adducting the thumb metacarpal and keeping it there produces a webspace contracture!
Digital amputations: try replanting all thumbs; single digits that have been amputated DISTAL to the FDS insertion, and multiple digit injuries. Avoid trying to replant an avulsed, degloving-type amputation.
An intrinsic plus contracture or deformity usually shows up as MCP flexion, and IP joint extension. Intrinsic minus contracture (clawing) shows up as MCP extension, IP joint flexion.
The oblique pulley is the most important structure supporting thumb flexion (akin to the A2 pulley of the finger)
Hook of hamate fractures are best seen on CT or carpal tunnel views.
When excising hook of hamate fractures, beware of the deep branch of the ulnar nerve.
The best tendon transfer for opponensplasty is probably FDS of 4, brought through a little pulley made in FCU. (in the relevance of a low median nerve palsy, where opposition is severely limited by abductor pollicis brevis paralysis). “The motor has adequate power, more than sufficient excursion, and requires only slight change of direction by a pulley.” In high median nerve palsy, where FDS is also involved, probably have to do an extensor indices transfer through the 3rd metacarpal interspace.
Swan neck deformity can occur as the result of a long-standing mallet deformity. The distal extensor mechanism is lengthened, and allows dorsal migration of the lateral bands at the PIP joint.
If you cut your finger 1 mm proximal to the distal flexion crease and are unable to demonstrate DIP motion, you’ve cut the FDP. However, if you are also unable to demonstrate flexion of PIP with the other fingers held in extension, then you probably have a congenital absence of FDS, because 1 mm proximal to the distal flexion crease is probably still quite a bit distal to the broad insertion of FDS. Even if you got some of the FDS insertion, it is pretty broad, encompassing much of the volar surface of the middle phalanx – you are unlikely to have cut the whole tendon at this level, so close to the distal flexion crease.
Wartenberg’s Syndrome is a painful neuroma of the superficial radial nerve. If bothersome enough, dissect out the ends, and bury them in muscle.
The collateral ligaments are directly attached to the volar plate at the PIP joint.
A contracture of the oblique retinacular ligament will cause an extension contracture of the DIP, thereby limiting DIP flexion (part of the pathophysiology of Boutonniere deformities.) The oblique retinacular ligament appears to lie volar to the axis of rotation of the PIP, but then curls dorsally to lie on dorsal to the axis of rotation of the DIP. When contracted (as in the Boutonniere deformity), it maintains the extension of the DIP. Because it lies volar to the axis of the PIP, it contributes to the flexion deformity of the PIP.
The tight structures in a chronic Boutonniere deformity are the oblique retinacular ligament and the transverse retinacular ligament. The oblique retinacular ligament maintains the DIP extension, while the transverse retinacular ligament keeps the lateral bands subluxed volarly and maintains the PIP flexion. The oblique retinacular ligament, being volar to the axis of the PIP, also contributes to maintaining the PIP in flexion. The triangular ligament is attenuated because the lateral bands are pulled volarly.
If the intrinsics are paralyzed, the long extensors are best able to extend the IP joints with the MCPs in flexion. If they are not held in flexion, the long extensors tend to hyperextend the MCPs and lose there extension force on the proximal phalanges.
During the open volar approach to a complex MCP dislocation, the neurovascular bundle is most at risk.
Complex MCP dislocations are associated with skin dimpling, parallelism between the metacarpal and proximal phalanx, and a sesamoid within a widened joint space.
During the complex dislocation, the metacarpal head ruptures between the lumbrical radially and the flexor tendons ulnarly. These two