Adhesive Capsulitis CPG: Clinical Course and Differential Diagnosis

Since adhesive capsulitis is the only shoulder diagnosis for which we currently have a CPG, it's worth spending two episodes to cover this in a bit more depth. Today Austin covers part 1 of the adhesive capsulitis CPG, including the sections on prevalence, clinical course, and diagnosis.

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Transcript

Hello and welcome back to the OCS field guide podcast. Today we are beginning our long anticipated series on the shoulder with the only CPG we have at this time: the 2013 shoulder pain and mobility deficits, aka adhesive capsulitis, clinical practice guideline. The shoulder/shoulder girdle is the second largest content region for the OCS, just behind the lumbar spine, at 15%. This is kind of intimidating to know in light of the fact that this is the only diagnosis for which we have a CPG. Supposedly, CPGs on rotator cuff syndrome and instability are in the works, but we’ll see how quickly that happens. So after this episode, bear with us as we assemble the available information to cover the rest of the shoulder. Preambles aside, I get the joy of presenting what is likely the most cut-and-dry diagnosis in the shoulder: Adhesive capsulitis. This is an older CPG, so I’ll be supplementing with a few recent articles as we go.  

As I like to do, let’s start with a practice question to get you thinking. 

A physical therapist has been treating a 55-year-old female patient with a diagnosis of adhesive capsulitis 2 times per week for the last 4 weeks. The patient had symptoms that began about 8 months prior to beginning physical therapy. At last session the patient reported that they were no longer having any night or resting pain, her average pain was about 2/10 on the NPRS, and it was noted that active and passive range of motion were equal at 135 degrees of flexion, and 50 degrees of external rotation at 90 degrees abduction. Thus, the PT instructed the patient to increase stretch duration from 3 bouts of 30 second holds just short of pain to 3 bouts of 1 minute holds, just short of pain. Today the patient reports that for the next 24 hours they had intermittent pain at rest in the shoulder at rest and that she was awoken by pain in that shoulder that night. Thus she did not perform her home stretches since last session. She reports that by today she feels that she is back to where she was prior to last session. The physical therapist should:

a.      Instruct the patient to decrease stretch duration back to previous level

b.      Apply heat and electrical stimulation modalities following stretching at the same duration to decrease post-treatment pain

c.      Educate the patient that posttreatment soreness up to 24 hours is normal and encouraged in her stage of the disease process

d.      Continue the longer duration stretching in today’s session, but instruct the patient to take the next day off of stretching and then resume home stretching

The correct answer is A. Contrary to principles we would apply for other conditions like tendinopathy, post-treatment increases in pain or signs of increased inflammation such as pain at rest and night pain are signs we went to far with adhesive capsulitis. This will be true in all levels of irritability, but especially with moderate to high irritability and/or in the earlier stages of the disease process. Thus, although heating modalities and electrical stimulation do get a recommendation in this CPG it won’t be appropriate to keep stretching at the same duration, nor would we tell the patient this is a good thing, or have the patient stretch hard enough that they had to take a day off.

Now let’s jump into the CPG:

First off, let’s talk definition of this condition. For the purpose of this CPG, the definition of adhesive capsulitis, or shoulder pain with mobility deficits, includes idiopathic primary adhesive capsulitis, and three groups of secondary causes of adhesive capsulitis, including secondary systemic, secondary intrinsic, and secondary extrinsic. Secondary systemic causes include systemic diseases like diabetes mellitus and thyroid issues. Secondary intrinsic factors (as in intrinsic to the shoulder) include dislocation, rotator cuff or labral pathology, etc. Secondary extrinsic (as in extrinsic to the shoulder) include things like CVA, cervical disc disease, or distal upper extremity fracture. Whatever the secondary intrinsic or extrinsic factor is, it is usually due to prolonged immobilization due to pain, fear-avoidance, or inability to move the upper extremity. They also note that pain and stiffness following a surgical procedure should not be considered adhesive capsulitis. 

The overall prevalence of primary adhesive capsulitis is 2-5.3% of the general population. Among people that have adhesive capsulitis, there is a much higher rate of diabetes and hypothyroidism compared to the general population. As such, the strongest risk factors for development adhesive capsulitis are presence of diabetes mellitus and/or hypothyroidism. Among individuals with hypothyroidism, females are more likely to develop adhesive capsulitis, while among individuals with diabetes, a greater proportion of males than females develop adhesive capsulitis. Beyond those with systemic factors, adhesive capsulitis is most prevalent in individuals age 40-65, with peak incidence between 51-55, who are female, and who have had contralateral adhesive capsulitis.                                                                                                              

The pathoanatomic features and details of what causes primary adhesive capsulitis are not perfectly understood, but we know that there is evidence of multi regional synovitis and/or vascular and synovial angiogenesis which progresses and  results in fibrosis of the capsuloligamentous complex, particularly anteriorly, and in the rotator interval. 

Clinical course: 

Historically, the clinical course of adhesive capsulitis has been considered a 12-18 month, 4 stage, self-limiting disease, though newer evidence shows that people may have symptoms, though milder, for years depending on extent of fibroplasia and the amount of resorption. In fact, around 40% of patients will still report disability 2 years after onset, and at 3 years, around 40% will still have residual ROM loss, though minimal reported disability. Furthermore, individuals with diabetes have demonstrated an even longer course with high likelihood of relapse. This highlights the need for treatment and education in this population. It will be important for us to combat the idea that this will just go away on it’s own, as that is often not the case, and we know that people can get back to functioning far quicker with proper care.

Let’s quickly walk through the classic way to stage this condition. Stage 1, or pre-freezing stage, can last up to three months and is characterized by sharp pain only at end ranges, aching at rest, and can have sleep disturbance. It is often mistaken for impingement in this stage due to minimal loss of range of motion. Examination may reveal some loss of external rotation range of motion, but intact rotator cuff strength. Stage 2, or the “freezing” stage is characterized by a gradual loss of ROM in all planes limited by pain. You likely will not feel a true end feel here, as under anesthesia, individuals in this stage have only minor loss of ROM. At the tissue level, there is aggressive synovitis and angiogenesis occurring, but not significant contracture or fibrosis of the capsuloligamentous complex yet. This can last around 3-9 months. Stage 3 or “frozen” stage is characterized by lessening of the synovitis and angiogenesis, and thus lessening of the severity of pain, but at this point fibrosis has progressed significantly and the axillary folds of the capsule are usually lost. Thus ROM will be the most limited. Frozen stage is said to last from 9 to 15 months. Stage 4, or the “thawing” stage is characterized by significant lessening of pain, which in many cases will resolve, and gradual improvement of ROM over potentially a 15 to 24 month period. Remember that this is the clinical course of adhesive capsulitis WITHOUT intervention, when we just observe what happens. In other words, without intervention, uncomplicated cases will likely have pain for a year to a year and half that then resolves, but they may keep ROM loss on to 3 years or more if not addressed. Also remember that there is a wide range in how each individual may go through these stages, and at each point, intervention or other factors can prolong or decrease time spent in a given stage. Thus the CPG advocates for classifying patients based on their symptom irritability at any given point, and allowing that to guide treatment rather than just trying to guess what stage they are in based on time.

On that note, let’s touch on the evaluation/intervension decision making guide included in the CPG. It consists of 4 components: medical screening, differential evaluation, diagnosis of tissue irritability level, and intervention based on irritability level. Medical screening is where we will gather information to decide if the patient is appropriate for PT evaluation and intervention, appropriate for PT and referral, or not appropriate for PT and rather referral only. Obviously, this is where we want to recognize if the symptoms could be coming from a more serious pathology such as a tumor or infection. Now, spoiler alert for the treatment section, since many of these patients will benefit from a corticosteroid injection, they are often optimal patients for PT AND referral. Also consider referral in these cases if the patient has signs of either poorly controlled or undiagnosed diabetes or hypothyroidism, as optimal management will involve treating these underlying conditions. This is also where we would screen for psychosocial factors that may affect the case. Though understated in this CPG, there has been a recent push for recognizing and addressing signs of central sensitization such as fear avoidance, catastrophizing, kinesiophobia, tactile discrimination deficits, and other psychosocial factors in people with adhesive capsulitis, as these are related to greater chronicity. A case study in JOSPT in 2018 by Sawyer et al demonstrated signs of central sensitization such as decreased tactile discrimination, poor limb laterality, and fear avoidance in a patient with frozen shoulder after a failed intensive therapy program. They began with a top-down approach focused on pain neuroscience education, graded motor imagery, and tactile discrimination for 6 weeks, and then focused on a more typical impairment based approach with excellent improvement across all measures. If nothing else, this highlights the need to screen for signs of central sensitization, fear avoidance beliefs, and apply appropriate interventions for deficits found in these areas. In that same vein, one RCT by Baskaya et al in 2018 showed greater improvement in pain, function, and ROM with addition of mirror therapy to patient’s active ROM exercises with adhesive capsulitis. So we may see more on this coming out in the literature.

The second component is differential evaluation.  If you have the CPG out, you may note that they include two main other diagnostic classifications, which they say are the most common other classifications or diagnoses with shoulder pain: shoulder stability and movement coordination impairments which includes dislocation or sprain and strain of the shoulder, and shoulder pain and muscle power deficits which includes rotator cuff syndrome, rotator cuff or biceps tendinopathy, things we would call subacromial pain, etc. We’ll dive into those and what seems to be the leading classification system for the shoulder in future episodes, so for now we’ll focus on ruling in or out adhesive capsulitis. 

Criteria for ruling IN adhesive capsulitis are as follows: 

●       Age between 40 and 65

●       Gradual, insidious onset with progressively worsening of pain and stiffness

●       Pain and stiffness limit sleeping, grooming, dress, and reaching activities

●       Glenohumeral passive range of motion is limited in multiple directions with external rotation most limited and worse in greater abduction

●       Glenohumeral external or internal rotation decreases as the humerus is abducted from 45 to 90 degrees

●       Passive motions into the end range reproduce the patient’s familiar pain, and

●       Glenohumeral accessory glides are limited in all directions

You can probably rule OUT adhesive capsulitis if one of the following exist:

●       Normal passive range of motion

●       Radiographic evidence of glenohumeral OA

●       Internal or external rotation improve with greater abduction, or familiar pain is reproduced with palpation of the subscap, aka, if the issue is actually the subscap limiting their ROM and causing pain.

●       Upper-limb neural tension testing reproduces the familiar pain, or if shoulder pain can be altered by altering neural tension in different positions, or if…

●       Shoulder pain is reproduced with placatory provocation of a relative peripheral nerve entrapment site

Pretty much all of that is to say: you’re really only considering this diagnosis between 40 and 65 with insidious onset, with similar active and passive ROM loss that is brought on by ROM into the restriction and not signs of some other pathology. Let’s quickly go through how you would differentiate this from other painful, ROM limiting conditions. Though glenohumeral OA may have a gradual insidious onset, the history and age range are going to be different. Primary OA will likely have a much more gradual intermittent onset over years rather than weeks and months, and will be most prevalent beginning at 60 years old and up. Also consider rheumatoid arthritis, as someone with a flare-up or new onset of RA could present with painfully limited shoulders. Remember that for whatever reason, though people may end up getting adhesive cap in their other shoulder, it doesn’t really happen at the same time, so red flags should be going up if you see bilateral symptoms or multi joint pains and inflammation. Beyond this, I’d look out for acute calcific tendinitis of the shoulder. As this masquerades most closely to frozen shoulder. It is similar in that it has higher prevalence in women, individuals age 40-60, and higher prevalence with thyroid and metabolic disorders such as diabetes. Just as primary adhesive capsulitis, it is not precipitated by any specific injury, but rather comes on insidiously. The main differentiator clinically to look for is that adhesive capsulitis will have a slow gradual onset, while acute calcific tendinitis will come very quickly, such as someone waking up early one morning with severe debilitating pain in the shoulder. Calcific tendinitis is characterized deposition of calcium hydroxyapatite crystals in the rotator cuff tendons, bursa or other structures in the shoulder. This can develop into chronic calcific tendinitis, but most cases actually go through somewhat similar stages for which there are various theories, but mostly center around some kind of pre-calcifying, calcifying, rest, and then resorptive phases. Thus it is also considered to be self-limiting in many cases. It can also limit ROM due to pain and mechanical blocking of ROM dependent on where calcium deposits most. This can even be included in the list of secondary causes of adhesive capsulitis. Just remember that true adhesive capsulitis will likely begin more slowly and then have progressively worsening pain and ROM loss rather than the quick severe onset of pain. When in doubt, a simple radiograph should be able to reveal the presence or lack of calcification. On that note, let’s move on to imaging considerations. 

The diagnosis of adhesive capsulitis is primarily determined clinically by the history and physical examination, so there is not significant need for imaging in clear cases of adhesive capsulitis. Rather we use it primarily to rule in/out other potential pathologies. Radiographs can rule in or out osseous abnormalities such as that are consistent with osteoarthritis, or the aforementioned calcium crystals with calcific tendonitis. MRI is also primarily used if there is need to rule out other pathology rather than diagnosing the condition, but there are some tell-tale signs that can be seen with adhesive capsulitis such as thickening of the coracohumeral ligament and the joint capsule within the rotator cuff interval, as well as joint volume reduction, and signs of synovitis. So if the OCS exam asks if a patient with signs and symptoms of adhesive capsulitis needs to be referred for imaging, the answer is likely going to be no, unless they have items in their history or examination that lead you to need to rule out other pathology.