeon's skill set. In other words, > there is greater opportunity for surgeon error. Given that > surgeon error is still the major cause of failure with the > standard single-bundle ACL grafts, it could be argued that > only a small number of surgeons are ready to tackle the > challenge of correctly installing double-bundle ACL grafts. > More information on double-bundle ACL grafting can be found > in the Knee Library.) > It should be kept in mind that the ACL fulfills multiple > biomechanical roles: not only is it responsible to > controlling forwards tibial sliding as well as inwards > tibial twisting, but it also plays a key role in limiting > how far the knee extends (this is a role it shares with the > PCL, which is why both cruciate ligaments must be intact > for the knee to function normally). Also, in situations > where the collateral ligaments (MCL and LCL) are > compromised, the ACL helps resist sideways forcing (in > conjunction with the PCL). > As well, correct functioning of the ACL is essential to > meniscal longevity (and so a missing ACL will result in > meniscal deterioration, hence osteoarthritis). Note that > each and every giving-way incident of the knee, as well as > any time the knee is left ACL-deficient, will bring > cumulative, permanent damage (which could be termed > "collateral damage") in terms of an increased > predisposition to osteoarthritis. This is why it is > surprising that the physiotherapist and surgeon apparently > did not rigorously test your nephew's knee (i.e. the same > manual-manipulation tests as would have been done after the > initial injury: Lachmann drawer test, anterior drawer test, > pivot-shift test, Macintosh test, dial test, and so > on...and all these tests ideally would be done under > anesthesia in order to ensure that muscle tenseness cannot > mask ligamentous deficiencies), prior to releasing him to > return to sports. Simply allowing the athlete with a > questionable knee to return to knee-demanding sports > "to see how the knee holds up" is inherently very > risky because of the collateral damage that invariably > occurs in conjunction with an ACL tear/retear. > Evaluation of an ACL-reconstructed knee is not something to > be done only at the very end of the long and gruelling > rehabilitation period. The knee's progress throughout the > rehabilitation stages should be tracked and recorded. Any > worrisome signs of graft failure should not be ignored, and > should be followed up on meticulously. A graft that has > stretched out (or completely failed) at, say, three months > post-op will never be useful, and so revision > reconstruction should be pursued without further delay. > Looking back on your nephew's rehabilitation progress over > the past eight months, were there any warning signs during > this period? Were there any missed milestones on the > rehabilitation timeline? Was there anything that triggered > a delay in progress? > It is also important to keep in mind that a natural ACL is > filled with tension-sensitive nerve endings, which serve to > keep the brain informed as to what is going on inside the > ligament. (This process is known as proprioception, and it > plays a key role in optimal athletic performance as well as > injury avoidance. Proprioceptive feedback occurs > automatically in the natural ACL, but neurologically it is > similar to the pain-sensation aspect I noted earlier.) Such > nerve endings may never regrow in a reconstructed ligament > (although there is some reason for hope; more information > on this can be found in articles in this forum's Knee > Library). This means that, in a person with a > torn-and-reconstructed ACL, the brain can be expected to > have less information regarding position in space > (including movement parameters such as speed and direction) > from the affected limb than from the never-injured limb. > This means that the brain's movement-related decisions > (most of which are done completely automatically, and which > involve tensing muscles in a certain sequence with > split-second timing precision) are affected. Even small > changes in which muscles are tensed when, and by how much, > can result in increased stresses on the knee ligaments. > One strategy to compensate for the missing proprioception > includes regimens of sports-specific training exercises. > Such exercises should have been included in the latter > stages of your nephew's physiotherapy program...and he > should have been advised to continue with these exercises > on his own, after returning to sports. (Of course, now that > the ACL has been retorn, all knee-demanding activities > should be halted until an orthopedist has examined the > knee.) The wearing of devices on the leg, including > anything ranging from a simple neoprene sleeve to a > high-end functional knee brace, stimulates skin-subsurface > nerve endings and can provide a surrogate form of > proprioception too. (Articles on this topic can be found in > the Knee Library's Functional Knee Bracing section, as well > as elsewhere.) > I think the key thing to keep in mind is that modern ACL > reconstruction, despite being a tremendously common > surgery, is still a technically very demanding pursuit. It > makes major demands on the surgeon's skill set, and it > requires a surgeon who is diligent, exceedingly careful, > caring, thoughtful, analytical, patient, knowledgeable, > experienced, and painstakingly thorough. There are many > excellent surgeons out there who are highly skilled and > highly experienced, and who have very low failure rates. > But there are also surgeons who are not so skilled and not > so experienced, and these ones might be turning out higher > failure rates. It is also important to keep in mind that > surgeons are human too. Even the best surgeon can make a > mistake. And, even if the surgeon does not make a mistake, > it is still possible for the graft to fail to ligamentize. > My advice here is to consult another orthopedist, and to > pursue a revision reconstruction as promptly as possible. > It is worthwhile to have standard X-rays of the knee taken: > these show the bone tunnels, thus providing insight into > whether the graft failure was due to surgeon error, patient > error, or some other cause. The failure cause (or causes, > since multiple factors can contribute to a given failure) > should be addressed. For example, incorrectly placed bone > tunnels will need to be bone-grafted prior to new tunnels > being drilled in the correct location. > After the revision reconstruction and a thorough > rehabilitation (with protocol carefully followed), the knee > should be tested carefully (as noted above). The > sports-specific exercises, including both the > knee-injury-preventive and the proprioceptive-regainment > exercises, should also be pursued as part of a > comprehensive return-to-sports program, but only after the > successful ligamentization of the revision-reconstructed > ACL graft has been confirmed. > Yours truly, > Michael Frind. > Knee Library http://factotem.org/library
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