Treatment of Fourth and Fifth Carpometacarpal Fracture-Dislocations in Punching Injuries With Motion-Sparing Hamate Fixation Spring Plates: "Rabbit Ears" Plating.

Punching injuries to the hand are frequent and can result in fourth and fifth carpometacarpal (CMC) fracture-dislocations. Fourth and fifth CMC fracture-dislocations are unstable, and dorsal metacarpal dislocations are most common. Operative management for maintaining reduction of the unstable fracture-dislocation was closed reduction and percutaneous pinning; however, in delayed fractures, open reduction is necessary. We report on a plating technique used for acute and delayed, unstable fourth and/or fifth CMC fracture-dislocations. This method of plating is novel and allows for physiological motion at the CMC joint through a dorsal buttressing mechanism while maintaining joint reduction. The range of motion begins within the first week postoperatively, and full composite fist formation and digital extension occur 4 to 6 weeks postoperatively. This novel technique affords an alternative effective surgical treatment option with excellent outcomes for patients presenting with fourth and fifth CMC fracture-dislocations up to 12 weeks following the injury.

Open anterior-inferior hip dislocation.

Traumatic hip dislocations result from high-energy trauma. These dislocations are usually posterior in direction and have severe associated injuries. The less common anterior dislocation is usually of the inferior type. We report a case of an open anterior-inferior hip dislocation secondary to a high-speed motor vehicle collision. The wound was in the medial upper ipsilateral thigh. To our knowledge, this is the first reported case of an adult with an open inferior-type anterior hip dislocation.

Carpal tunnel syndrome in children.

CTS is uncommon in children. A number of conditions predispose children to developing CTS. These conditions include the lysosomal storage diseases, a multigenerational history of CTS, and macrodactyly. Because many case are idiopathic, isolated cases are possible even in the normal child or adolescent. Children with CTS often have modest complaints in spite of long-standing difficulties such as decreased manual dexterity in one hand or poorly localized pain. Physical findings tend to be dramatic abnormalities such as severe thenar weakness and atrophy. These findings suggest that many children are diagnosed late in the course of their nerve compression. Because some patients have profound atrophy at a young age, the condition can be confused with primary thenar hypoplasia. Provocative tests, the Tinel and Phalen tests, are often normal in children with long-standing nerve compression. Electrodiagnostic studies are essential to establishing the diagnosis in many children. Pediatric cases of CTS tend to demonstrate bilateral electrophysiologic abnormalities, even if only one hand is primarily involved clinically. Therefore, it is recommended that EMG and NCS be performed bilaterally in all suspected children. Sedation may be helpful in obtaining electrodiagnostic studies in a small child. Open operative release is the only treatment documented to be effective in the treatment of childhood CTS.

Biologic behavior of an in vitro hydrated collagen gel-human tenocyte tendon model.

An in vitro human tenocyte-collagen gel model was developed to study tenocyte-mediated Type I collagen fibril reorganization, proliferation, and Type I collagen gene expression. Human tenocytes, obtained from extrasynovial forearm flexor tendons from children 5 to 10 years of age were cultured on plastic or in a cylinder of hydrated Type I collagen gel. Collagen solution was seeded with human tenocytes at 5 x 10(5) cells/mL and gelled in cylinder molds; gel cylinders without human tenocytes served as controls. Gel cylinders were pinned to troughs to create noncompliance. The gel cylinders were analyzed for collagen birefringence and cell shape at 7 and 21 days and for proliferation and gene expression for Type I collagen at 7 days. Under conditions of noncompliance, human tenocytes reoriented Type I collagen into longitudinal bundles resembling the parallel organization of collagen in native tendons. Tenocyte shape became fusiform between the collagen bundles which mimics the morphologic features of a tenocyte in vivo. The structural changes in the tenocytes and matrix are accompanied by downregulation of human tenocyte proliferation and Type I collagen gene expression. When released from the gel cylinder and grown again on plastic, human tenocytes resume proliferation and Type I collagen gene expression. The human tenocytes in this in vitro gel cylinder model system control fibril reorganization and proliferation, resembling their behavior during the development and repair of native tendons.