Flexor Tenolysis Workup
- Author: Cato T Laurencin, MD, PhD; Chief Editor: Harris Gellman, MD more...
No specific laboratory tests are indicated.
The major utility of imaging studies prior to flexor tenolysis is to evaluate whether the patient has a failure of tendon reconstruction, elongated callus, or tendon adhesions that lead to the clinical presentation.
Initially, radiographs should be taken to ensure proper anatomical alignment of the skeletal elements. Ultrasound has proven effective to assess both the presence and location of a ruptured tendon repair.[12, 13] Additionally, the mechanism of ultrasound allows dynamic assessment of flexor tendon injuries, and thus ultrasound is recommended for evaluation of zone 1 (DIP joint) tendon injuries. Ultrasound, however, is not effective in discerning pure adherence from elongated callus, and thus the type of surgical intervention required. Additionally, ultrasound of the ligaments in zone 2 (MCP and PIP joints) are a difficult endeavor and strongly operator dependent.
MRI has proven to be effective as a noninvasive imaging procedure to differentiate between tendon rupture and tendon adhesions in zone 2. Imaging artifacts from implanted devices, including metal plates or screws, can limit the effectiveness of MRI in evaluating tendon injuries.
In a rabbit model of tendon repair, once a tendon is injured, within 24 hours a noticeable increase in cellularity, predominantly from neutrophils, is seen. In the same model, cells in the tendon sheath are seen to migrate into the tendon, and cells from the periphery of the tendon are seen to migrate to the interior of the tendon core within 7 days. By 7 days, alpha smooth muscle actin expression is high, which marks the presence of myofibroblasts and pericytes in the wound area. From 7 to 21 days, cells are both depositing and remodeling collagen bundles, which correlate with a peak in heat shock protein 47 around day 21. As intrinsic healing of affected tendons progresses, alignment of collagen fibers along the axis of contraction, as well as a decrease in inflammatory cellularity, is usually seen, with a peak in apoptosis around 84 days in rabbits.[4, 11]
In human subjects, studies that closely track cell origin and type are lacking, but when looking at histological sections of adhesions, noninflammatory cells resemble myofibroblasts and secrete types I and III collagen, and epitenon cells are also involved in the process of both collagen production and collagen debris clearance.
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