Abstract
Sir:FigureAlthough the appearance of peripheral nerves related to lipofibromatosis (hamartoma) and intraneural or extraneural lipoma has been documented, the appearance of peripheral nerves at known sites of anatomical compression in the lower extremity, in people with diabetes,1 has not been reported previously. It is the purpose of this communication to document the appearance of nerves in patients with diabetes compared with patients without diabetes at the fibular tunnel and in the tarsal tunnel. A nonquantitative case-control approach to analysis of this problem was undertaken using intraoperative photographs previously taken of peripheral nerves in patients of the senior author (A.L.D.) with neurolysis for chronic compression related to either an underlying susceptibility to compression, as in diabetes, or a posttraumatic cause, such as ankle stretch/traction or fracture/dislocation injury. Sites chosen for this documentation were the common peroneal nerve at the fibular tunnel and tibial nerve in the tarsal tunnel. The only selection used in choosing these photographs was related to matching the left and right sides and cropping to show the nerves in a similar view and magnification. No change of the lighting or brightness of any of the original photographs was done. Five matched pairs of patients/nerves are included. From the figures, it can be seen that the peroneal nerve at the fibular tunnel (Fig. 1) and the tibial nerve in the tarsal tunnel (Figs. 2 and 3) are more yellow and larger in the patient with diabetes than in the nondiabetic, posttraumatic patient.Fig. 1: (Above) The left common peroneal nerve, in a diabetic, is exposed just proximal to the fibular neck, demonstrating fatty infiltration that appears like a lipoma. (Below) The left common peroneal nerve, in a nondiabetic, with similar exposure to that in the image above is seen after the neurolysis. The normal white-appearing common peroneal nerve is noted proximally, and the flattened region of compression is noted adjacent to the peroneus muscle.Fig. 2: (Above) The tibial nerve in the right tarsal tunnel is shown in a patient with diabetes. The nerve is in the usual location and has not yet divided into its medial and lateral branches. The large size of the yellow tibial nerve is noted. (Below) The tibial nerve is shown in a view comparable to that in a nondiabetic. The whitish coloration of the nerve is noted.Fig. 3: The tibial nerve in the left tarsal tunnel is shown (above) in a diabetic and (below) in a nondiabetic. The difference in color and size between the two nerves is noted.It has been documented experimentally that the peripheral nerve in the diabetic is susceptible to nerve compression, with this having been demonstrated in experimental models of diabetes2–5 and observed in clinical practice.6 The actual appearance of the human diabetic peripheral nerve in anatomical areas known for being a site of chronic nerve compression has never been documented. The present communication clearly contrasts the white appearance of the normal common peroneal nerve at the fibular tunnel and the tibial nerve at the tarsal tunnel with the yellow, swollen appearance of the same nerves in the patient with diabetes. Once the swollen yellow appearance of the lower extremity peripheral nerve in the diabetic is appreciated, its susceptibility to chronic compression at a site of anatomical narrowing is, at least mechanically, understandable. Although the basis for the swelling is known to be related to increased aldose reductase activity, conversion of glucose to the hydrophilic sorbitol,7 the basis for the yellow coloring and the extent to which the yellow represents fat deposition within the connective tissue portions of the nerve or lipid deposition is unknown and is likely not to be known from patients having neurolysis of chronic compression because these nerves cannot be harvested for histologic evaluation. However, this study could be conducted on freshly amputated limbs in a future study. A. Lee Dellon, M.D., Ph.D. Eric H. Williams, M.D. Gedge D. Rosson, M.D. Department of Plastic Surgery, The Johns Hopkins University, Baltimore, Md.
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