Hi everyone. So today we're going to be talking about shoulder adhesive capsulitis, pearls, and pitfalls. I'm Priya Patel, and with me I have Dr. Nadia Zaman and Dr. Gerardo Miranda-Comes, who will be up here shortly. So this talk we're going to go through, we came up with this topic because despite being a common and debilitating complaint, it's still a subject of considerable uncertainty within the scientific literature and clinical practice as well. Not only is it difficult to define and diagnose, but also to treat effectively. And this is due to lack of knowledge about the risk factors involved and the pathophysiology. And then unique to this talk, we're going to talk about any correlations with the SARS-CoV-2 virus or the COVID vaccine as well. So specifically, I'm going to be talking about the pathophysiology of shoulder adhesive capsulitis. I'm an assistant professor at Albert Einstein College of Medicine, and I work with the Department of Orthopedics in a large level one trauma center in Bronx, New York. I have no financial disclosures. And the objectives of my talk are going to be to understand the pathophysiology of adhesive capsulitis, understand any associated disorders that can lead to it, and any associations between adhesive capsulitis and the SARS-CoV-2 and COVID vaccine. So Simon Emmanuel Dupleix is widely recognized as the first physician to describe this pathology in 1872, which he called scapulohumeral periarthritis. Periarthritis describes a painful shoulder syndrome that is distinct from arthritis, with a general radiographic preservation of the joint. In 1934, Ernest Codman coined the term frozen shoulder to emphasize the debilitating loss of shoulder motion in patients afflicted with this condition. He described this condition as difficult to define, difficult to treat, and difficult to explain from the point of view of pathology. In histological study published in 1945, Julius Nevesier redefined this condition as adhesive capsulitis. For the purposes of this talk, I will be using adhesive capsulitis and frozen shoulder interchangeably. The incidence of adhesive capsulitis in the general population is about 3 to 5%, but can be as high as 20% with patients with diabetes. The condition most commonly affects people in their 50s to 60s, and demographic studies have shown that patients fall with about 84.4% fall within this age group. Women are more affected than men, with 70% of those with frozen shoulder are women. And usually one shoulder is affected, often the non-dominant extremity, and patients can go on to develop it on the other side. A 2016 meta-analysis study suggested a genetic predisposition to adhesive capsulitis, noting a higher correlation in white patients, patients with a positive family history, and patients with HLA-B27 positivity. Adhesive capsulitis can be primary or secondary. Primary, or idiopathic, can occur spontaneously without any specific trauma or inciting event. Secondary adhesive capsulitis can be due to a multitude of factors, which we will go into detail. So from an evolutionary perspective, manual work and the use of the upper limb used to be much higher than today. Today's lifestyle has dramatically decreased the use of the upper limbs in contrast to its evolutionary design, most likely leading to atrophy, parts of the complex ligament capsule of the shoulder. The idiopathic route is associated with neglect syndrome and a sedentary lifestyle. Sedentary living is the main risk factor for the development of insulin resistance and the accumulation of advanced glycogen end products in the ligamentary and capsule areas of the shoulder. Secondary adhesive capsulitis can be broken down to intrinsic, extrinsic, and systemic factors. Intrinsic factors include rotator cuff disorders, bicep tendon disorders, and glenohumeral and AC joint arthritis. It can also be a severe complication after open or arthroscopic shoulder surgery, including rotator cuff repair and shoulder arthroplasty. All of the systemic and intrinsic causes are associated with inflammation. It is most commonly associated with syndromes such as diabetes, thyroid disease, cerebrovascular disease, coronary artery disease, autoimmune disease, and duptrins. The mechanism of the action related to these pathologies include low-grade inflammation and chronic hypoxia. Inflammation is the critical factor in setting off what appears to be a cascade of chemicals in the body that specifically irritate the shoulder joint. Oxidative stress associated with the presence of inflammatory cytokines affecting different parts of the shoulder ligament capsule complex can lead to an increase in accumulation of free radicals, advanced glycogen end products, and subclinical alterations in both the connective tissue and the extracellular matrix. However, what triggers the onset of frozen shoulder in these pathologies is still unclear, and further investigation is needed to give a better understanding. Since this pathology was first described in 1872, there's been a debate about its true pathogenesis. As discussed previously, inflammation plays a critical role. However, it has long been considered to be a primarily fibrotic disorder similar to Duptrin's disease because the histology of affected specimens primarily show fibroblasts mixed with type 1 and type 2 collagen. These fibroblasts were absorbed to transform into smooth muscle phenotype myofibroblasts, which is assumed to be responsible for capsular contraction. Another theory proposed a solely inflammatory process due to multiple studies showing elevated inflammatory cytokines in capsular and bursular tissues of patients. It is now more widely accepted that the pathogenesis is primarily an inflammatory process that eventually leads to fibrotic changes in the capsule. There are a few studies that examine synovial biopsies of patients with frozen shoulder. Of note is a prospective case control study comparing those undergoing arthroscopic treatment for frozen shoulder and those with subacromial bursitis. Frozen shoulder biopsies were found to have a chronic presence of immune cells, such as inflammatory mediators, including cytokines, tumor necrosis factor alpha, and matrix metalloproteinases. They concluded that the altered levels of inflammatory cytokines may be associated with the pathogenesis of inflammation evolving into fibrosis. So in terms of pathoanatomy, contracture of the glenohumeral capsule is the hallmark of adhesive capsulitis. Findings include loss of the synovial layer of the capsule, adhesions of the axillary to itself and to the anatomical neck of the humerus, and overall decreased capsular volume. A thickened and fibrotic rotator interval, a structure that's critical for glenohumeral joint stability, is also seen. The rotator interval is a triangular space between the supraspinatus tendon, subscapularis tendon, and the base of the coracoid process. It contains the coracohumeral ligament, superior glenohumeral ligament, bicep tendon, and glenohumeral capsule. A contracted coracohumeral ligament is considered the essential finding in frozen shoulder. The coracohumeral ligament is placed under tension with maximal external rotation, therefore it is the main target of operative treatment for adhesive capsulitis. In advanced stages, thickening and contraction of the glenohumeral joint capsule develops, further limiting the range of motion in all directions. So the discussion to have a talk about adhesive capsulitis initially came up when we all started noticing an increase of patients being diagnosed with it in our respective clinic in the past two years. A literature search found a few case reports discussing any associations with the SARS-CoV-2 or the COVID-19 pandemic. So as many of us are aware, SARS-CoV-2 can have multiple extrapulmonary complications and reports illustrate that the musculoskeletal consequences include fatigue, malaisia, and transient arthralgia. So considering the wide spectrum of complications, frozen shoulder could be triggered through an inflammatory and immunological pathway. Other possible associations that the studies reported included correlations with mental health and a sedentary lifestyle as a result of the pandemic and quarantine. Recent literature discussed the impact of COVID-19 pandemic on mental health and an increase in mental health distress overall. It is hypothesized that mental health distress can be linked to an incidence of frozen shoulder through low-grade inflammatory process. So of the limited published studies, there are two to know. There was a retrospective cohort study that evaluated patients during March 2020 to January 2021 and compared patients from the year prior. The pandemic group was found to have a significant increase in the incidence of frozen shoulder, a relative increase about 39.8%. It was concluded that the pandemic played a role in the increase of cases of frozen shoulder. However, they did not assess any correlations after the COVID-19 infection and or the vaccine and thought it was more due to sedentary lifestyle of the pandemic and quarantine. But then Asani et al. reviewed a case series of 12 patients who developed frozen shoulder after COVID-19 infection in the time period of November 2020 to January 2021. They found that all 12 patients exhibited shoulder stiffness and pain diagnosed as frozen shoulder about one and a half to three months after COVID-19 infection. Seven patients were asymptomatic and five had mild symptoms. It was concluded that a direct effect can be considered since cellular penetration of the SARS-CoV-2 occurs via the angiotensin converting enzyme 2 receptor and the transmembrane protease serine 2, which are also expressed by several cells in the synovium, including the fibroblasts and monocytes. An indirect effect can be due to systemic inflammatory response of the host to the infection, which includes a cytokine storm. So as the previous study discussed an indirect cause due to systemic inflammatory response, then would the COVID-19 vaccine have any correlation with the increase of incidence of e-capsulitis? So regarding studying any association with vaccine, it's important to consider if the correlation is due to shoulder injury related to vaccine administration itself or an immune immediate response of the vaccine. Serva is a broad term used to encompass atypical shoulder pain and dysfunction following deltoid IM injection. It is a well-described preventable injury resulting from improper injection technique into anatomic structures adjacent to the deltoid muscle, resulting in chemical and or mechanical trauma. The most reported cause of Serva is an injection into the bursa, which can lead to both subacromial bursitis as well as adhesive e-capsulitis. So Bass et al. conducted a large scale review of reports of Serva after the COVID-19 vaccination in August 2022. Compared with previous systemic reviews of Serva, Serva in the setting of COVID-19 vaccination had a few similarities, including a female predominance with approximately 73% of cases being female and symptoms of pain and limited range of motion being the most common symptoms. Though a key difference is that the previous studies have suggested rotator cuff tendinopathy and bursal injury as the most common manifestation of Serva, this study showed that adhesive capsulitis was the most common finding in the study. From the same study, the comparative delay in symptom onset and increase in adhesive capsulitis is better visualized in this chart, which shows that most cases in the greater than 72-hour timeframe were cases due to adhesive capsulitis, which is shown in gray. Now this can be incidental, but the second chart shows a similar bimodal distribution within the mRNA group, which is seen in blue, and this could suggest an immune-mediated phenomenon specific to COVID-19 vaccination. However, further research is still needed. So in conclusion, adhesive capsulitis pathogenesis is primarily an inflammatory process that eventually leads to fibrotic changes to the capsule. Their hallmark findings include contracture of the glenohumeral capsule and contracted chloro-humeral ligament. With the limited data available, there may be a direct or indirect correlation with the SARS-CoV-2 and or COVID-19 vaccine. And those are my references, and thank you. All right, good afternoon, thanks for being here, first of all. So my role here in this clinical session is to talk a little bit about the diagnosis of adhesive capsulitis. Some of the concepts that we're going to review are concepts that might be a little bit older, and the reason is because there's nothing, there's not much new information in terms of diagnosing it. My name is Gerardo Miranda, I'm an associate professor at the Department of Rehabilitation and Human Performance at Mount Sinai, and an assistant professor at the University of Puerto Rico as well. How do I go forward? So, the next slide, I don't have anything to, no financial disclosures. The learning objectives, so hopefully we all will be able to educate our patients about the etiology and prognosis of adhesive capsulitis, evaluate the shoulder pain, shoulder pain related to this etiology, and identify some clinical and imaging findings related to this. We're going to divide, my talk is going to be divided in a little bit of brief epidemiology just to talk about the scope of the problem. We're going to talk about some initial pearls when diagnosing this condition. The natural progression, I'm going to talk just a little bit about that and confuse everybody a little bit more than we are already confused about this condition. We're going to talk about clinical evaluation and common imaging findings. So the scope of the problem, it is in the general population, three to five percent of the population can be affected by this condition, and in diabetic individuals even as high as 20 percent of them. It usually is more common in the non-dominant hand, but there's a high percentage of cases that can be presented bilaterally. It is usually a self-limiting condition. It can resolve by itself anywhere from one year to three years. That can be, and a high percentage of individuals can have long-lasting symptoms. So in terms of diagnosis, the initial pearl, if I'm going to say anything else, is that it's a clinical diagnosis based on medical history and physical exam, and it's more often than not, it's a diagnosis of exclusion, right? You have to rule out other shoulder pain etiologies such as rotator cuff pathology, ulnar humeral arthritis, cervical reticulopathy, septic arthritis, malposition of any orthopedic hardware prior surgeries, or fractures and malunion fractures or the fracture itself depending on the history. So the natural progression. The natural progression of the condition or the stages or phases like different authors and different authors classify them. They can be classified in four stages that are mainly based on arthroscopic findings or the most common one that we might see are the classification of three stages that's more of the painful, freezing, and tolling phases. So stage one, I try to put them all together and make a little bit of sense of them. So stage one is a painful stage, painful phase. The symptom, the most common symptom is pain, especially at night. The arthroscopic findings during this stage are going to be synovitis without adhesion of contracture, and histologically, you can see inflammatory self-proliferation, the synovium. Stage two and three are the ones that are falling to the frozen stage that we mostly know and maybe we talk to our patients more often. This is a stiff, freezing phase that can last anywhere from four to 12 months. The number one symptom is stiffness. Arthroscopic findings include synovitis, loss of axillary fold or that's secondary to early adhesions at the information at the capsule and capsule contracture. And histologically, you can see synovial proliferation. Stage three is part of this freezing or frozen phase, which is a maturation stage. It can be long, anywhere from four to 12 months as well. The number one symptom is global loss of range of motion, and this is maybe one of the most frustrating stages, and pain with the extremes of motion. Arthroscopic findings includes resolution of the synovitis, so that inflammation, that inflammatory process can be resolving. And there's definitely obliteration of the axillary fold due to significant adhesions. And histologically, you can see dense collagenous tissue in the capsule. And then stage four, which is the, it can be the longest stage, the chronic stage, is persistent stiffness but minimal pain and slow improvement of range of motion. In arthroscopy, you can see advanced adhesions and restriction in the glenohumeral joint space. So when we talk about this clinical diagnosis in the medical history, then we have to mention the risk factors, and that's where our history should focus. So more prevalent in female sex, men less prevalent, but maybe less responsive to treatment. Most cases are within the 40 to 59 years of age range. Any preceding trauma is important to know. And other medical conditions, such as diabetes, cerebrovascular accidents or strokes, coronary artery disease, thyroid disease, autoimmune diseases, Dupuytren's disease, hypercholesterolemia, or other inflammatory lipoproteinemia as well. Prolonged glenohumeral joint immobilization, for whatever reason, is one of the risk factors. And there's a thought that, there's some suggestion that there can be some genetic predisposition. The history of adhesive capsulitis can be a risk factor. White individuals and people that are HLB27 positive can also have a higher predisposition to this condition. So clinical presentation. The initial presentation is shoulder pain, especially in the extremes of range of motion, where you actually stretch that capsule. There's a gradual loss of both active and passive range of motion, which is important secondary to that fibrosis and glenohumeral joint capsule. The first movement that's lost is the external rotation, like Dr. Patel just mentioned earlier, that coracohumeral ligament is where it's stretched with external rotation. And something that's very important is that that passive range of motion that is lost, you can feel a firm end to it that is less likely related to any painful arc or pain limiting range of motion. So when we talk about pitfalls, the number one pitfall is that we don't need imaging. So during this talk, I started reviewing the different imaging modalities that we have available to help out with this diagnosis. And the reality is that imaging is not necessary for the diagnosis. It is a clinical diagnosis. The most important thing about imaging is to rule out any other conditions that you might be suspecting. So within imaging, we can use plain films are useful. And plain films, radiography, and arthrography, especially arthrography, you can see several findings like, for example, medial contrast leakage. This is a normal flow, and this is medial contrast leakage. You can have subscapularis bursa distension, and that can be seen like this, or they can be seen as fluid in the anterior aspect of the scapula. And then you can see abnormal tendon sheath fluid extravasation. For more of the chronic patients or the chronic stage patients, you might see this used osteopenia. And for that, this can be useful. And obviously, to rule out any other conditions such as arthritis, any malposition of hardware, orthopedic hardware, or any fractures. When we talk about further imaging, we should mention MRIs or MRAs, which are very useful. It has the most evidence in terms of findings, so we're going to talk ultrasound a little bit, but MRI has the most evidence. You can see contracture of the glenoma joint capsule, especially when there's volume loss. For example, this is a normal MRI, and you can see contracture at this axillary fold in those coronal views. That's part of it. You can see also extravasation of the fluid medially, and you can see in the anterior part of the scapula, those are signs of adhesive scapulitis. And you can see a periscapular signal, right? You can see signal around this increased signal in the capsule area, periscapular, and that's suggestive of this as well, and those T2 cuts. You can see thickening of the capsule and periscapular tissues, like the hallmark that Dr. Patel mentioned. Looking at that rotator interval plays a big role, where you have the coracohumeral ligament, and you have the superior glenohumeral ligament, the biceps tendon, and the capsule itself. There's good evidence that thickening of the coracohumeral ligament correlates with this condition, especially when compared to the contralateral side. There's going to be capsule thickening, right? Here you have thickening of the coracohumeral ligament, and here you have thickening of the capsule itself. It is suggestive that capsule thickening more than three millimeters can be very specific to adhesive capsulitis. And you can also see increased signal in the inferior glenohumeral ligament, which is useful for the diagnosis as well. Then ultrasound. Ultrasound, for me personally, in my practice, I use ultrasound for many diagnostic purposes. And for frozen shoulder alone, I used it a little bit less, until we started talking about this a little bit more, just because when a person comes in for frozen shoulder type pain, their range of motion is so limited that your actual exam with ultrasound is going to be limited just by the position of the individual. But there are certain findings that you can assess very easily, and one of them is thickening of the joint capsule. You can assess limited movement of the supraspinatus tendon underneath the acromion, especially when doing the impingement dynamic evaluation, and thickening of the coracohumeral ligament. For example, in here you can see the coracoid, the humeral, and this is the coracohumeral ligament, and it's thickening more than close to three millimeters can be suggestive of this. So there is hypoecogenicity of the coracoglenohumeral ligament and there is hypervascularity around the rotator cuff interval. All those are signs of possible adhesive gastrolitis or frozen shoulder type of picture. So lastly, the main pearl here is that adhesive gastrolitis is a diagnosis based on clinical findings, medical history and physical exam. There's no need for imaging studies to confirm the diagnosis, although there are findings that may suggest a diagnosis and can be very useful. For example, the capsule contracture and thickening of the glenohumeral joint, the thickening of the coracohumeral ligament and the inferior glenohumeral ligament and hypervascularity around the rotator interval. So that's it for me. Now Dr. Zaman is going to talk a little bit about treatment. All right, so good afternoon everyone. My name is Nadia Zaman. I'm going to be talking about management for shoulder adhesive capsulitis. So kind of building off of what my colleagues have talked about, the one thing I want to mention before we start is you will see as I get into the management, there are a lot of different options. Not everything has great level of evidence, but my job is essentially to try to synthesize as much of this for you so that you can apply this the best as possible. But you can literally do hours of a talk just on management alone for this condition and you'll see what I mean in just a bit. So I'm an assistant professor of PM&R in the Department of Orthopedics and Rehabilitation in Tufts Medical Center in Boston. And I have no financial disclosures. As I was saying before, lots of options, no real gold standards. So this is something that, as you saw, can be very difficult to diagnose. Oftentimes it's a diagnosis of exclusion, rather, so you're oftentimes working to figure out if there's other things that are going on as well. And in the same token, it can often be difficult to treat. The goals ultimately are to relieve pain and to restore mobility the best that you can. There are several non-operative and operative approaches for management. However, few have high level of evidence and there's actually an appraisal article that I'll go over at the very end that tries to synthesize level A through level F in terms of evidence for each of these things. So what are some of your management options? If you're thinking more conservative, non-operative, you can do non-steroidal anti-inflammatory medications. Oftentimes patients are in a lot of pain and you're considering other things that you're going to add on top of that. Doing a short course of anti-inflammatories, especially early on in adhesive capsulitis can be very useful. There's physical therapy, there's oral corticosteroids, and then there's modalities like short-wave diathermy, shockwave therapy, laser therapy. Of those, the ones in red are the things that I'm going to go into a little bit deeper to give you a little bit more information in terms of how you can apply them to your patients. Now if we're trying to get a little bit more invasive, there are injection components such as just even regular intra-articular injection, like a corticosteroid injection. And then we'll talk a little bit more about capsular hydrodilatation under image guidance. You can also do suprascapular nerve blocks, and then obviously there are surgical options if patients are not responding to the more conservative options, which is translational manipulation under anesthesia, arthroscopic release, and then rarely an open capsulotomy. So I'm going to focus the most on injections because as physiatrists, a lot of us are using image-guided injections as part of our treatments, but I will touch on when it is that you need to sort of maybe consider to have a patient see a surgeon. So physical therapy. So again, as I said before, goals here to try to minimize the adhesions. You want to work on the restrictions and motion that the patient has. You want to reduce pain. And really the main focus of all is really trying to improve functional movement. So often this is in conjunction with either injections or medications that you're going to be giving the patient. What the therapist will often work on, and especially if you have a great network of therapists that you work with the most often for certain pathologies, you can actually kind of put a protocol together that you guys kind of put together based on the evidence that's available. But essentially, they're going to work on joint mobilization. They can use wax therapies, TENS units, Codman exercises, myofascial release, muscle energy techniques. And then more recently, one of the main things that's been studied is the use of proprioceptive neuromuscular facilitation, or PNF techniques. And the reason for that is because numerous studies have actually found that PNF can actually have statistically significant improvement in outcomes related to both VAS, or visual analog pain scores, as well as the shoulder pain and disability index. And one of the reasons why they think that is the case is because PNF is probably one of our most functional ways of applying physical therapy. The whole use of diagonal movements and contract and release can actually kind of mimic a lot of the uses and the range of motions that the shoulder needs to go through in order to do certain activities, like getting dressed, showering, et cetera. A little bit on modalities. So this is probably one of the things that has, right now, unfortunately, some of the weakest evidence that's out there. A lot of the evidence related to modality use has really been in those that have a lot of other comorbidities associated with adhesive capsulitis in the shoulder. For laser therapy, in particular, there was a study done just last year, in 2021, looking at the use of low-level, high-intensity laser five times a week over a three-week period. And they actually found that there was some good evidence in terms of improving mobility, as well as decreasing pain, versus like sham laser therapy. Another thing that many of you may have come across in your practices, and have maybe even heard of some talks or articles coming out recently, is the use of electro-shockwave, sorry, extracorporeal shockwave therapy in musculoskeletal dysfunctions. So as a little intro here, essentially, there's been actually a few different things that have come out in terms of shockwave therapy and the use of MSK conditions. However, it's really not understood how to apply it in a uniform, effective manner. There's different articles that have different protocols, how often patients are getting it, what energy flux densities are being used, the number of impulses that are being applied, whether there's focal versus radial, focal meaning getting deeper into tissue versus radial being more superficial tissue, whether or not there's application of analgesia prior to or after application of shockwave. But the idea behind it is similar to kind of our regenerative techniques. It's this usage of sound waves in order to cause cell migration, proliferation, and upregulation of the collagen in areas where there's MSK pathologies. So in terms of use in adhesive capsulitis, two different studies that were probably kind of recently published. One looked at the use of shockwave in those that have adhesive capsulitis due to diabetes, and they actually found that there was functional improvement in pain relief. However, that was not a controlled study or a randomized study. It was just an observational study. And then there was a similar study previous to that that compared the use of shockwave versus oral corticosteroids, and they actually found significant improvement both in range of motion and visual analog scores with the use of shockwave. And this was unfortunately only a small study, or sorry, rather a short study. They only looked at six-week outcomes. And you'll find that a lot of the studies out there right now are either looking at six weeks, 12 weeks, or at most six months. There's actually very few studies that are looking at a year. So now kind of getting to the meat of what we do, right? So how can we apply injections, and specifically capsular hydrodilatations? So these are basically modalities that you can, or interventions rather, that you kind of include in order to see if you can expedite the recovery in conjunction with corticosteroid injections or other measures of treatments that you're doing. As Dr. Miranda mentioned, you know, oftentimes the clinical phase of this pathology can last anywhere from one to three years. So our goal is really to not have these patients be out of commission for what they're essentially trying to do either at work or at home for one to three years, right? So here we apply image guidance. So often a lot of the studies in the past have been done using fluoroscopy. More recently we're finding that ultrasound can be just as good, or if not better, for a number of reasons to perform these procedures. And then there are actually some much older studies that actually did these palpation guided using landmarks. But again, just like with everything else that we talked about so far, there's a lot of variability in how these procedures are performed. The volume of injectate that's being used, the composition of the injectate itself, whether or not you include steroid or not, and then the frequency of these injections, some leaning towards doing one injection and then waiting a longer period of time versus doing multiple injections in a row, you know, closer together, like four to six weeks apart. And then lastly, there's some controversy about whether or not really you should be going to capsular rupture versus capsular preservation. Sorry, it's just a little video of me actually performing the procedure. Okay, so this was a great article that came out in actually the PM&R Journal, the Purple Journal. So the Catapano article in 2018 initially started as a systematic review where they had over 2,000 papers. And then after their inclusion criteria, they actually ended up with only six studies that they ended up including. And the inclusion criteria was essentially that it had to be level one evidence, that it had to be, the studies had to be in English, and that the control group that was being compared to had to be intra-articular cortisone injections. So they're comparing doing the hydrodilatation to just an injection alone. Two of the studies essentially found clinical and statistical significant improvement in both function and range of motion. Three studies found no significant benefit, and one study found clinical but no statistical significance. So to dive a little deeper, what we have here is I've laid out what each of the studies had in terms of their sample sizes, how they performed the injection, and what outcome measures they looked at. So this is looking at the two studies that actually found both statistically significant and clinically significant benefit. You can see one of them is a much larger study at N of 100 versus the other was an N of 20. The Reza et al. study was actually fluoroscopic guidance versus the smaller study, Gamm et al., was actually only landmark-based, so not using any imaging guidance. And then the first study here, Reza et al., also used a much larger volume. It's actually one of the largest volumes of the studies that were looked at in this paper. They actually went to capsule rupture versus the Gamm et al., which actually did 20 milliliters and did capsule preservation. However, both of them actually found that there was statistically significant improvement both in VAS scores as well as in range of motion, with Gamm et al. also including what I put in quotes, physician impression of severity, whatever that meant. Then there's the three articles, two here and one in the next page, looking at the same thing and actually finding that there was no benefit. So Tevita, both of these actually are much larger studies, one using fluoroscopic, the other one using landmark. Here there was some question about volume being maybe a potential limiting factor for finding whether or not there was a benefit, but both of them used about 20 mLs, one going to capsule rupture, the other one there was questionable capsular effect. But they essentially found no difference with just the comparison to cortisone injection. The Tevita et al. only looking at a short course of six weeks, Sharma et al. looking at a one year. And the last study that found no benefit was a much smaller study, fluoroscopic guidance using 45 mLs with capsular rupture. They actually found that there was some initial improvement at the three-week follow-up but no difference at six months. So now let's talk about ultrasound. So this has been kind of a more recent, and when I say recent, probably in the last longer than five years, but more so the better studies have been coming out more recently. If you noticed in my systematic review article, none of them were ultrasound. And at that time it was unfortunately because none of the studies that were done under ultrasound met the level one evidence criteria. The next two studies that I'm going to talk about did. So now ultrasound has actually become a more preferred method. A lot of it is literally because for many of us it's right in our offices. It avoids any kind of ionizing radiation. And the nice thing is you kind of can do a two for one. You can actually get a little bit of a limited look at the rotator cuff and the shoulder in general, as kind of Dr. Miranda was mentioning before. There have been numerous studies, and I cited a number of them at the bottom. And then if you look at my resources, you can actually go deeper into a lot of these studies as well. But they showed a lot of... So it showed short term up to 26 weeks of effectiveness in the use of the injection under ultrasound guidance versus palpation guided. The traditional approach under ultrasound has been posterior via the glenohumeral joint. But recently there's been some good articles looking at the anterior approach to the rotator interval as a better option. And the reason for that I think makes a lot of sense considering everything that you heard from Dr. Patel and Dr. Miranda saying that there's a lot of thickening of the coracohumeral ligament. And there's a lot of changes in the anterior capsule that it would make sense to do the actual procedure through the anterior. So a little visual here for the posterior approach. So oftentimes you're going to have your patient in a lateral recumbent. You're kind of coming in this area here. And so this is kind of the visual of the head of the humerus, the glenoid. And then this is the needle coming into the joint. For anterior approach, this is the image here. So this is kind of just another visual of what we talked about, or rather what my colleagues talked about before. The rotator interval here between the subscapularis and the supraspinatus tendons. This is your biceps tendon right here. Your coracohumeral ligament is right above it. Your superior glenohumeral ligament is right around here. And your needle oftentimes ends up kind of adjacent to the biceps tendon in this rotator interval. So this over here is actually a great study from a couple years back that looked at the anterior versus posterior approach for injections. And what they actually found was both groups had significant improvement three months after the injection. But the anterior approach actually had improvements that were seen earlier, as well as improvements that were actually seen in range of motion and not just pain relief. However, the two main range of motion that did not improve regardless of anterior or posterior approach in this particular study was extension and internal rotation. And I found even in my patients, oftentimes when patients are coming back after they've had the procedure done, their main complaint is still that they can't internally rotate to put their jackets on or whatever it is. And that's one of the conversations that I oftentimes have to have, that a lot of times the injection may not be enough to improve that. A more recent study from last year, also a randomized control trial, also looking at posterior versus anterior approach, found kind of very similar findings. Looking at both six and 12 weeks, they found improvements in both the shoulder pain and disability index, the visual analog scale, as well as range of motion. There was better and earlier pain relief in the anterior approach versus the posterior. However, in the long term, they had very similar kind of findings in terms of function and range of motion recovery. So even with that said, however, with everything that we know, they still concluded the anterior approach may be more effective, especially in early onset disease. So a little bit about, so what is my approach, right? So we talked about how there's so many different types of approaches, so many different volumes, so many different ways you can do this. So oftentimes, I've been doing it more as a posterior approach via the glenohumeral joint. A lot of this was essentially because when I was seeing a lot of these patients post-COVID, this was before some of these articles regarding anterior approach existed. I often have the patient in a lateral recumbent with the affected shoulder up, similar to this picture here. If they're not diabetic, I will oftentimes include one ml of trimicin alone, which is about 40 milligrams, with four ml's of ropivacain, and then 25 ml's of normal saline for a total of 30 cc's. And I actually do capsular preservation. I found that if you use the extension tubing, oftentimes there's a little bit less resistance when you're doing this injection, so you have a little bit of an easier time from just your finger perspective in terms of getting the volume in. And it also kind of pushes it in in a less powerful way, so the patient, it's not as painful for them. And the whole goal here is essentially you're distending the capsule using that hydrostatic pressure that you create with this larger volume of fluid. So the trimicin alone really is more of a preference thing. There's really no evidence to say that that can make or break your injection, because if the point of the injection is more the hydrostatic pressure, you can do that even without the trimicin alone. And then I often have them follow up at about the 8 to 12 week stage, and at that point we decide if we need to do a repeat injection. So right now, actually, kind of spoiler alert, we're working on a little bit of a retrospective analysis in my practice. Because I have a high volume injection practice, we're actually taking a look at data post-procedure of all of my ultrasound-guided capsular distensions based on the volumes and things that I'm doing in the entire year of 2021. So we had about 120 patients in that 12-month period with a presumed diagnosis of adhesive capsulitis, and we're looking at some very similar outcome measures, such as the spotty and the degree of range of motion improvement, as well as the visual analog scale. So hopefully we'll have results for that soon. We just got IRB approval to actually do this, and maybe we'll have a follow-up talk to this in the future. So what if none of that works, right? So when do you want to see the surgeon? Or when do you want your patients to see the surgeon? So there's a lot of varied literature on this, and a lot of this is essentially because the time points of this disorder is just so long. But the general consensus is, if conservative management fails, it may be time to see a surgeon. That could be two to three months. That could be six months. That could be a year. Some patients are more likely to see a surgeon earlier. Some of that could be younger patients that maybe have a need to get back to something sooner. So if they have manual labor, if they're athletes. If there's trauma involved, they may be going to surgery earlier. If there's less comorbidities, so you're not worried about things like diabetes or thyroid disease or hypertension being a factor of causing a recurrence of the disorder or occurrence on the other side. And then there was actually, the last point here is a little bit of a gray area. There was actually a study done by the Boston Medical Center a couple years back that actually found that patients being on workers' compensation were eight times more likely than private insurance to actually undergo surgery. And they were contemplating whether or not there was something to do with the fact that the reimbursement rate is almost two and a half times higher. Keep in mind, though, this is only looking at the state of Massachusetts, so this doesn't explain other places and other reasons why. But just a very interesting point that I came across and I wanted to include. And then what are the surgical options? So a lot of you may have heard of manipulation under anesthesia. It's the controlled rupture of the contractions that are in the capsule. It's less invasive compared to an open capsulotomy, for example, or even an arthroscopic release. There have been some studies that have actually shown that the outcomes for manipulation under anesthesia and an image-guided capsular hydrodilatation actually have very similar outcomes. So a lot of the surgeons are kind of relying on people like us actually first before they want to go in and do any of these procedures. There's some good evidence out there for arthroscopic release in conjunction with manipulation versus manipulation alone. And then very rarely is the open capsulotomy used these days, more so because the time for recovery is just so much longer. So this is the appraisal article I mentioned previously. So this was actually originally published in 2013 and then revised in 2017 and again in 2020. Keep in mind, this is an expert panel, so this is not necessarily an article that necessarily itself went through peer review. But essentially the goal of it was to come up with some evidence-based clinical practice guidelines that we can use in order to manage people that have shoulder aches of capsulitis. They looked at lots of clinical research articles and they basically established a level of evidence based on the level of the criteria established by the Center for Evidence-Based Medicine in Oxford. And so what they did is they assigned the level of evidence from A, meaning strong opinion, to F, as an expert opinion. And of course the strongest recommendation right now exists for an injection combined with shoulder mobility and stretching exercises. It's found to have the best outcomes in terms of short-term four to six weeks pain relief and improved function. There's weaker evidence as you go down. There's level B evidence for essentially allowing it to go through its clinical course, allowing patient education and stretching exercises. There's level C evidence for manipulation under anesthesia when it's not responsive to conservative management. And the weakest level of evidence really exists for just modalities and a combination with mobilization and stretching. So what's my approach putting all that together, right? So this is kind of a very simple graphic, but essentially what it's getting at is once a patient has a diagnosis or a presumed diagnosis of shoulder adhesive capsulitis, this is oftentimes the way you might like to approach it. So the very first thing that you do is trying to be the most conservative and oftentimes can come down to what the patient wants to do. So you have the option to do kind of anti-inflammatories and physical therapy. And when I say injection here, I mean either injection or capsular distension. Oftentimes you're going to lean towards capsular distension maybe after this talk in conjunction with physical therapy or a combination of all those three together, right? If you have patients that have diabetes, you may actually consider the addition of shockwave at this stage. And you may also want to counsel the patient that especially if they're coming to you early in the disorder, they're more likely to have a benefit from a combination of these things than maybe if they're later in the disease process. You can also include other modalities here, so things that we talked about before like laser and TENS. You just want to explain to the patient that they may not have as big of an impact as some of these other things here. Oftentimes we'll have them come back for a follow-up about six to eight weeks. It's usually because the clinical course of physical therapy is right around this timeframe. At that point, you may want to consider, if you haven't done an injection at this period, you may want to consider an injection. Keep in mind, again, explaining that as you get later in the disease, the effectiveness of the injection may not be as good. You may want to consider a second injection in this area as well. And then you can have the patient go and kind of either do some physical therapy or some of these other modalities or potentially shockwave therapy. But on this next initial, essentially the next follow-up, if they're not improving or they've plateaued, that may be a good time to actually have them see the surgeon. It doesn't mean that they're going to have surgery at that time point, because we're only about three to four months out. And as I mentioned before, some surgeons do believe that due to the clinical course, they may not want to touch a patient until six months to a year out, but it might be a good time to have the conversation get started. And that's it. Those are my resources. I can leave this up for anyone who's interested. And then we'll open this up for any questions. Great talk. Can you hear me? Yeah. Anyway, great talk. Very informative. Just when do you or do not consider adding a suprascapular nerve block to your injection? Yeah. That's a great question. Does this, is this working? Yes. Okay. So that is actually a great question and that was something that we were just actually recently talking about. So I personally have not been doing suprascapular nerve blocks, but I think part of the reason why it is used is because if you're using these higher volumes, it can create a lot of pressure within the joint and actually can increase pain for these patients for a period of time. So a suprascapular nerve block can actually be very useful in that scenario because you can kind of basically anesthetize that region and it should last anywhere from, you know, four to six hours up until even the next day, depending on how quickly the patient is metabolizing that anesthetic. But it is something that I think can be valuable. I just haven't needed it because based on my... Hi, thanks for the talk. Question is about using Shockwave. I haven't used it for adhesive capsulitis. Do you use it posterior, anterior? What's your approach to that? And has it been regional? Like, what do you found to be successful for that, for anyone who uses Shockwave? So I've been using Shockwave for this type of patients. I do a little bit of scanning, right? But yeah, usually I do three sessions and wait it out a little bit. I have a question over here. Thank you for the talk. I was just wondering if you could comment on. How does your paradigm change in regards to how quickly you would want to intervene and is there recommendations in regards to how to sort of guide therapy versus trying to be more interventional at that point? So no, so that's actually a great question So I think one of the things and I'm sorry if I didn't mention this before but we do know that in terms of evidence injections and capsular distention Oftentimes will have a much better benefit for patients the earlier you do it So it's stage one and two right so I would almost say in that kind of a setting if that patient doesn't have any contraindications to having an intervention you may want to do that much earlier than just relying just on like you know range of motion and stuff because as we talked About some of the mobility stuff doesn't have as high a level of evidence as the injection So Interestingly enough when I started doing more of the capsular distention was in that population because I've been I was getting consultations from the inpatient from the inpatient unit and trying to figure out procedures that were That could potentially benefit early on so so the answer to your question is I would definitely do it early on and there's Multiple reasons for that part of it is evidence. The other one is the system the system, right? So our patients are not there for a long period of time, right? For the shockwave therapy, are there any absolute or relative contraindications Dr. Zaman, you were talking about how it causes proliferation of cells in the shoulder. Would cancer be something that you'd consider being aware of? Maybe a contraindication? Yeah. Great presentation. I experience that sometimes when we are doing the injection I may feel like a pop followed by loss of resistance. Most of the time when I feel that I stop, I don't keep going, and I just was wondering if you've experienced that yourself. Yeah, so do you do them under fluoroscopy, ultrasound, palpation? I usually do them blind or it depends on the patient, on the body habitus. Okay, so I will comment. So based on my experience, oftentimes when you feel that pop and a loss of resistance So, not necessarily a bad thing, because a lot of the literature... same benefit. But in some cases, I even have observed it in 10 mLs. Yeah. And so it may be, even if you go with 20, you may get it if you're not doing it on the monitoring. Absolutely. And I think that's, so what I was saying is my goal is usually go to capsular preservation, as I was saying from my approach. That doesn't mean that I haven't ruptured, but it's just interesting because when I do them under ultrasound, I can actually, I feel the pop and then I can see almost the outcome of it on the screen. Thank you. Yep. How about the role of rest? I was at a conference just a few months ago, it was actually an orthopedic surgeon presenting and saying, when things are inflamed, it's like a blister, you don't want to rub it, and resting for the first four to six weeks before doing therapy and doing all the things which can be more aggravating. My end of one since then did pretty well. You know, we did let it calm down, we did injection and mobilization after the six weeks. would be tightening, right? Loss of range of motion. So I was, again, surprised at my end of one that he actually improved, you know, as we went on. Was there any data you saw that you definitely don't want to rescue? Do you all do a breezement after your hydrodilations, so manipulation after your hydrodilations, or do you just let the hydrodilation... So I'm sorry, day after or... Even the day after, yes. Yeah, okay. I set it up something similar to what people are having in elective surgery, things like that. And just a quick second question. So on capsular rupture, I haven't really seen all that much in terms of that being like some sort of horrible outcome. It certainly hasn't been the case for mine, my patients, but you had that 120 patient series. I didn't know if you had noticed some things for those people who did rupture having worse out... I have two questions. First one, just in my clinical practice I'm more in neurologic rehabilitation so I don't see too much adhesive capsulitis per se, but in evaluation tend to see a lot of shoulder impingement, et cetera, you know, a lot of positive Hawkins, MTK, et cetera. In your practice, do you see just isolated adhesive capsulitis or is it a combination of things, like are many tests positive? So, in my practice I see a combination. All right. So then I'm validated kind of. Other question. Is that with the... I agree. I second what you said. It's more... Very often you see concomitant conditions. When you had this, Dr. Miranda, when you had the slides of MRA, MR angiogram, but I guess to me I can't say I know this very well, but some of these looked more like arthrograms or whatever, but you did mention angiogram and vessels. Can you just be a little more... Just elucidate a little bit what was going on. Why would you use an angiogram? Yeah, more of an arthrogram. I'm sorry. I'm sorry? It is an arthrogram. Oh, okay. Thank you. Sorry. I'm too scared of that one. Hello. So I want to implement the rotator interval approach more based on the literature as well as ease of visualization, but I found that even if I visualize the needle in the correct position, I kind of have to use some trial and error to find that sweet spot where I have no resistance. I'm wondering if any of you guys have any tips or tricks in finding that sweet spot. It is cool when you do it anterior and then you scan posterior. I had another question, I'm just wondering, it's a little more general, but if a patient comes in and let's say you're not sure, they have frozen shoulder or they have rotator cuff tendinopathy and it's just too painful and you want to do a diagnostic, let's say subacromial injection to see. If you don't have... Thank you.

sweet spot for injection

rotator interval approach

trial and error

correct position

scanning posteriorly

anterior injection

frozen shoulder

rotator cuff tendinopathy

diagnostic subacromial injection

pain relief