Diabetic neuropathic arthropathy
- Lesley D Hordon, MD
Lesley D Hordon, MD
- Consultant in Rheumatology
- University of Leeds, United Kingdom
- Section Editors
- Simon M Helfgott, MD
Simon M Helfgott, MD
- Section Editor — General Rheumatology and Related Topics
- Associate Professor of Medicine
- Harvard Medical School
- David M Nathan, MD
David M Nathan, MD
- Editor-in-Chief — Endocrinology
- Section Editor — Diabetes Mellitus
- Professor of Medicine
- Harvard Medical School
In patients with diabetes mellitus, the loss of sensation to a joint may result in a chronic, progressive, and destructive arthropathy. The prototype of this disorder was described by Charcot in relation to tabes dorsalis. Similar changes are seen with other neurologic disorders, such as syringomyelia, although diabetes is the most common cause of neuropathic (Charcot) arthropathy in the western world. Diabetic neuropathic arthropathy is also called diabetic osteoarthropathy.
A variety of other musculoskeletal conditions have also been associated with diabetes mellitus, including specific arthropathies of the hand and shoulder, limited joint mobility, and spontaneous infarction of skeletal muscle.
Diabetic neuropathic arthropathy will be reviewed here. Other musculoskeletal conditions associated with diabetes, limited joint mobility in diabetes, and diabetic muscle infarction are described separately. (See "Musculoskeletal complications in diabetes mellitus" and "Diabetic muscle infarction" and "Limited joint mobility in diabetes mellitus".)
The pathogenesis of this condition remains uncertain; it is likely to be multifactorial, due to a combination of mechanical and vascular factors resulting from diabetic peripheral and autonomic neuropathy and metabolic abnormalities of bone (algorithm 1) [1-4].
It is thought that lack of proprioception secondary to peripheral neuropathy may result in ligamentous laxity, increased range of joint movement, instability, and damage by minor trauma, to which the relatively insensitive neuropathic foot is prone. In addition, the resulting change in the architecture of the foot causes a change in weightbearing and subsequent localized trauma. Finally, autonomic neuropathy may result in vasomotor changes and in the formation of arteriovenous shunts. These, in turn, result in reductions in effective skin and bone blood flow, despite the good and sometimes bounding foot pulses in these patients.
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- CLINICAL FEATURES
- History and physical findings
- Laboratory findings
- Clinical and radiographic staging
- Diagnostic features
- Initial diagnostic evaluation
- Further testing in selected patients
- Differential diagnosis
- - Infections
- - Noninfectious disorders
- Acute and subacute disease
- Joint disorganization and surgical correction
- SUMMARY AND RECOMMENDATIONS