Capsular Releases for Shoulder Stiffness: Considerations for Treatment and Rehabilitation
Jacqueline Munch, MD
Andrea Tychanski, PT, DPT, ATC, CSCS
Sarah E. McLean, PT, MSPT
Samuel Arthur Taylor, MD
Scott Alan Rodeo, MD
Dr. Munch or an immediate family member has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research–related funding (such as paid travel) from Acumed and Arthrex. Dr. Rodeo or an immediate family member has stock or stock options in Rotation Medical and Ortho RTI (not paid consultant to Ortho RTI). Also—consultant to Joint Restoration Foundation. None of the following authors or any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Taylor and Dr. Tychanski.
Introduction
Frozen shoulder, or adhesive capsulitis, is a common cause of loss of both active and passive shoulder motion. Originally described by Duplay in 1872, Codman and Neviaser lent the terms “frozen shoulder” and then “adhesive capsulitis” to this condition. Idiopathic adhesive capsulitis presents in the absence of any underlying shoulder pathology, trauma, or systemic condition. Risk factors for idiopathic adhesive capsulitis include female sex, diabetes, thyroid disease, or other autoimmune disease, age over 40 years, stroke, and cardiopulmonary disease. Frozen shoulder can also be a significant cause of delay and difficulty in reestablishing shoulder range of motion (ROM) in the postoperative or posttraumatic setting. The precise cause of this condition remains unknown, but our understanding of the pathologic process has improved substantially.
In the absence of any surgery or known trauma, idiopathic adhesive capsulitis generally manifests as a gradual onset of global shoulder pain and stiffness. This global loss of motion is in contrast to directional capsular tightness, as in the case of the throwing shoulder (in which the posterior capsule is typically tight, due to adaptive changes secondary to repetitive high-velocity external rotation [ER]) or an iatrogenic motion loss such as that seen in the setting of an overly tight anterior instability repair, such as the now-defunct Putti Platt procedure.
Pain associated with adhesive capsulitis is typically constant in the early period. Patients have trouble sleeping, and find particular difficulty with activities involving reaching to the extremes of their motion, including overhead or behind the back. Rapid shoulder movement—a vigorous handshake or unexpected “bump,” for instance—often causes particularly severe pain. In the early presentation, before there is severe loss of motion, the condition is often confused with rotator cuff or impingement syndromes. Patients can avoid pain by minimizing or avoiding movements that cause pain.
As our understanding of the pathogenesis of adhesive capsulitis has improved, the process has been divided into four typical stages. In stage 1, adhesive capsulitis, which typically lasts for about 3 months, patients note pain with active and passive motion, and progressive limitation of shoulder motion in all directions. If pain is controlled or eliminated (such as by injection or nerve block), examination will demonstrate minimal loss of passive motion. The glenohumeral joint has diffuse synovitis on arthroscopic examination, and microscopic examination demonstrates a normal capsule, with a hypertrophic synovium.
In stage 2, or “freezing” adhesive capsulitis, from 3 to 9 months from the onset of symptoms, patients continue to suffer from pain with active and passive motion, but experience true loss of passive range of motion (PROM) as well as limited glenohumeral translation that can be demonstrated on physical examination. Pathologic evaluation reveals synovitis as in stage 1, but with additional scarring and changes in the glenohumeral capsule.
Patients in stage 3, or “frozen” adhesive capsulitis, from 9 to 15 months from the onset of symptoms, have relief of pain except at the extremes of motion, but continue to suffer from significant limitation of active range of motion (AROM) and PROM. The capsule is dense and shows global volume loss. Histologic evaluation demonstrates a synovium that is no longer hypervascular, but the capsule has fibroblastic scarring (Figure 4.1).
Stage 4 adhesive capsulitis is called the “thawing” phase, which can last from 15 to 24 months after the onset of symptoms. During this time, patients have diminishing pain, and gradually regain their ROM.
The diagnosis of adhesive capsulitis is made primarily based on history and physical examination, with imaging studies utilized mainly to rule out other known causes of shoulder pain and stiffness, such as rotator cuff disease, osteoarthritis, or
calcific tendinitis. Plain radiographs may demonstrate disuse osteopenia, and depending on the stage in which the imaging is obtained, MRI may show a thickened capsule with loss of overall intra-articular volume.
calcific tendinitis. Plain radiographs may demonstrate disuse osteopenia, and depending on the stage in which the imaging is obtained, MRI may show a thickened capsule with loss of overall intra-articular volume.
Treatment
Treatment of adhesive capsulitis is individualized. Underlying risk factors should be addressed, such as optimizing glucose control or thyroid balance. Patients are treated with oral nonsteroidal anti-inflammatory drugs (NSAIDs), activity modifications, and PT aimed at preserving and restoring ROM while avoiding pain. Intra-articular corticosteroid injection can be a useful adjunct if patients are diagnosed within 3 months of symptom onset. The therapeutic effects of corticosteroids are lessened in chronic cases. Injections can be both diagnostic and therapeutic in stage 1. If a patient regains full active shoulder motion following intra-articular injection of local anesthetic, the diagnosis of early stage adhesive capsulitis is confirmed.
Surgical Procedure: Arthroscopic Capsular Release with Manipulation under Anesthesia
Indications
As mentioned earlier, the natural history of adhesive capsulitis involves a prolonged course of pain followed by progressive stiffness for up to 2 years, which eventually resolves in the vast majority of cases. Many patients are dependent on their shoulder ROM for their livelihood; thus, if no progress is being made after 6 months of conservative treatment, more aggressive intervention may be considered.
Contraindications
Patients who are deemed too high risk for surgery for medical reasons are counseled to continue PT until their stiffness improves, rather than attempt to accelerate their course by undergoing capsular release. Many arthroscopic shoulder surgeries are performed in a “beach chair” position, which
involves sitting relatively upright. This positioning, combined with general anesthesia, can result in intraoperative hypotension that is dangerous for patients with heart disease, hypertension, a history of stroke, and so on. If a patient is cleared for surgery from a medical standpoint, however, the procedure is generally straightforward.
involves sitting relatively upright. This positioning, combined with general anesthesia, can result in intraoperative hypotension that is dangerous for patients with heart disease, hypertension, a history of stroke, and so on. If a patient is cleared for surgery from a medical standpoint, however, the procedure is generally straightforward.
Procedure
Closed manipulation under anesthesia can result in improvements in ROM, but risks involved in exertion of significant force against relatively thickened and rigid tissues include fracture, dislocation, rotator cuff or labral tears, or possible neurovascular injury. As a result, the surgeon may recommend arthroscopic capsular release prior to manipulation. Arthroscopy allows synovectomy to be performed, and any coexisting shoulder pathology can be documented and treated. After direct arthroscopic capsular release, a controlled manipulation is carried out, allowing predictable improvement in ROM while minimizing the risk of bone or soft-tissue injury.
Arthroscopic capsular release is accomplished in a stepwise fashion. Preoperative ROM and stability under anesthesia are carefully documented prior to introducing the arthroscope into the glenohumeral joint. Given the thickness of the joint capsule, a blunt trocar is essential to avoid injury to articular structures as the capsule is penetrated. Distension of the joint with an intra-articular injection may aid insertion of the arthroscope into the joint. The global capsular volume loss is documented on diagnostic arthroscopy, and the capsule is released in a systematic fashion. It is important for the arthroscopic capsular release to be carried out expediently, under low fluid distension pressures when possible, since fluid will quickly extravasate from the joint after the capsule is incised. The rotator interval is released first, typically using an intra-articular cautery device. Once the rotator interval has been addressed, the instruments are removed from the joint, and ROM and joint stability are assessed again. If the ROM has not normalized, the anterior capsule is released next: the plane between the subscapularis and the middle glenohumeral ligament (MGHL) is developed in order to protect the subscapularis tendon while releasing the MGHL. The anterior portion of the inferior glenohumeral ligament (IGHL) is also released (Figure 4.2). Again, the instruments are removed and the ROM and stability are evaluated. In some cases, the stiffness is sufficiently profound as to require release of the inferior glenohumeral capsule. This anatomic location is perilous due to the proximity of the axillary nerve. As a result, care is taken to release the inferior capsule, and consideration is given to keeping the inferior capsule intact to be released with the manipulation. The arthroscope is switched to an anterior viewing position to allow the posteroinferior capsule to be released. Once the capsule is completely released, the shoulder is manipulated to release any remaining capsular scaring and assess the shoulder ROM.
Once the glenohumeral portion of the procedure is complete, some surgeons will also perform a subacromial bursectomy in order to completely release any remaining adhesions, and treat any symptoms of impingement that may arise as patients work to improve their ROM. A final assessment of ROM and stability is performed and documented. When the bursectomy is complete, the subacromial space may be injected with corticosteroid. The glenohumeral joint is generally not injected in the perioperative setting, because the capsular releases will allow extravasation of the corticosteroid into the surrounding tissues. Some surgeons elect to treat patients with systemic steroids to prevent recurrence of synovitis and subsequent adhesive capsulitis.
Figure 4.2 Arthroscopic anterior capsule release of the left shoulder using an electrocautery device, as viewed from a standard posterior viewing portal. GL = glenoid labrum, HH = humeral head. |
Interscalene regional anesthesia may be used as a perioperative adjunct for assistance with intraoperative pain control. In addition, an indwelling interscalene catheter can be used to administer long-acting anesthetic to help the patient regain ROM before early postoperative pain might become prohibitive.
Postoperative Rehabilitation
Patients are referred immediately to PT, in order to maintain the ROM that was obtained intraoperatively. Focused rehabilitation after capsular release is essential to restore function and achieve patient goals. As this surgical procedure is indicated and performed on patients who have failed conservative measures, it is important to consider that a patient may be frustrated with the process and the prospect of more PT. Patient education on the importance of regaining ROM in a timely manner is critical to the success of this procedure.