The pain associated with SIS is caused by compression of the rotator cuff and subacromial bursa against the acromion.
2,12 The subacromial space is reduced when the arm is raised (ie, abducted and externally or internally rotated), impinging the subacromial structures (rotator cuff, long head of the biceps, and bursa), which explains the association of SIS with repetitive overhead activities, such as throwing.
13
Patients with SIS experience pain and disability, which are the primary clinical features that treatment seeks to address. Exhaustive but conservative management is the initial approach to treatment before proceeding to surgical intervention.
2,13 Nonoperative treatment typically consists of NSAIDs and physical therapy, aimed at increasing range of motion (ROM) and strengthening the rotator cuff.
14-16 This approach has been shown to produce a “satisfactory response” among approximately two-thirds of patients.
14 A retrospective study
14 of 616 patients with SIS assessed 3-week indomethacin therapy followed by 6 weeks of physical therapy; after their shoulders became pain free, patients continued home exercise for 4 weeks. Sixty-seven percent of patients had a satisfactory result, and 28% had no improvement and went on to have subacromial decompression.
14 If pain persists despite use of NSAIDs, a therapeutic subacromial injection of lidocaine and a corticosteroid may address pain and allow the patient to continue a home-based physical therapy program.
14-16 Cummins et al
17 reported the results of 100 SIS patients treated with a nonsurgical treatment protocol consisting of subacromial cortisone injection and physical therapy, with 79% of patients not requiring surgery after a 2-year follow-up. Kuhn
18 reviewed 11 randomized controlled trials of exercise and SIS and found that, although exercise had both clinically and statistically significant effects in decreasing pain and improving function, it was ineffective at improving ROM or strength. To my knowledge, no direct comparisons of SIS treatments have been reported; an ongoing study by Rhon et al,
19 however, is comparing outcomes in pain and disability between patients with SIS who are receiving either manual physical therapy or subacromial corticosteroid injection.
Osteopathic physicians use a variety of methods to manage dysfunctions of the shoulder joint, such as the Spencer technique,
20 developed in 1916, and the Jones technique.
21 Whereas both are used for a variety of shoulder complaints, to my knowledge neither has been systematically studied for use in patients with SIS.
It has been suggested that SIS is optimally managed by eliminating pain first—before restoring shoulder joint stability and movement patterns, increasing ROM, or enhancing strength.
22 Progressive resistance training for the rotator cuff muscles has been shown to effectively reduce pain, as well as to improve function and quality of life in patients with chronic shoulder complaints, including SIS.
5,23 Pain relief observed in 1 study
23 was attributed, in part, to the strengthening and resulting stabilization of the shoulder joint. Because effective strengthening of the rotator cuff muscles can initially aggravate symptoms and because pain relief as a consequence of strengthening typically has a slow onset, there is a need to immediately and directly address pain caused by SIS.
Substantial evidence supports the premise that pain should be addressed early in the management of chronic shoulder conditions. Fear that emerges in response to musculoskeletal pain may contribute to the development of chronic pain and disability.
24-26 The “fear-avoidance” model of musculoskeletal pain links pain-related fear with the development of chronic pain and long-term disability, where pain is catastrophically misinterpreted by the patient, therefore giving rise to fear of pain, fear of movement, hypervigilance to body sensations, avoidance, and disuse.
27 This behavior then perpetuates a cycle that results in disability, which lowers the patient's threshold for pain and activity tolerance, and thus reinforces the cycle.
28
The heated lidocaine-tetracaine patch can begin to break the fear-avoidance pattern. The controlled heat of the lidocaine-tetracaine patch enhances the delivery of the respective agents. It was approved by the US Food and Drug Administration in June 2005 “for use on intact skin to provide local dermal analgesia for superficial venous access and superficial dermatological procedures.”
29 In my practice, the heated lidocaine-tetracaine patch has demonstrated excellent pain relief, convenient self-administration, and lack of cognitive impairment because of the little meaningful systemic exposure. The most common adverse events reported in clinical studies were erythema, blanching, and edema during or immediately after treatment in the area where the heated lidocaine-tetracaine patch was applied.
29 Localized reactions were generally mild, and no treatment-related serious adverse events have occurred in clinical studies.
29 Results of a randomized, double-blind, crossover study
30 of healthy adults showed that the heated lidocaine-tetracaine patch provided greater depth and duration of topical anesthesia (based on pain and sensory depth evaluations and sensory and thermal stimuli testing) when compared with a placebo patch.
The understanding of how medications are absorbed transdermally has evolved considerably. Whereas topical treatments tend to exert effects primarily in subcutaneous tissues, researchers have at times observed a deeper saturation. Preclinical and small pharmacokinetic studies have shown that pharmacologically active agents that have been compounded with carriers and made into topical gels, liquids, or patches can extend into a joint space after topical application.
31-35 For example, a study of 27 patients
31 compared semitendinosus muscle/tendon concentrations between ketoprofen topical 20 mg patch absorption at intervals up to 20 hours prior to anterior cruciate ligament reconstruction and oral 150 mg ketoprofen capsule administration 14 hours prior to reconstruction. One hour after topical application, ketoprofen was detected in the semitendinosus muscle and tendon and gradually increased to a peak concentration at 6 hours after application.
31 There was no statistically significant difference in tissue concentration between oral and topical groups 14 hours after administration or application.
31 The amount of medication present in the tissues varies as a result of factors such as the characteristics of the medication, vehicle, tissue being penetrated, and application time. I propose that once within the joint, the mechanism of action of the drug is the same as it would be if the drug was delivered via injection. For the 2 cases presented, the prolonged effect of the treatment with the heated lidocaine-tetracaine patch was an unanticipated response. Clearly, something other than anesthetic effect took place, and further study is warranted.