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adhesive capsulitis

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adhesive capsulitis - July 6, 2004 8:05:00 PM   


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I know there are stages of adhesive capsulitis and that often times a person will get better on their own over time, but how long do each of these phases usually last? What are reasonable range of motion goals with relation to time? If a person is only displaying slight improvements in range of motion, when do you seek other alternatives?
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Re: adhesive capsulitis - July 7, 2004 9:03:00 PM   


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From: Bay City, MI
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There are three statges:
Freezing - (10-36 weeks)
Frozen - (4-12 months)
Thawing - (5-26 months
I believe every case is different with adhesive capsulitis. I had a pt with it and after no improvements they may need to have a manipulation under anesthesia. ROM messurements may be different in different stages. In early states it is good to do ROM in pain free range. Try joint mobs I and II. Once in the advanced stages you may start strengthening and joint mobs III and IV.


Thanks for taking the time!

(in reply to mgalkows)
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Re: adhesive capsulitis - July 8, 2004 12:46:00 AM   


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From: colorado usa
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I strongly disagree with the current thinking about adhesive capsulitis and the classification of stages. Along with this classification are guidelines to treat or not treat, based on the belief patients will spontaneously recover or are so acute treatment is useless.

I have seen all clients benefit from joint mobilization etc. no matter what stage they are supposed to be in. Letting someone go without treatment and then imposing a manipulation on their shoulder is certainly a contradiction to the extreme.

Posterior and inferior capsular mobilization at end range and restoration of full internal and external rotation can help immensely.

Curious, what these classifications are even based on. Anyone know the evidence for these as well as the treatment directives?



(in reply to mgalkows)
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Re: adhesive capsulitis - July 8, 2004 4:47:00 AM   


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I have not seen any evidence that the phases of adhesive capsulitis are genuine; and it is of interest to me, being a neurophysiology freak.

Some folk present with a couple of months of severe pain, particularly at night, and start losing ROM because of the pain. We need to see these people BEFORE the ROM starts to fail; but usually we don't.
If you consider that this condition can occur bilaterally, or swaps around from one shoulder to the other over a period of time, there can really be only one cause - central sensitisation where the brain keeps on interpreting that the shoulder/s need pain to protect the body.
Try mobilisations as coloradojulie suggests, and perform the upper limb neural tests, as far as you are able to. Mobilise the cervico-thoracic joint, check the cervical spine out and treat what you find....
,,,but go carefully, as this condition flares easily and the patient will not appreciate this.
Forget strengthening - it is only likely to stir it up, look at strengthening down the track when the pain has settled. Keep repetitions well down - maybe no more than 5 at a time..
Manipulation under GA does not have a good track record. There is a debate on whether the capsule is truly stuck; the jury is out on that one. Not all capsules show up as affected, given the same loss of ROM and pain.
The general tendency is to monitor and encourage, do very low key neural mobes, don't aim for too much, just ease on gradually. No stretches...guaranteed to flare.

It remains a rather mysterious condition, and therefore treatment is grey; there is some indication that the process is the same as for Dupuytren's contracture histologically, and the cause may well be the same for both.

Good luck


(in reply to mgalkows)
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Re: adhesive capsulitis - July 9, 2004 5:11:00 PM   


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I agree with coloradojulie. I don't put much emphasis on a stage. Nor do I with an MD Dx. of adhesive capsulitis. I say this because I continuously change a pts. posture and re-assess ROM....which becomes full or near full and pt. is surprised. If you range a shoulder with a pt. in forward head posture you will not get an a correct assessment. I explain the mechanics of the GH joint to the pt. and then treat them for a postural dysfunction associated with shoulder strengthening...with proper positioning.


Jason, PT
Board Certified Orthopaedic Specialist

(in reply to mgalkows)
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Re: adhesive capsulitis - July 9, 2004 5:34:00 PM   


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From: Madison WI USA
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The stages are based on arthroscopic and histologic appearance of the capsular tissue.

Here is an exerpt from a presentation I did a few years ago.
Stage Characteristics, Histological and Arthroscopic Findings for Adhesive Capsulitis

Stage One, the ?soreness? phase.
This stage is really not discernible from some other shoulder problems, such as tendonitis, bursitis, impingement, and the like. The patient presents with little or no loss of ROM, active and passive. I disagree with the feeling that they actually notice the slight loss that may be present. Pain has been present for 0-3 months, and is reportedly present at rest, with an achy sensation, and with end-range movements, as a more sharp pain. Sounds like tendonitis, bursitis, impingement, doesn?t it? To be able to decide that this person has stage one adhesive capsulitis is a guess at this point. In terms of ROM loss, Hannafin and Chiaia note that this person will present with loss of IR, fwd flexion, and ABD, along with a subtle loss in ER. It is important to note that some authors essentially skip this stage in their studies and/or reviews, and move right on to the ?freezing? stage.
Arthroscopically, these capsules show ?diffuse glenohumeral synovitis, most pronounced in the anterosuperior capsule. (Hannafin and Chiaia)
Histologically, there is hypertrophic, hypervascular synovitis, rare inflammatory cell infiltrates, with a normal underlying capsule. (Hannafin and Chiaia)
It is thought that the hypervascularity of the synovial hyperplasia leads to fibrosis and shortening of the capsule. This is based on studies in which patients with early onset shoulder pain (stage one) were treated with corticosteroid injections and did not go on to get adhesive capsulitis.

Stage Two, or the ?Freezing? Stage
This stage is characterized as the start of the significant pain. It is present with active and passive ROM, which is now limited into flexion, ABD, IR, ER. Sleep is now affected, as lying on the shoulder increases pain. ADL?s become restricted by both lack of ROM and pain. Inability to don clothing is a primary complaint. If you can get the patient to relax, you will feel a thick, capsular end-feel. Unfortunately, relaxation is not likely at this point, due to pain and guarding, so you will more likely get a sense of an empty end-feel due to guarding. Scapular hypermobility is clearly present.
Arthroscopically, there is ?diffuse, pedunculated synovitis (tight capsule with rubbery or dense feel on insertion of the arthroscope)? (Hannafin and Chiaia)
Histologically, there is ?hypertrophic hypervascular synovitis with perivascular and subsynovial scar, fibroplasias and deposition of disorganized collagen fibrils in the underlying capsule? (Hannafin and Chiaia)

Stage Three, or the ?Frozen? Stage
Pain in this stage is less overall, but really no different at end ranges. ROM is severely limited, in the capsular pattern of ER greater than IR, and flexion greater than ABD. All ADL?s above the shoulder height are limited, as are those involving rotation of the humerus. End feel is still capsular, but even more rigid. Getting to actually feel this is not necessarily common, again due to muscle guarding and pain. Scapular hypermobility is rampant.
Arthroscopically there is no longer hypervascularity. Capsule still feels thick upon insertion of the scope. Capsular volume diminished.
Histologically, vascularity is returned to normal, capsule shows dense scar formation.

Stage Four, or the ?Thawing? Phase
Pain is now minimal, yet still can be present at end-ranges. ROM is improving, as is function and ability to perform ADL?s. Recovery is thought to be ?spontaneous but frequently incomplete? (Siegel, Cohen and Gall)
Arthroscopic and histologic data is unavailable, as these people are now improving, and therefore surgical intervention is not necessary.

The A.M. Wiley study did not separate the subjects into stages of the condition, but they did find synovitis in all patients with adhesive capsulitis. This ranged from brisk red appearance to watery and gelatinous. The location for these changes was most often the supraglenoid tubercle, near the upper border of the subscapularis, and in the ?mouth of the subscapularis bursa.? The most interesting finding in this study was that the infraglenoid recess was not obliterated by adhesions, but was inflamed and appeared contracted. There were also no intraarticular adhesions! They went on to say that due to the contracted joint space, it was difficult to examine these recesses in the subjects.

Another study by Rodeo, Hannafin, Tom, Warren, and Wickiewicz found both synovial hyperplasia and capsular fibrosis. Specific cytokines including transforming growth factor-beta and platelet-derived growth factor may be involved in the inflammatory and fibrotic processes. They go on to suggest that developing antifibrotic agents may be helpful in treating the condition.
Adhesive Capsulitis Treatments Involving Other Than Just Physical Means

Manipulation under General Anesthesia.
This is performed by orthopedic surgeons, utilizing long lever arm motions, with an assistant stabilizing the scapula. While this has been shown to result in increased motion, this is not without risk. Risks include fracture, especially in those with osteopenia, which can be caused by the condition itself, according to Leppala et al. Further risks include soft tissue injury, and of course those risks associated with general anesthesia itself. Expense is also an issue with this type of manipulation.

Manipulation or Mobilization after Interscalene Brachial Plexus Block.
Three of the resources in the bibliography for this teleconference directly address this type of treatment. Two involve research studies dealing with adhesive capsulitis, and the third explains the interscalene block procedure in great detail.

Placzek, Roubal, et al studied the long-term effectiveness of translational manipulation for adhesive capsulitis. They had a larger study size (n=31), and showed that significant gains in ROM could be obtained by performing both inferior and posterior translational manipulations following the interscalene brachial plexus block.

Roubal, Placzek, and Dobritt found similar results with a much smaller study size (n=8).

Both of these studies showed not just acute benefit, but long-term results. The majority of patients experience marked decrease in overall pain as well as function in the long-term.

Arthroscopic release
This procedure is of course more involved than the simple manipulation procedures, but Zanoti and Kuhn have shown that it can be performed safely if done correctly. They gathered data for the proximity of neurovascular structures to the capsule, and found the safest location for the release. Hannafin and Chiaia delve into the Arthroscopic release a bit deeper, and describe how it can be performed along with manipulation, with the release prior to the manipulation, which results in less force needed for the manipulation.

Distension Arthrography
This technique involves injecting fluid (contrast medium, corticosteroid, and lidocaine, followed by 30-40 ml of refrigerated sterile saline) into the joint. It has been found that a joint with adhesive capsulitis has considerably less volume.

Laroche et al found that with intraarticular corticosteroid injection, followed by high-intensity physical therapy and an abduction splint, significant gains in ROM could be obtained within the first 5 days. These gains were maintained after one month as well.

Parlier-Cuau et al had similar results, but with the injection of the contrast medium, steroid, lidocaine and sterile saline.


Steve Hill PT

(in reply to mgalkows)
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