Search

This study determines the change in tension after an acute nerve lengthening, as would occur in peripheral nerve repair. Stress relaxation, a viscoelastic property, was studied with the use of 24 rabbit tibial nerves. The nerves were divided into three groups and were stretched 6%, 9%, or 12% beyond their original resting length. The mean 1-hour stress relaxations for the three groups were 48%, 34%, and 34%, respectively. Nerve stress relaxation was significantly greater at 6% strain than at 9% or 12% strain. These biomechanical findings have important clinical implications for nerve-stretch injury and for nerve repair.

Previous recommendations regarding the "safe" period of tourniquet hemostasis were based largely on studies of ischemia distal to the tourniquet. This study quantitatively analyzed skeletal muscle injury induced beneath and distal to a pneumatic tourniquet applied to the hindlimbs of rabbits for 1, 2, or 4 hours with a cuff inflation pressure of 125, 200, or 350 mm Hg. Technetium Tc 99m pyrophosphate incorporation after systemic injection (Tc 99 uptake) and correlative histology were used to evaluate tissue damage 2 days after tourniquet application. Compared with the contralateral control limbs, compression and ischemia induced statistically significant increases in Tc 99 uptake in the thigh and leg regions of all groups. Pyrophosphate incorporation was significantly greater in the thigh region than in the leg region after 2 hours of compression in the 200 and 350 mm Hg pressure groups and following 4 hours of compression in all pressure groups. Focal and regional fiber necrosis and degeneration were observed in thigh muscles after 2 hours of tourniquet compression. Two hours of continuous tourniquet application at clinically relevant cuff inflation pressures induced significant skeletal muscle necrosis beneath the tourniquet. Use of the lowest possible inflation pressure for a limited duration should minimize the degree of tissue injury caused by tourniquet application.

We describe the morphologic changes that follow division of the transverse carpal ligament in patients with carpal tunnel syndrome. Fifteen hands in 12 patients with carpal tunnel syndrome were studied with magnetic resonance imaging before operation and for 6 weeks after operation. Eight hands were studied at 8 months after operation. Carpal arch width, anterior displacement of the carpal canal contents, and carpal canal volume were measured by use of multiplanar reformation and three-dimensional reconstruction of magnetic resonance images. There was a 24.2 +/- 11.6% increase in carpal canal volume 6 weeks after carpal tunnel release (p less than 0.001). This difference persisted at 8-month follow-up. There was an anterior displacement of carpal canal contents 3.5 +/- 1.9 mm from its original position 6 weeks after operation (p less than 0.001). This palmar displacement persisted at the 8-month follow-up. There was no statistically significant increase in carpal arch width 8 months after carpal tunnel release. We believe that division of the transverse carpal ligament restores median nerve function by increasing the volume of the carpal canal. This volumetric increase results from an anterior displacement of the newly formed transverse carpal ligament and not from a widening of the bony carpal arch.

Compression applied to a peripheral nerve may easily interfere with intraneural blood flow. In the present experimental study, a vital microscopic technique was used to observe changes in intraneural microcirculation (intrafascicularly and extrafascicularly) when graded compression was applied to a rabbit's tibial nerve by a specially designed minicompression device. Interference with venular flow was observed already at a pressure of 20 to 30 mm Hg while arteriolar and intrafascicular capillary flow was impaired at about 40 to 50 mm Hg. At 60 to 80 mm Hg no blood flow could be observed in the nerve. Nerves observed 3 or 7 days after 2 hours of compression at 400 mm Hg showed no or very slow stagnant blood flow within the previously compressed segment. It is concluded that acute compression of nerve may cause persistent impairment of intraneural microcirculation due to mechanical injury to blood vessels.

Severed and subsequently sutured rabbit flexor tendons were kept free and isolated in the synovial cavity of the knee joint. In one series the tendon specimens were surrounded by a dialyzing membrane to avoid cell seeding from the synovial fluid. At different intervals of time over a period of 3 weeks, the tendons were studied morphologically with special reference to scanning electron microscopy. Adhesions were not observed and, with synovial fluid as the nutrient medium, the tendons showed an intrinsic ability to repair in the superficial layers, also bridging the suture gap. Moreover, cell seeding, mainly of macrophages, from the synovial fluid could be demonstrated on the very surface of the tendon. When this cell seeding was prevented, the fibroplasia in the superficial layer of the tendon did decrease slightly, but tendon cell morphology was that of active fibroblasts. The results support the concept that flexor tendons may show intrinsic fibroplasia when nourished by synovial fluid, while macrophages, mainly, of extrinsic origin, contribute to restoration of the tendon surface.