Der Unfallchirurg
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Magnetic resonance imaging (MRI) is routinely used for the diagnostic assessment of diseases of the shoulder joint. Depending on the clinical presentation native imaging, intravenous (IV) or intra-articular injection of contrast medium can be performed (MR arthrography). Advances in imaging technology nowadays enable early detection of characteristic changes in the clinical picture of frozen shoulder. ⋯ Furthermore, obliteration of the subcoracoidal fat pad can also be observed. The MRI examinations also show a hyperintensity in the T2-weighted imaging and a contrast enhancement of the joint capsule. The alterations can show a temporal correlation with the clinical symptoms of the patient.
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Shoulder stiffness is characterized by restriction of the active and passive movement of the glenohumeral joint. The stiffness is ultimately caused by fibrosis and the resulting contracture of the glenohumeral joint capsule and its ligaments; however, the term stiff shoulder is only a descriptive umbrella term that must be further defined as the course of the disease and the recommended treatment are decisively influenced by the cause of the shoulder stiffness. Primary shoulder stiffness, also known as idiopathic shoulder stiffness or "frozen shoulder", must be distinguished from various forms of secondary shoulder stiffness and often occurs in three stages, which can all last for several months to years: the initial "freezing phase", followed by a "frozen phase" and finally a "thawing phase". Although primary shoulder stiffness is a frequent pathological alteration with an prevalence of 2-5% in the general population, the exact etiology remains largely unknown; however, there is consensus throughout the literature that certain systemic pathologies, such as diabetes mellitus are associated with a higher incidence of primary shoulder stiffness.
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Apart from primary or idiopathic frozen shoulder, the secondary form of glenohumeral stiffness can also develop after trauma or surgery. The cause for these secondary forms of restricted range of motion can be distinguished into intra-articular and extra-articular factors. Posttraumatic stiffness can develop after minor or major trauma to the bony or soft tissues of the shoulder girdle. ⋯ Stiffness after shoulder arthroplasty is rare and should prompt further diagnostic work-up to differentiate implant, surgery or patient-specific causes. Furthermore, an inflammatory shoulder stiffness similar to the primary or minor trauma form can develop after surgery. Reviewing the literature, shoulder stiffness has been reported most often after rotator cuff reconstruction surgery, followed by fracture fixation surgery, instability operations and lastly shoulder arthroplasty.
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Idiopathic shoulder stiffness (i.e. frozen shoulder, FS) is a common pathology of the glenohumeral joint characterized by a sudden onset of pain syndrome and progressive restriction of the range of motion. While the histological changes of FS are accompanied by synovial inflammation and increasing capsular fibrosis, the underlying cause of FS is still unknown. ⋯ As the disease is usually self-limiting and the symptoms resolve after 2-3 years, especially conservative treatment measures are often clinically applied; however, in this context there is still no scientifically based consensus on which treatment measures are most likely to contribute to symptom relief in which phase of the disease. For this reason, this article focuses on the description of the scientifically investigated conservative treatment methods in FS and their temporal classification into the classical three-phase course of the disease.
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The morbidity and mortality of polytrauma patients are substantially influenced by the extent of the posttraumatic inflammatory reaction. Studies have shown that TIMP‑1 and MMP‑9 play a major role in posttraumatic immune disorder in genome-wide mRNA microarray analyses. Furthermore, both showed differential gene expression profiles depending on the clinical parameters massive blood transfusion and traumatic brain injury. ⋯ Polytraumatized patients who received massive blood transfusions following major trauma showed significantly higher TIMP‑1 levels than patients who did not receive massive transfusions. This seems to be an expression of a massively excessive inflammatory reaction and therefore represents a substantial factor in the pathogenesis of severe posttraumatic immune dysfunction in this collective. Furthermore, the significant increase in MMP‑9 with accompanying traumatic brain injury reflects the pivotal role of matrix metalloproteinases in the pathophysiology of traumatic brain injury.