Study protocol subacromial impingement syndrome: the identification of pathophysiologic mechanisms (SISTIM)

Abstract

Background: The subacromial impingement syndrome (SIS) is the most common diagnosed disorder of the shoulder in primary health care, but its aetiology is unclear. Conservative treatment regimes focus at reduction of subacromial inflammatory reactions or pathologic scapulohumeral motion patterns (intrinsic aetiology). Long-lasting symptoms are often treated with surgery, which is focused at enlarging the subacromial space by resection of the anterior part of the acromion (based on extrinsic aetiology). Despite that acromionplasty is in the top-10 of orthopaedic surgical procedures, there is no consensus on its indications and reported results are variable (successful in 48-90%). We hypothesize that the aetiology of SIS, i.e. an increase in subacromial pressure or decrease of subacromial space, is multi-factorial. SIS can be the consequence of pathologic scapulohumeral motion patterns leading to humerus cranialisation, anatomical variations of the scapula and the humerus (e.g. hooked acromion), a subacromial inflammatory reaction (e.g. due to overuse or micro-trauma), or adjoining pathology (e.g. osteoarthritis in the acromion-clavicular-joint with subacromial osteophytes).We believe patients should be treated according to their predominant etiological mechanism(s). Therefore, the objective of our study is to identify and discriminate etiological mechanisms occurring in SIS patients, in order to develop tailored diagnostic and therapeutic strategies.

Methods: In this cross-sectional descriptive study, applied clinical and experimental methods to identify intrinsic and extrinsic etiologic mechanisms comprise: MRI-arthrography (eligibility criteria, cuff status, 3D-segmented bony contours); 3D-motion tracking (scapulohumeral rhythm, arm range of motion, dynamic subacromial volume assessment by combining the 3D bony contours and 3D-kinematics); EMG (adductor co-activation) and dynamometry instrumented shoulder radiographs during arm tasks (force and muscle activation controlled acromiohumeral translation assessments); Clinical phenotyping (Constant Score, DASH, WORC, and SF-36 scores).

Discussion: By relating anatomic properties, kinematics and muscle dynamics to subacromial volume, we expect to identify one or more predominant pathophysiological mechanisms in every SIS patient. These differences in underlying mechanisms are a reflection of the variations in symptoms, clinical scores and outcomes reported in literature. More insight in these mechanisms is necessary in order to optimize future diagnostic and treatment strategies for patients with SIS symptoms.

Trial registration: Dutch Trial Registry (Nederlands Trial Register) NTR2283.

Figures

Figure 1

A. Schematic anatomy of a healthy glenohumeral joint and subacromial space. B. Schematic anatomy of a shoulder joint with the presence of several etiologic mechanisms for Subacromial Impingement Syndrome. In theory, impingement ("a disbalance between acromial space and the space needed for subacromial structures") can be caused by 1) A dynamically reduced subacromial space due to a pathologic pattern of arm-shoulder movements (e.g. scapular dyskinesia), resulting in relative cranialisation of the humerus with respect to the scapula/acromion, or 2) A more statically reduced subacromial space, due to 2a) structural anatomic variations (e.g. a hooked acromion), eventually in combination with altered arm-scapula motion patterns; 2b) A subacromial inflammatory reaction (e.g. caused by micro-trauma or overuse) causing subacromial oedema, fibrosis and tendinosis; 2c) Encroachment of subacromial tissues by an adjoining pathology or structures other than the acromion (e.g. acromioclavicular (AC)-joint osteoarthritis and subacromial osteophytes, calcifying tendinitis, and coracoid impingement).

Figure 2

Set-up for EMG-recorded isometric abduction and adduction force tasks. Subjects are positioned in front of the radiographic plate, in standing position with the concerning arm in external rotation at his/her side (i.e. hand in frontal plane), enabling the use of this set-up during concomitant acquirement of standard shoulder radiographs. The arm is attached to a 1-dimensional force transducer at the wrist, enabling subject specific force tasks, visual feedback, and equal task force magnitude for abduction and adduction tasks.

Figure 3

Experimental setup for isometric arm-shoulder force tasks in 24 directions. The subject has the arm in a splint, which is connected to a force transducer. Subjects must bring the arm force driven red cursor into the blue target area, which indicates force direction (n = 24 directions) and force magnitude. The exerted force, perpendicular to the humerus long axis, is recorded together with EMG to measure the activity of 10 individual shoulder muscles.

Figure 4

Schematic outline for relating outcome measures to pathophysiological mechanisms. We expect to identify one or more of the hypothesized etiological mechanisms in each SIS patient. These mechanisms might be related to the reported variations in SIS symptoms, course, and treatment outcome. (MRI = Magnetic Resonance Imaging, X-ray & EMG task = radiographs during EMG recorded abduction and adduction tasks for measurements of acromiohumeral distance, and FoB = 3D kinematics with Flock of Birds system).