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Author Topic: Trying to understand Arthrofibrosis  (Read 22767 times)

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Offline sreinhard

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Trying to understand Arthrofibrosis
« on: September 10, 2011, 12:08:34 AM »
I read quite some stuff about AF. Some "tutorials", some papers, some book chapters, several patient stories here around. Certainly only a tiny bit of what is available. And nonetheless I neither do get a really clear picture at all, nor do I have the impression that reading more could bring a true break through. I do not see it anywhere, instead it is often claimed AF is not fully understood. This does not satisfy me. Even if there cannot be a clear picture because of lacking data as a foundation for true insight in the scientific sense, I do believe in something like a "best guess". I believe that a "most likely hypotheses" is better than no hypotheses at all. Perhaps such a paradigm is not wise or a waste of time. Call it naive, senseless or stubborn. May it be the superstitious nature of man trying to find an explanation for everything, no matter how far it is really from evidence. Or call it just curiosity.
I have no claim for knowledge, nor for inflexible dogma, certainly not for the truth. Enough of the preface. Here is my belief-picture:

AF is the growth of excessive fibrotic scar tissue within a joint triggered by an inflammation condition. Inflammation mediators are distributed from damaged tissue and proliferate growth of fibrotic tissue structures.
Such structures can be

a) Single-sidedly attached scar strings or plates, reaching into free joint space (e.g. the "grass plains" seen on some arthroscopic pictures)
b) Double-sidedly attached scar strings or plates, connecting different tissues and reaching through free joint space
c) Growth of harder fibrotic tissue within tissue structures of a different type, thus strings and plates reaching through other, usually softer, tissues
and of course intermediate forms of all those categories, like interconnected webs going through tissue, between tissue and through free (liquid, non-tissue) joint space

Primary triggers for the inflammation encompass

a) Sharp mechanical injury of in-joint tissue (ligaments, cartilage?, capsule) e.g. through surgery instruments, bone splinters or implants like screws
b) Abrasion injury between tissues of different hardness, e.g. misplaced ACL replacements, bone bulges with ligaments, and produced scar tissue with itself or other joint parts (feedback process) from micro-injury
c) Infection within or close to the joint
d) Scar tissue, non-mechanical (mediator discharge feedback process)

Excessive bleeding can be considered semi-secondary as it proliferates the transport and presence of inflammation mediators.
Secondary "leverage" (multiplication) factors are of genetic nature, regulating the inflammation reaction extent. Concerning AF itself, in literature the notions of primary and secondary are used differently, as "secondary" is seen towards the primary triggers, while genetic is often presented as assumed to be without significant primary triggers.
My belief is the following: there is always a primary trigger. The primary trigger can be more or less strong. Its effect is then "leveraged" (multiplied) by genetic factors. Thus, an initially weak expression can be turned by further strong primary triggers (e.g. further bad surgery) into a strong expression with medium genetic leverage. Weak triggers can be leveraged into strong expression by extensive genetic leverage. Thus, I do not believe in a clear distinction between secondary and primary AF, instead it is a continuum and in a way both are always present. Especially infections can be very strong primary triggers, creating strong expressions with only mild or medium genetic leverage.

Expression can be manifold. It is mostly characterized by intensity and duration of the proliferation process. The stronger the expression, the further reaching the effect of inflammation mediators. Inflammation mediators can spread locally alongside the grow of scar strings or through the liquid medium. It usually starts within the original joint capsule from the source of the primary trigger but with high intensity and duration may spread beyond, e.g. under the patella. You wont find patella baja without or before extensive intra-capsule scarring, except with patella-only surgery. Proliferation stops, when the inflammation dissolves. Mature scar strings will remain, while young, weak may vanish unter motion conditions. Excessive presence of scar tissue will make stopping more unlikely, as it is itself an (although weak) primary trigger and can also be a (strong) abrasion trigger in the face of joint motion.

Impacts of scar tissue are being an obstacle within natural joint free-space (e.g. type a) above), glueing different joint parts together (b) or changing the flexibility of functional tissue (c). This results in joint motion limitation, crepidus and pain. Terminal secondary effects can be necrosis in ligaments or abrasion of cartilage. The latter is currently in any case irreparable damage.
Swelling and heat on the other hand are a result of the inflammation process itself. Thus, those are only present during a proliferation stage, while scar effects remain afterwards. Ongoing heat is a sign of continuous proliferation.

How do scar effects feel like? That depends very much on where in or near the joint did scar tissue form.

I do not like the Shelbourne classification. What does a flexion deficit beyond 25° or 30° mean? Affected persons may reach 135° flexion (after extensive stretching, mobilisation and more or less strong pain) yet reach only 100° after getting up from bed. There are various forms of expression possible with hard or soft ROM restrictions, different kinds of pain, very differing "cold" and mobilised maxima. It all depends on the exact pose of scar tissue.

Subjective feelings are theoretically much better suited, yet cannot be easily evaluated and compared scientifically.
Good indications are a feeling of tightness and stiffness during joint motion, even within the central parts of the ROM (usually between 30 and 70°), even without any swelling present. Tightness is expressed by a feeling of "not that much space down there" which reflects scar tissue occupying needed natural free space and exerting pressure on neighbouring tissue. Such a feeling might not be that balanced as with pure swelling, but of different strength at different joint angles and especially during different joint velocities and directions. Some forms can be described as "popping, clutching". Scar strings catch joint structures during motion, are a resistance for some degrees of motion and then suddenly give way as the joint motion finally pushes the scar string away. Crepidus is an expression of rough scarred surfaces rubbing on each other.
Stiffness and pain are emphasized in motions after longer rest. Here, the scar tissue first has to be pushed aside by some motion and also be made a bit softer and thus more flexible for a short term under pressure. Also, increasing crepidus and pain towards both end limitations of the ROM indicate an impingement of moving joint structures onto scar tissue. Functionally decreased ROM is therefore present. When standing or otherwise exerting pressure on the joint, increased tightness and pain is felt as scar tissue presses on neighbouring tissue or in the (c) type case) hampers flexible deformation of tissue usually being able to do that.
In severe expression, b) and c) types can fixate down structures, usually mobile relative to others, completely, e.g. fixed patalla (baja).


How can the condition overcome? There is only a chance when the product of primary trigger and genetic leverage do not surpass a certain hypothetical threshold. Best treatment can reach furthest, when removing all present scarring (a potential primary trigger) with a surgery the least invasive possible (surgery is always a primary trigger, but may be minimized in impact). Then, controlling the inflammation process and avoiding attachment of scar tissue within the joint has to be achieved at the same time. There is always an inflammation process, initially. The best way to tackle that is cold, rest, elevation, anti-inflammation medication. The other aspect has to be tackled with exactly the opposite: mobilisation and ROM extension. Because of this contradiction, the condition is so hard to cure. Only a very balanced way of walking the fine line between the two together at the same time in the face of not too much expression (from the product of primary and secondary) will be successful.

I believe AF is not that rare. It is just often underestimated or not recognised correctly. Many surgeons do not see a mild form when it is present or treat it or a severe form wrong - because even a mild form is not that easy to cure. Patient compliance with a therapy procedure they do not know - haha - is of course very low and standard PT approach is not helpful. Most expressions are mild to moderate. The patient accepts at some point that they have to limp with some minor pain for the rest of their lives because they are told that nothing further can be done for them. As they trust doctors, but do not like being operated and it is not life threatening, they leave it as that. Subsequently, not enough cases can be operated, cured and studied by experts on the one hand and on the other, the condition is thought to be rare, thus too few resources spent for research. It is a vicious circle: not enough research - not enough known among OSs - not enough specific treatment - not enough data - not enough known and not considered relevant (research). Additionally, because of so many complex primary triggers and genetic leverage variation, leading to various symptoms and expressions, very large sets of cases would be needed to isolate specific aspects for scientific study. So there is research, but much more cases and research would be needed ...


That's my story. My belief. Why do I post it here, then? Because of curiosity, because I believe your knowledge, stories, experience can help to correct and improve it further towards the truth. I would be very glad for anything pointed out. And if you think, it's all nonsense, please do not hesitate to explain why.
You think there is somewhere already a very nice, continuous story? Please post it, I am very interested! All stories I read so far, did not fully please me in content, logic, scope, continuity or compactness.

Many thanks and best regards,
S.R.

Offline Decruz

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Re: Trying to understand Arthrofibrosis
« Reply #1 on: September 10, 2011, 11:54:03 AM »
I share the fact that the Shelbourne classification isn't complete, it simply miss many other cases.
Here:

Type 1: <10° extension loss and normal flexion;
Type 2: >10° extension loss and normal flexion;
Type 3: >10° extension loss and >25° flexion loss with a tight patella;
Type 4: >10° extension loss, 30° or more flexion loss, and patella infera with marked patellar tightness

What about case (like mine) with <10° extension loss and >25° flexion loss with a tight patella?
Or cases I've seen myself with <10° extension loss and 30° or more flexion loss with a tight patella/patella infera?
Why in the world extension loss should be > of 10° when flexion loss is >25°?
It's totally unsensed, always thought so.
Bye
Decruz

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Offline starpolisher

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Re: Trying to understand Arthrofibrosis
« Reply #2 on: September 11, 2011, 10:34:12 AM »
I agree with you both, wholeheartedly.  We moved to Indiana (not just to see Dr. Shelbourne but my son had chosen college here) and all my surgery had been done in NY and at one of the best Ortho hospitals in the U.S.....with a brilliant surgeon.  I had extensive physical therapy and went to a very good rehab hospital the 2nd, 3rd, and 4th time around.  When I first visited Dr. Shelbourne's clinic, I never met him because he is more familiar with this condition from accidents....and not tkr's.  My doctor there was familiar with tkr's.  I kept my mouth shut because I didn't want to anger any doctor who might help me (even though I didn't agree with him) when he said they didn't believe it was genetic....it was due to improper PT after surgery!  It no longer exists in Indiana!  I had the same therapy as everyone else and yet ALWAYS lagged so far behind.  I did all  the exercises and all of us were in a lot of pain, but we all wanted to do well after what we'd been through!  Why was I ALWAYS the one would couldn't achieve good ROM?  At it turned out, I did have some improvement with their Elite seat.....and getting my legs straighter was a big help but when they moved on to bending, I would lose degrees in straightening!  Finally after months of not progressing anymore and needing a lot of pain meds, I was told nothing further could be done and they were short term care doctors.  They wouldn't even do paperwork for long term parking placards!  The wouldn't do paperwork for a scooter.  I was in serious pain!  Why didn't they refer me to Astym?  The doctor said as soon as they see a patient with AF problems, they immediately work on PT .... perhaps the elite seat and different exercises to prevent it from worsening?  Not sure.  I think they said mine wasn't caught in time.  Well Astym certainly was able to give me enormous pain relief and my last surgery was in 2008 and just had my first of 16 treatments in May of 2011!  I am still stiff with less than desirable ROM although it's certainly improved.  They can't break down Scar tissue inside the joint itself.....but I had a lot of scar tissue wrapped around both knees and they have broken down a very large amount of this scar tissue!  I never expected to be like I was before all the operations but I was almost bedridden with chronic pain and now my pain is far more easier to deal with.....I have a lot less!  I have a life.....limited to an extent, but able to do much more.

Offline Decruz

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Re: Trying to understand Arthrofibrosis
« Reply #3 on: September 12, 2011, 04:03:16 AM »
Please check the new thread I just opened about ASTYM in Europe (for who is interested): http://www.kneeguru.co.uk/KNEEtalk/index.php?topic=57405.0

Thank you - bye
Decruz

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Offline sreinhard

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Re: Trying to understand Arthrofibrosis
« Reply #4 on: October 16, 2011, 03:11:49 PM »
A month has gone by since my first post, I have consumed more literature and seen one of our national AF gurus, who diagnosed ' AF "at" reflex dystrophy ' with me. Accordingly, I have been digging deeper on the inflammation and especially (S)RD/CRPS literature. That gurus latest research indicates, that generalized AF is often maintained by latent (S)RD.

Thus, I would like to update my belief. I would not completely retract any paragraph, I had written, but my point of view has shifted quite a bit.

First of all, my (S)RD/CRPS/Sudek is NOT really obvious. The most prominent symptom of that desease is missing completely: the pain! There is also hardly any swelling or obvious skin changes. But I have most of the not so obvious typical other symptoms: the increased hair growth, the pre-stage to osteoporosis, the heat pulsations and ... generalized arthrofibrosis! I want to make clear, that an (S)RD/CRPS can be easily overlooked. Only the AF is really obvious on the MRT and with crepidus/decreased ROM.

Thus, I have to add an e) inflammation trigger: neuropathlogical triggers or leverages.

From this observation grew the insight with me, that the AF is not the main point, the inflammation is what really matters. In my first post I was writing about the inflammation, but even more about the AF tissue stuff, how I believe it forms, grows etc. That may be interesting but it misses the point.

Thus, the core perspective of my current belief: AF is just the most pronounced symptom of a range of complex post-operative inflammation conditions.

This sentence is not in any way a contradiction to what I wrote in my first post (inflammation triggers AF), but the point of view is. It means, that treating the inflammation condition has to be at the center and not necessarily "treating" the AF (e.g. by LOA).

No matter if the inflammation is a (S)RD/CRPS/Sudek or a latent infection or something else, those are classes of inflammations which become chronic after some time. (S)RD/CRPS is chronic after a year at the latest. Such chronic inflammations are very difficult to heal. Somewhere here around I read about someone with a latent bone infection. Might be similar for such a condition.

This also explains a few things:
a) The elusive genetic factor is just the sensitivity for these complex inflammation conditions. There may be even a psychopathological cause among those factors, although studies are mixed concerning at least the (S)RD/CRPS.
b) Why does surgery often not help and often make a mild AF even worse? Well if you just operate one symptom and the (chronic) inflammation is still present or even more likely re-ignited by this, the symptom will of course come back!
c) The more surgeries and longer the time frame, the worse the prognosis. The inflammation - by then always in a chronic stage - is deeply entrenched in the joint and surrounding region.
d) Why AF is more frequent with TKR. Well, a TKR is a strong inflammation "fuel".

The surgery topic, however is more complex. There is still another dimension in it: secondary effects of the AF symptom, e.g. Patella Baja (PB) or Retropatella-OA. So in fact you have three layers: the primary illness (complex inflammation), the secondary symptom of Arthrofibrosis and tertiary, irreversible (!) effects of the decreased ROM and Patella contracture, e.g. PB or P-OA.
Those tertiary effects are the worst in the long run.

Thus, there has always to be considered a balance when making a decision about a LOA. The primary condition requires a LOA as late as possible, that is when the inflammation has hopefully completely subsided. Tertiary effects on the other hand require a LOA as early as possible because they worsen over time.
Yet, these tertiary effects also depend a lot on the extension ROM deficit. Extension deficits >15° lead to increasing Patella contracture, while a deficit between 0° and 5° should be harmless when not stressing the joint much for a long time.

Thus, I have to amend my "how can it be overcome" section from the first post. Walking the balance is true for severe extensions deficits, where one "has to take the risks" and it is very difficult to achieve while the inflammation is still active - and likely refreshed/strengthened by the surgery. Yet the threshold of "trigger" and genetic concept is only a complicated description of what really matters: the stage of the inflammation and its reaction to surgery and AF-rehabilitation procedure!

However, for lesser extension deficits, another path has to be taken: avoid LOA at all costs, as long as possible! Take all load from the joint, only light PT, no leg sports. And wait, wait, wait. In many such "milder" AF cases, the fibrosis as a symptom might even decrease when the inflammation has subsided and has not become chronic. Hard, mature fibrotic tissue might take long to change in form or diminish, but there are cases where it did over range of years.
If ROM is still insufficient after 2 or 3 years, a LOA comes at least with less risks. There are studies showing exactly that statistical causality.

Or in the word of the AF-expert "Patients usually want to have surgery quickly, to return to full activity quickly. But that is by no means wise."

So much about my latest belief. I will post again, when it has reached a new stage  ;)



Juneau

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Re: Trying to understand Arthrofibrosis
« Reply #5 on: October 18, 2011, 06:57:18 AM »
Wow, that's quite some research you have been doing. Thanks so much for all of that information. The information comes to me at an important time when I am considering next steps to do for my AF.

My AF expert OS had told me before my LOA that I might need more than one surgery because my AF was so extensive and he does not want to remove too much scar tissue at once so that he can 'trick the knee into thinking no trauma was done so that it does not react with excessive swelling'. He usually does not do a second surgery until 6 months after the first one (except if there is a risk of infection like for a portal issue).

I am supposed to see the OS again in January and discuss next steps so I need to start to plan my trip to California again soon. On one hand, I have been eager to have more done, to get better results but my gut level has been telling me that I need extra time (since I have been healing so slowly) to let my knee fully heal again before I should even consider undertaking any more surgery. Your research seem to support that feeling.

Offline starpolisher

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Re: Trying to understand Arthrofibrosis
« Reply #6 on: October 21, 2011, 03:16:04 AM »
What you say makes so much sense!  I've had a variety of medical conditions that involve inflammation....just one example is chronic, very painful rosacea.  I have laser surgery a lot and it really controls it....but as it is considered "cosmetic" I have to always pay for it....however, it is worth it.  I have heard that the omega oils are great for inflammation but I am allergic to every single omega capsule on the market....no matter what the source is.  I am also allergic to seafood!  I can't eat flax cereal.  About the only source I can consume without problems are walnuts!  I believe this IS a genetic factor.  I had  a double tkr.....so AF in BOTH knees.  My pt was grueling and never worked.....it made it worse!  I had a revision for each knee, 5 months apart in 2008 and it all came back.  I also have panic disorder and my panic attacks (now pretty much under control) feel as if I am on fire.  When I had my first surgery....double tkr....I literally had to lie on bags of ice at the rehab hospital as my panic disorder was so out of control due to the pain.  The pain mgt. was sub par at the first hospital and rehab....the 2nd hospital was far better and having surgery on one knee at a time plus much better pain control kept my panic disorder under control.

May of this year I have had 18 Astym treatments and that is the ONLY thing that really helped reduce the pain!  I have been on morphine as the pain was so severe.  I couldn't stand more than a minute without a lot of pain and the ONLY time I wasn't in constant pain (the morphine only took the edge off) was laying in bed....no way to live....so I just tried to deal with the pain as best I could.  The ASTYM was incredible.  After 2 treatments (very gentle) I could feel less pain!  While I still am not to 100 ROM....I am improved.....but the degree of pain is so much less.  I have far less pain and can get around better.  It is tiring if you are in a continual cycle of breaking down tissue and healing....though Astym is very gentle....so taking time off lets your system rest.  Right now am having problems with something else....on a med I think is starting to bother my panic disorder....so taking time off from my Astym until I get something else resolved.  Astym is very dependent on the PT knowing they have to be gentle and you do best with one treatment a week (at least for me).  I am so grateful for this therapy.  I never had an LOA and of course no doctor will do anymore surgery on my knees....just as well.  For those who go the Astym route, make sure the therapist has a good talk with headquarters (as my therapist did) because Dr. Sevier did a great job of advising her to be gentle, not to hurt me (I have experienced discomfort with it but nowhere near the pain I've had with my regular PT in the past) and "less is more"....once a week treatment only.  This has kept me from having any flare ups.  I think the doctors who worry about Astym get it mixed up with Graston, which everyone has acknowledged is much more painful.  A slow and steady reduction of scar tissue has really eased the pain. 

I've had a lifetime of health issues.....and a surprising number of people with AF have noted they have either had panic attacks or have panic disorder....not everyone but more than not!  I was not diagnosed with panic disorder until about 12 years ago and I've had it for years.  I participated in a study at Columbia University (gave my DNA) and they have found several faulty chromosomes.  Unfortunately, so many doctors know so little about it.  The best ones I've found are those who have it themselves....they've been the most helpful.  A lot of biological problems go hand in hand with this disorder.   

Offline sreinhard

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Re: Trying to understand Arthrofibrosis
« Reply #7 on: November 05, 2011, 09:21:55 AM »
When I had understood, that the inflammation complex is the key to arthrofibrosis, my search went on trying get to the root of everything.

As the inflammation is fueled by something, I will now call this the

Inflammation support compound (ISC).

The inflammation complex which creates AF is by itself only local, not global, however the ISC may also be global! Such an ISC encompasses general hormonal levels, immune system state, metabolic state and sympathetic/parasympathetic activities. The main part of this post will be about dealing with these things.

I believe now, that the ISC is the most complex aspect of the whole story!

Lets summarize the layers of the condition, AF is embedded in, first:

1) Inflammation support compound
2) Inflammation complex
3) Fibrotic tissue (AF)
4) Tertiary effects from changed joint conditions and biomechanic as a result of 2) and 3): e.g. Patella Baja, Cartilage damage (both from abnormal cytokine IL level AND mechanic load changes), ligament tissue necrosis etc.
5) Pain, ROM restrictions as a result of 3) and 4)

What you see and feel is mainly 5) - everything else are more or less hidden variables - you can see 3) and 4) on MRI, though. Peeling off the onion has therefore to take place mainly in the mind.

Concentrating back on 2) and 1): the inflammation complex is certainly triggered by primary surgery. The type of the inflammation complex may vary greatly among patients. Research on molecular factors showing emphasized behavior during an AF points clearly to the inflammatory response factors being crucial stages of the cascade, e.g. Cytokine IL-1 and friends.

Influence on these factors is known to be both local and global. Thus, the ISC must be tackled both local and global.

I will define two dimension, one for local handling and one for global handling.

I) Local treatment stands on two pillars:

I.A) Joint load relief - I.B) Joint immobility avoidance

I.A) Joint load relief is probably the most important aspect of ISC handling. Its aim is to minimize stress and irritation on local tissues. Among involved local tissues are cartilage tissues, bones, ligaments, muscles, skin, free joint liquid, capsule, the abnormal fibrotic AF tissue and more.
Load stresses occur as a result of biomechanical forces and torques between tissues. In the AF damaged knee, two factors lower the threshold for load stresses: inflamed tissues are more sensible on the one hand and biomechanical settings are altered because of fibrotic tissue and tertiary joint changes on the other.
Load on the patellofemoral joint is least in full extension, where the patella is relaxed. Load is high during dynamic movements covering a wide range of flexion under acceleration and high "payload" weight. This is especially true for walking stairs up and down, walking slopes up and down and exercises like squatting. These have to be avoided at all costs until the inflammation and AF have completely subsided. Cycling provides intermediate load and is better to be avoided - its mobilizing aspect should be substituted by other, less load intensive exercises.
Walking on even grounds is safer, as acceleration and spring-damping is performed closer to full extension. Yet, walking should be avoided at high extension deficits.
Standing is mostly safe at low extension deficits as the patella is relaxed and muscle tension is not very high. Sitting is preferably always done with maximum available extension to minimize patellofermoral load and avoid patella contracture. It can also help to increase extension, although very slowly at most.

I.B) Like with everything, too little is as bad as too much concerning joint stimulus. Joint load relief avoids too much stimulus and accordingly immobility avoidance has to avoid too little stimulus. Stimulus avoids tissue atrophy, helps to keep positive healing processes active, dynamic and can channel the inflammation complex onto more natural paths by liquid influx etc. However, mobility exercise has always to take care not to conflict with joint load relief. Thus, exercises have to be free of load, acceleration and larger forces in general. These exercises have to be performed carefully, slowly and within a pain free range. Examples are manual patella mobilization, supported wall slides, free dangling of the lower leg, passive flexion motions, but also straight leg raises (which are patella neutral) and similar exercises.
The frequency has to be adjusted so that no negative subjective feeling (heat, swelling, pain) arises from these exercises as a distinct source. It has to be remembered that there is no urgency concerning muscle atrophy. Any permanent muscle atrophy is caused by nerve damage, not by long enduring temporary atrophy becoming hypothetically chronic.

II) Global treatment stands on the three pillars of life hygiene:

II.A) Psychological - II.B) Activity - II.C) Nutrition

I.A) Psychological treatment centers around stress levels, affecting both hormonal level and (para)sympathetic level, also leading to secondary and tertiary effects by self-feedback together with activity and nutrition. Stress is an intense inflammation fuel and thus a central aspect of the global ISC share.
Stress levels are controlled by ways dealing with the illness itself mentally, by positive and negative social parameters, by mental load and sleeping patterns.

I.A.1) Confronting and accepting the condition itself - direct condition generated stress
One of the largest hurdles is probably the pain. Pain increases stress levels massively and therefore leads to a vicious circle. If there is no clear tendency of the pain levels to subside, only smart and well adjusted pain medication therapy can help to break that circle, making stress levels manageable.
Beyond the pain, the uncertain outlook concerning both work and leisure life are another piece of condition generated stress. Dealing with that is very personality dependent, thus finding a sufficient method of confrontation has to be adjusted individually. In general, it can be said that active confrontation is important. Trying to arrange everyday life by behavior changes in a way that life could be managed if the condition would not improve anymore indefinitely can be extremely relieving. An inner coming to terms with the disability can reduce stress levels massively and thus actually help to turn things to the better.

I.A.2) Minimizing external negative social stress
External negative social stress usually arises from being embedded into hierarchical organisations. Most job environments are of that kind. Extensive studies on baboon groups have investigated the stress levels of individuals on all levels of social stratigraphy. Stress levels are highest at the top and at the bottom - which is most certainly also true for human beings. Bosses and peons are under the most intense pressure. From this insight follows that not being strongly involved in a stratified environment is best for the stress level.
While being healthy, one might have only moderate problems living and performing under these conditions. With an active inflammation complex, it is most helpful to retreat as much as possible from the squabbling of human organisations during treatment. "Career" and financial aspects are overrated compared to health. Assuming every reader comes from an economically advanced society, it is those in which financial needs are overrated by cultural pressure.
However, this argumentation assumes, of course, a generalized health care system.

I.A.3) Maximizing external positive social impulse
It is known from both primate and human studies that being embedded into a small, non-stratified, but close social context is beneficial for stress levels. Being around close people is not only practical for physical help in times of disability, but significantly reduces anxiety, depression, stress. That should be very clear, nothing further has to be said about this one.

I.A.4) Mental overload
Reducing mental overload means to thin schedules. No travel, no involvement in intense organisations, no plans. Just relaxing. Mental load is a source of stress.

I.A.5) Sleep
Good sleep over a long time is important for healing complex inflammations. First, the pain has to be relieved as discussed in I.A.1) and other stress factors reduced as mentioned in the previous points. If the foundation is set, you can further experiment with times, temperature, light, earplugs in case you have not done so previously.
Once, when I was still healthy, I tried all available earplugs from a specialized online shop. I found a type of earplugs that is so good in damping and wearability that I can sleep anywhere now. Setting up the bedroom in a way that it is nearly totally dark even at summer noon does also help a lot. Even the change in temperature conditions induced by a different blanket can help a lot.
Furthermore, the concept of Siesta can help during insomnia. Sometimes insomnia is induced by being tired too quickly during the day and then hanging around for some time which leads to not being able to sleep well a night. A 2h Siesta may avoid this.
I have found out for myself that the need for a Siesta depends on season and overall activity levels. In very active stages in the winter, when I get a lot done, I need a Siesta. I organize the work schedule around the sleeping pattern. I experimented even with two Siestas during the day and a very short night - but that did not lead to good results.
Experimenting with different patterns can help you to find your own best. Do not take given what society tries to impose you, especially in times of need!

I.B) Activity targets cardio-vascular conditions but also levels of many hormones. Long-term full body inactivity is very dangerous and a great fuel for inflammation complexes becoming chronic. This is a very well investigated and known fact and has not to be discussed further here.
However, nearly all relevant exercise activities known to man require healthy leg functionality which is definitely not present at the discussed condition.
Yet, there is a great source of ideas for activities which can be performed without leg functionality: the tetraplegic community.
Several sports which do not need leg functionality - and thus do not conflict at all with the joint relief paradigm - can be found there:
Handcycling (there are even mountainbikes with electric support now!), swimming with a buoyant leg pad, cross country ski sledding, sitting monoski and upper body strength exercises (bench press, pull ups, curls etc.).
I am especially a fan of the Handbike (I have a Sophur Shark S racebike), which can fully substitute running and cycling as both a sport and a means of transportation.
Like with every other activity, endurance and strength training should be mixed. As only the upper body is available, it is a bit difficult to schedule enough training of both aspects together with sufficient regeneration. Yet, a lower overall intensity than with full body health activity training should be sufficient.
A recommendation can be (which is exactly my program):
3-5x per week 1-2h endurance (Handbike, pad swimming or cross country sled) exercises
2-3x per week short (20-30 min) intensive sessions for strength, each either pull (bizeps/latissimus and friends) or push (triceps, pectoralis and friends)

I.C Nutrition influences all types of hormonal activity. Both macronutrients and micronutrients play important roles. Sadly, even in the year 2011, we as a society, are far from a general consensus about what is healthy and what is not. Science is entrenched in deep battles and it is hard to find convincing food advice through the fog of that war.
And still there are some undisputed facts, you will find in nearly any modern dietary recommendation:

- Eat meals from food as basic (unprocessed), as possible (and non-toxic)
- Avoid all kinds of industrial sweets
- Avoid fructose corn sirup or any large intake of fructose
- Eat a lot of colorful vegetables (only legumes are disputed)
- Eat omega-3 rich fish
- Drink mostly tea

Sadly that's it. From potato over chicken to bread and egg, from different kinds of oil over milk to chocolate - it's all disputed! The only thing we know is, it is important to eat right, but what is right depends, on whom you believe.

In the meantime, I believe in moderate paleo diets. Recent studies are very convincing. Some very deep literature:

http://www.amazon.com/Perfect-Health-Diet-Youthful-Vitality/dp/0982720904
http://www.amazon.com/Food-Western-Disease-evolutionary-perspective/dp/1405197714

If you are not totally convinced, you can still go even a little more moderate. More potato/rice, less beef - there is always a place for your truth, for you not wanting to be too radical. But be conscious, be clear - not laissez-faire - and you have that pillar under control. And if it is just cutting out any sugar. Your joint will thank you a lot.


I believe, that global treatment of the ISC is an underestimated aspect of AF handling. If one really wants to overcome AF, it means to overcome it on all fronts and with all necessary means. It is total war and you are the one who has been assaulted. So mobilise everything. As long, as there is no targeted medication, directly breaking the inflammation complex, outshining all other means - or to keep to the analogy you are "having the h-bomb" - general purpose global treatment is a promising attack vector beyond and in support of the local treatment.

The summarized message of this post:
While being somewhat lax about the three pillars of life hygiene might be ok when otherwise healthy, it is not ok when treating a complex inflammation condition!

Best regards
from S. Reinhard who has now reached 0/0/125 cold and /137 max, feeling better every week

Offline sreinhard

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Re: Trying to understand Arthrofibrosis
« Reply #8 on: November 10, 2011, 06:51:02 AM »
I just stumbled over this article:

http://www.jaapa.com/infrapatellar-contracture-syndrome-following-acl-reconstruction/article/128854/

The section concerning the gluten is very interesting. This finding is fully in line with trying to change the diet, e.g. to a Palaeo.

Offline sreinhard

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Re: Trying to understand Arthrofibrosis
« Reply #9 on: November 22, 2011, 09:43:12 AM »
Another AF expert doctor has assured me, that he can clearly see "generalized Arthrofibrosis" in my 4 months post-original-surgery MRI.
Which was 10 weeks ago and before which there was no improvement in ROM and subjective feeling, more like worsening for 3 months.

Since then, I have made the following progress with the above therapy plan:

Cold ROM: 0/5/115 became 0/0/127
Max ROM: 0/3/130 became 2/0/140

(Healthy leg: 5/0/140)

Not to talk about the subjective improvements.

As there was no LOA, MUA or something like that, I guess it refutes the common notion that it is hardly possible to improve (hard max) extension conservatively after a long time post-op. At least for not too severe deficits.

Offline mlbbarry

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Re: Trying to understand Arthrofibrosis
« Reply #10 on: December 15, 2011, 06:49:00 AM »
After reading all this, I realize how complicated this condition is. ??? I am 1 year out  from a tkr at age 42.  This came after approx. 12 surgeries in twenty two years on my left knee. The initial injury was torn ACL, MCL, LCL.  back then it was major surgery, five days in the hospital, with another surgery during that stay due to complications.  Wearing a brace for literally nine months, not walking for 7 months and absolutely no PT.  that is just crazy in today's standards :o. So I guess I was wondering if what I have is AF or I am just not working hard enough. ROM is 107 extension is decent, but not normal.  Did PT TILL 5 months out, three days a week, then they sent me on my way, telling me to keep stretching.  I did and still try and do all the exercises was not lazy, but this is it I think. Somehow I feel it is going backwards, harder to go up and down stairs then it was 6 months ago, can't sit for long without pain. Go to a movie with the kids is very uncomfortable, where at three months out I thought it was wonderful to finally sit through a movie.  I don't quite understand the change ::)  but after reading up I am thinking it doesn't get any better then this, and I would be risking so much to try and fix it.

So is it best to leave well enough alone?  I sleep okay, can get up out of a chair fine, walk a mile or two each day.  Tough stuff; getting in and out of a car, can't squat down to save my life, stairs suck, can't get down and up from the floor easily, etc...I guess it could be way worse then 107 and pain. Maybe just waiting it out will heal things over the next several years and it will get easier? Let's hope so.

Thanks for all the knowledge, although a bit difficult to understand it did help.

Monica
88' torn ACL, MCL, LCL repair
92' clean up
95' clean up
96' lateral release
99' meniscus repair, and clean up
2004 meniscus repair, & failed micro fracture attempt
2010 April, arthritis clean up and meniscus repair, poor outcome.
2010 Nov. 8th tkr left knee

Offline captainruss

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Re: Trying to understand Arthrofibrosis
« Reply #11 on: February 13, 2012, 09:08:10 PM »
Monica,

I would kill for 107 degrees and no pain.  I have had the multiple TKR's and have ROM of < 40 degrees.  I had the scar tissue removed 5 months ago and now have bone (Heterotropic Ossification) growing in the soft tissue.  It is terrible.  I limp which is hard on my back.  My shoulders have both been repaired multiple times (rotator cuff) so crutches/walker is difficult.  I have as a goal similar to your numbers.  I am not sure I will ever get there.

My doctor is telling me he can do no more for me besides fusing the leg straight or amputating it.  He wants me to live with it.

Russ
80 Shattered patella 5 surg
09  TKR 
09  MUA
09  MUA
09  Knee infected??
10  TKR  Scar Tissue
10  2nd OS  Diagnosis Infection
10  TKR with antibiotic spacer, no joint
4/11  TKR
11  TKR PT
11  TKR
11  TKR  AF diagosis
12/11  HO diagnosed
2012  Intractable Pain
2012  OS split
amputation possible?

Offline mlbbarry

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Re: Trying to understand Arthrofibrosis
« Reply #12 on: February 14, 2012, 03:06:12 PM »
Russ, so sorry to hear about the miserable leg. Your nightmare is my fear, so I will leave well enough alone.  The doc says when I start losing range of motion we will have to eventually clean it up. Take care;)
88' torn ACL, MCL, LCL repair
92' clean up
95' clean up
96' lateral release
99' meniscus repair, and clean up
2004 meniscus repair, & failed micro fracture attempt
2010 April, arthritis clean up and meniscus repair, poor outcome.
2010 Nov. 8th tkr left knee

Offline captainruss

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Re: Trying to understand Arthrofibrosis
« Reply #13 on: February 16, 2012, 07:39:31 PM »
S.R.

I hope your leg continues down the path of getting better.  I have to say waiting to see if you get AF is very risky.  I have not found one (1) person on this site who has AF and found a cure.  Not one.  So, I would read as much as you can from missmyknee as she is the resident expert and do anything/everything with supplements, anti inflammatories, PT recommendations, icing...and educating your OS to make sure that he/she is knowledgeable about AF and that they are looking for it every month.

I don't feel bad....if I was a horse they would just shoot me and eat me......I can take the pain most days...not working...not feeling like I am doing what a husband/father should be doing is wearing on me very heavily. 

Russ
80 Shattered patella 5 surg
09  TKR 
09  MUA
09  MUA
09  Knee infected??
10  TKR  Scar Tissue
10  2nd OS  Diagnosis Infection
10  TKR with antibiotic spacer, no joint
4/11  TKR
11  TKR PT
11  TKR
11  TKR  AF diagosis
12/11  HO diagnosed
2012  Intractable Pain
2012  OS split
amputation possible?

Offline starpolisher

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Re: Trying to understand Arthrofibrosis
« Reply #14 on: February 17, 2012, 05:28:20 AM »
Russ, I agree with you.  I think if you have the kind of AF we do, there is no cure.  I have, however, come to a variety of conclusions.  I think if I had much less aggressive pt after my surgery and had the type of pt more commonly used in Indiana (much more gentle and they seem more knowledgeable here......astym for one...and they recognize it much sooner and treat it immediately) and had either my second surgeon and then the therapy they do here, I would be much better off.  I AM much better off after astym but I think if I'd had multiple surgeries (even though I've had 5) I would have even more complications.  I am grateful I had less than a number of people on this site who have developed awful complications.  I wish I had decent rom.....I have asked my pt to ask Dr. Sevier if he has suggestions.  The fact that the astym helped my pain quite a bit has saved my sanity, I believe.  I can do more things but still quite limited.  Also, it seems that so many doctors are totally ignorant about what to do for us.  So frustrating to have an uncommon problem.















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