Tension-band wiring of displaced stable olecranon fractures with Eyelet-pins in the elderly: A series of 17 cases.

BACKGROUND: Tension-band wiring (TBW) and plate fixation are commonly used to fix displaced olecranon fractures. However, the high incidence of complications in the elderly, such as wound breakdown, infection, and loss of reduction, remain a concern for orthopaedic surgeons. Furthermore, patients frequently suffer from removal of the hardware. Even so, the operation seems to be indicated for independent elderly patients to return to their former activities of daily living. HYPOTHESIS: TBW of displaced stable olecranon fractures with Eyelet-pins in the independent elderly reduce the incidence of complications and allow early elbow joint exercise to keep their former activities. PATIENTS AND METHODS: We operated on the displaced stable olecranon fractures of 17 independent patients aged ≥ 70 using TBW with two Eyelet-pins. Eyelet-pins have an eyelet at the trailing end to prevent pin migration by passing a soft wire through it. The patients were reviewed clinically and radiologically at 2, 6, 12, and 24 weeks, and clinically at 1 year after the surgery. RESULTS: All fractures were united within 12 weeks, and the anatomic reduction was maintained. Mean radiographic proximal migration of the Eyelet-pins was 0.4mm (0.1 ∼ 1.2mm). Mean active elbow flexion was 136° (115° ∼ 145°) and extension 6.2° (0° ∼ 30°). Two patients had mild local pain and pain on motion at the tip of the eyelet. No patient required removal of the hardware. Other complications, such as superficial or deep wound infections, and neurological symptoms or signs, were not seen. All patients were able to maintain their former activities of daily living. CONCLUSION: TBW with Eyelet-pins for displaced stable olecranon fractures is useful for independent elderly patients to reduce the incidence of complications and to maintain their former activities of daily living without removal of the hardware. LEVEL OF EVIDENCE: IV; single-centre retrospective study.

Unstable Osteochondritis Dissecans of the Glenoid Fixed with Autogenous Osteochondral Plugs in a College Baseball Player: A Case Report.

CASE: A 19-year-old college baseball outfielder presented with a 3-month history of right shoulder pain. Radiographs, computed tomography, and magnetic resonance imaging showed a large osteochondral defect at the posterosuperior aspect of the glenoid. Arthroscopic evaluation identified an unstable fragment that was partially attached. Fixation of the osteochondral fragment was achieved with autogenous osteochondral plugs through a posterior arthrotomy. At 8 months after surgery, the patient was able to return to his former competitive level of performance. CONCLUSION: Osteochondritis dissecans (OCD) rarely affects the glenoid. Fixation of a large glenoid OCD lesion with autogenous osteochondral plugs was a successful treatment in this patient.

Case report: meralgia paresthetica in a baseball pitcher.

We report a case of meralgia paresthetica occurring in an amateur baseball pitcher who experienced inguinal pain and dysesthesia in the anterolateral thigh during pitching practice. The lateral femoral cutaneous nerve was pushed up by the iliac muscle to the inguinal ligament at the sharp ridge of its fascia and ensheathed in the tendinous origin of the sartorius muscle. Neurolysis of the lateral femoral cutaneous nerve and partial dissection of the inguinal ligament and sartorius muscle promptly relieved the symptoms and the patient resumed pitching 1 month later. These anatomic variations of the lateral femoral cutaneous nerve in the inguinal region might render the nerve susceptible to compression and irritation, and repetitive contraction of inguinal muscles during throwing motion might induce and exacerbate the neuropathy of the lateral femoral cutaneous nerve.

Distribution of sodium channels during nerve elongation in rat peripheral nerve.

A number of studies have investigated electrophysiological and morphological changes of peripheral nerves during gradual elongation. There has been, however, no report on the distribution of sodium channels at Ranvier's nodes during peripheral nerve elongation. We investigated peripheral nerve injury after the gradual elongation of rat sciatic nerves. Indirect nerve elongation was induced by leg lengthening at a rate of 3 mm/day by 15 or 30 mm. At 7 days after the leg lengthening, the electrophysiological properties of sciatic nerves, the ultrastructures of the Ranvier's nodes and axons, and the distribution of voltage-dependent sodium channels were examined. In the control nerves, most sodium channels were localized at Ranvier's nodes in myelinated axons, providing the physiological basis of saltatory conduction. In the elongated nerves, both the amplitude and conduction velocity of compound nerve action potential decreased following leg lengthening. The elongated nerves also showed paranodal demyelination in Ranvier's nodes longer than those in the control group. In addition, the distribution of sodium channels became diffuse or disappeared at Ranvier's nodes of elongated nerves. The diffuse distribution and/or disappearance of sodium channels may underlie the electrophysiological changes in compound nerve action potential induced by nerve elongation.

Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve.

Leg lengthening procedure is used increasingly to treat leg length discrepancy and some forms of dwarfism. We investigated adaptation in rat sciatic nerve to the gradual nerve elongation that occurs with leg lengthening. Indirect nerve elongation was produced by leg lengthening by a total of 15, 30, 45, or 70 mm at a rate of 1 mm/day. One day after leg lengthening completion, transverse semithin sections of sciatic nerve were prepared and examined; a teased-fiber study also was performed. Elongation decreased axon diameter, but not significantly. In teased-fiber preparations, internodal length was increased by 93%, and the longest internode measured 3000 microm after leg lengthening by 70 mm. Slopes of fiber diameter-internodal length regression lines increased with increasing elongation. Paranodal demyelination caused by nerve elongation worsened as elongation increased, stimulating remyelination (i.e., intercalation of a segment). Only 0.8% of axons showed degeneration in the group with 70 mm of elongation. We concluded that adult rat sciatic nerve can adapt itself to leg lengthening procedure with even doubling internodal length.

Pre-degenerated nerve shows enhanced regeneration after incremental elongation in rats.

Following nerve degeneration, we investigated effects of linear elongation on subsequent nerve regeneration in a total of 92 Wistar rats (weight 380-430 g). The nerve was ligated at the midthigh and then elongated incrementally by a total of 15 mm by leg lengthening at a rate of 3 or 5 mm/day. Seven days after initiation of nerve elongation, the external fixator was removed and normal leg length was restored with internal fixation. Then a 10 mm nerve segment at the ligature site was excised, and the nerve was repaired with sutures (group D). At 2, 4, 6, and 8 weeks after nerve suturing, we examined transverse semi-thin nerve sections compared with group I (severed and repaired after leg lengthening without a nerve ligature) and control group (severed and repaired without leg lengthening). After lengthening at 3 mm/day, nerve regeneration in group D was enhanced at 4 weeks. After lengthening at 5 mm/day, nerve regeneration in group D also was enhanced at 6 and 8 weeks. Pre-degenerated nerve showed better regeneration after suturing than intact nerve. Elongation holds promise as an alternative to nerve grafting in treatment of nerve injury.

P0 mRNA expression increases during gradual nerve elongation in adult rats.

Leg lengthening with nerve elongation is a common clinical treatment. We investigated morphological and molecular changes in peripheral nerves associated with femoral lengthening using animal models. Sciatic nerves of 13 week old male Wistar rats (n = 35) were elongated indirectly by leg lengthening for 14 days at 1 mm/day. At 3, 7, 14, 21, and 35 days following initiation of elongation, sciatic nerves on the elongated side and contralateral (control) side were excised at the midpoint of the femur. Internodal length was increased by 17%. Light and electron microscopic observation of transverse sections at 14 days showed elongated nerves appearing similar to control nerves with no degenerating axons and normal myelin thickness. We next examined changes of mRNA expression of a major myelin glycoprotein, P0, in elongated nerves using a quantitative reverse transcription-polymerase chain reaction and in situ hybridization. P0 mRNA expression in elongated nerves was increased during the first 3 weeks, with expression reaching 160% of control nerve expression at 14 days. Results of in situ hybridization were confirmatory. We concluded that myelin synthesis occurred during gradual nerve elongation. In adulthood, Schwann cells retain ability to synthesize myelin in response to nerve stretching.

Effect of the rate of prestretching a peripheral nerve on regeneration potential after transection and repair.

We tested the influence of nerve stretch injury on nerve regeneration after cutting and suturing. An external fixator was used to lengthen the femur, and consequently the sciatic nerve, progressively, by 3 mm/day (5%/day: group I) or 5 mm/day (9%/day: group II). In both groups the total lengthening was 15 mm, corresponding to approximately 23%-28% elongation of the sciatic nerve. Seven days after initiating nerve lengthening, the external fixator was removed and the nerve was transected and sutured. At 2, 4, 6, or 8 weeks after this suturing, semithin sections were prepared from the sciatic and tibial nerves. Although regeneration of nerve fibers was observed beginning at 2 weeks in all groups, nerve regeneration showed a delay only in group II at 6 weeks, when group I showed nerve regeneration as good as in the unstretched control group. Differences in nerve regeneration after nerve lengthening at different rates were considered the result of mechanical nerve injury, nerve degeneration, ischemia, and fibrosis, all made worse with more rapid lengthening. Nerve lengthening at a more moderate rate (3 mm/day) did not appear to compromise regeneration.

Paranodal demyelination by gradual nerve stretch can be repaired by elongation of internodes.

Nerve elongation resulting from leg-lengthening surgery can be injurious. We investigated peripheral nerve injury and recovery after gradual elongation of the rat sciatic nerve by progressive stretching. Indirect nerve elongation was produced by leg lengthening by 15 mm, at a rate of 3 mm/day (group I) or 5 mm/day (group II). The elongated length was then maintained. At 0 weeks, representing the 7th day after starting leg lengthening, and at weeks 2, 4, and 6, transverse semithin sections of sciatic nerve were examined. At the same time a teased fiber study was performed. As a result of nerve elongation axon diameter was decreased, although it later recovered. Axon diameter recovered more slowly in group II than I. Myelin thickness did not change compared with controls. In the teased fiber study, internodal length was increased by about 10% after nerve elongation in each group. Almost all nerve fibers showed demyelination at 0 weeks; myelination recovered with time, more slowly in group II than I. More obvious demyelination, axonal degeneration, and remyelination were observed in group II. We conclude that mild demyelination was repaired by elongation of internodes, while more severe demyelination was repaired by intercalation of segments.