Commentary & Perspective on
"The Role of Flexor Tenosynovectomy in the Operative Treatment of Carpal Tunnel Syndrome"
By Charlotte Shum, MD et al.

Commentary & Perspective by
James W. Strickland, MD*, Carmel, IN

The authors have conducted an excellent review and discussion of the pathomechanics of carpal tunnel syndrome and evaluated the effects of flexor tenosnovectomy as an adjunct to open carpal tunnel decompression. Their correlation of the gross (visual) appearance and microscopic histology of the flexor tenosynovium with postoperative symptoms and function is of interest to surgeons who treat carpal tunnel syndrome. In particular, Shum et al. have questioned the role of the tenosynovium in this condition with their finding that there was no significant correlation between either the histological findings or gross intraoperative findings of the flexor tenosynovium and the preoperative or postoperative clinical presentation (symptom-severity scores and functional assessment scores).

Irrespective of the duration or severity of the symptoms, the pathophysiological mechanism of carpal tunnel syndrome is the same. In normal hands, the average interstitial pressure within the carpal tunnel is 2.5 mm Hg. With maximum pressure elevations, which occur with the wrist in extension or flexion, the mean pressures increase to approximately 30 mm Hg¹. In animals, intraneural blood flow is impeded at pressures of 20 to 30 mm Hg, but the vascular retardation is readily reversible so long as the elevated pressures are of short duration¹. Any increase in pressure within the tunnel results in distortion or ischemia of the median nerve. Obstruction of venous return in the epineural or perineural vascular plexuses appears to result in anoxia and endoneural edema of the median nerve². The magnitude of edema formation and subsequent blockage of nerve conduction is related to the amount and duration of the compression³, which can also lead to venous congestion, hyperemia and circulatory slowing⁴.

As the pressure becomes higher and/or more sustained, swelling of the nerve bundles can occur within the endoneurium because of an accumulation of exudates and edema. In addition, endoneural edema itself interferes with nerve function due to alterations in the local ionic environment of the axons⁵. There are also data indicating that increased carpal canal interstitial pressure has a direct mechanical effect on axonal transport. Experimental outcomes suggest that persistent compression at 20 mm Hg results in a reduction of orthograde fast axonal transport with reductions in orthograde slow axonal transport at 30 mm Hg⁶. The longer the pressure increases continue, the more likely that the disturbances in blood flow and axonal transport will lead to permanent changes. Destruction of the epineurium and endoneurium resulting in dense fibrous scar tissue may be the final result of prolonged compression⁷.

The question is, then, does the increased pressure within the carpal tunnel result from inflammation or fibrous thickening of the flexor tenosynovium? Recent publications such as those of Lluch⁸ challenge the long-held belief that pathology of the tenosynovium is the culprit and question whether thickening of the tenosynovium is a result of carpal tunnel syndrome rather than a cause of it. The findings of Shum et al. corroborated those of histological studies in which "nonspecific fibrous changes and edema" instead of inflammatory changes were usually noted in specimens of tenosynovium removed from patients with carpal tunnel syndrome. In the absence of any pathology of the transverse carpal ligament or abnormality in the size of the carpal tunnel itself, it remains likely that the increased pressure within the carpal tunnel results from increases in the volume of the canal's contents, and the flexor tenosynovium is still the prime suspect.

The most important clinical lesson of this report is to dispel the notion that routine flexor tenosynovectomy is of any value in the management of carpal tunnel syndrome. The authors have conclusively demonstrated what many clinicians already believed: After the enlargement of the carpal tunnel, which results from transection of the transverse carpal ligament, synovectomy is unnecessary. Although there was little difference noted between patients who were managed with open carpal tunnel release with or without flexor tenosynovectomy, there is a distinct possibility that adhesions of the flexor tendon would develop, with resultant limitations in digital flexion or extension in those treated with flexor tenosynovectomy.

*The author did not receive grants or outside funding in support of this research or preparation of this manuscript. He did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author is affiliated or associated.

References

1. Gelberman RH, Hergenroeder PT, Hargens AR, Lundborg GN, Akeson WH. The carpal tunnel syndrome: A study of carpal canal pressures. J Bone Joint Surg Am. 1981;63:380-3.
2. Eversmann WW Jr. Entrapment and compression neuropathies. In: Green DP, editor. Operative hand surgery. 3rd ed., vol. 2. New York: Churchill Livingstone; 1993. p 1341-85.
3. Hargens AR, Romine JS, Sipe JC, Evans KL, Mubarek SJ, Akeson WH. Peripheral nerve-conduction blockage by high muscle-compartment pressure. J Bone Joint Surg Am. 1979;61:192-200.
4. Lundborg G, Gelberman RH, Minteer-Convery M, Lee YF, Hargens AR. Median nerve compression in the carpal tunnel—functional response to experimentally induced controlled pressure. J Hand Surg [Am]. 1982;7:252-9.
5. Rydevik B, Lundborg G. Permeability of intraneural microvessels and perineurium following acute, graded experimental nerve compression. Scand J Plast Reconstr Surg. 1977;11:179-87.
6. Dahlin LB, McLean WG. Effects of graded experimental compression on slow and fast axonal transport in rabbit vagus nerve. J. Neurol Sci. 1986;72:19-30.
7. Sunderland S. The nerve lesion in the carpal tunnel syndrome. J Neurol Neurosurg Psychiatry. 1976;39:615-26.
8. Lluch AL. Thickening of the synovium of the digital flexor tendons: cause or consequence of the carpal tunnel syndrome? J Hand Surg [Br]. 1992;17:209-12.