Adhesive Capsulitis (Frozen Shoulder)

Descriptive text is not available for this image BASICS

DESCRIPTION

  • Adhesive capsulitis (AC) or frozen shoulder:
    • Presents as progressive painful restriction in range of movement of the glenohumeral (GH) joint
    • Course usually involves diminishment of pain but can have residual pain and limits of active and passive range of motion (ROM).
  • Subtypes:
    • Primary AC:
      • Idiopathic
      • Usually associated with diabetes mellitus (DM)
      • Typically resolves in 9 to 24 months
    • Secondary AC:
      • Typically due to prolonged immobilization
      • Most commonly due to a complication of rotator cuff impingement syndrome (rotator cuff tendonitis) that remains incompletely treated
      • Sometimes called “shoulder-hand-syndrome,” which is a complex regional pain syndrome (CRPS) or reflex sympathetic dystrophy (RSD), if it is characterized by shoulder pain, diffuse swelling, and decreased ROM
  • Clinical course:
    • Phase 1 (2 to 9 months): painful phase; pain is constant; diagnosis may be difficult if restricted movement is not present in early disease.
    • Phase 2 (4 to 12 months): stiffening or freezing phase; movement becomes restricted, especially with external rotation.
    • Phase 3 (12 to 42 months): resolution or thawing phase; gradual return to normal shoulder mobility

EPIDEMIOLOGY

Incidence

  • 2.4/1,000 people per year
  • Female: male ratio (1.4:1)

Prevalence

2–5% in the general population, 10–20% among DM (1)

ETIOLOGY AND PATHOPHYSIOLOGY

Underlying fundamental processes:

  • Idiopathic
  • Inflammation: Mast cells, T cells, B cells, and macrophages have been identified histologically, suggesting an inflammatory process. Studies confirm presence of elevated inflammatory cytokines such as IL-1, IL-6, TNF-α, COX-1, and COX-2 (1).
  • Elevated markers for neoangiogenesis (CD34) and neoinnervation (GAP43, PGP9.5, NGFR/p75 NTR) have been associated with AC which helps explain the acute painful phase. Additionally, one study showed that over expression of TGF-β led to the development of AC in rats (1).
  • Scarring: Fibroblasts and myofibroblasts have been identified histologically. Capsular contracture reduces the joint volume to 3 to 4 mL compared to the normal 10 to 15 mL. Intracellular adhesion molecule-1 (ICAM-1) facilitates leukocyte endothelial transmigration. It is elevated in both AC and DM.
  • This scarring primarily effects the rotator interval (coracohumeral ligament [CHL], biceps tendon, and GH capsule). A contracted CHL is an essential finding in AC (1).
  • Contracture of the GH capsule from loss of synovial layer, capsular adhesions, and loss of capsular volume are seen in AC.

RISK FACTORS

  • Shoulder immobilization; often due to impingement syndrome (most significant risk factor)
  • Increasing age
  • Female gender
  • DM
  • Thyroid disease
  • Atherosclerotic cardiovascular disease (ASCVD): cerebrovascular accident (CVA)/myocardial infarction (MI)/hyperlipidemia
  • Antiretroviral medication use
  • Parkinson disease
  • Trauma/surgery
  • Prior history of AC in contralateral shoulder

GENERAL PREVENTION

  • Active lifestyle, while avoiding shoulder injury
  • Control of DM, atherosclerotic disease, thyroid, and autoimmune conditions

COMMONLY ASSOCIATED CONDITIONS

DM, autoimmune disorders, Parkinson disease, highly active antiretroviral therapy (HAART) use, CVA/MI, cervical disc disease, thyroid disorders

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