Frostbite and Diabetic Neuropathy

A. Lee Dellon, MD


Wounds. 2003;15(12) 

In This Article

Patient Management

The patient in this case was initially treated with antiprostaglandins, antibiotics, and bed rest for 48 hours. Gangrene did not occur. He was then taken to surgery where his wound was debrided and decompression of the peroneal nerve at the knee, the dorsum of the foot, and the tibial nerve in the four medial ankle tunnels was performed. Three months after surgery, the patient had recovered sensibility to his foot. By one year after surgery, he had recovered normal two-point discrimination in this right foot.

The patient was lost to follow up for six years; however, seven years after the frostbite episode, the patient returned for evaluation of his opposite foot. His left big toe had been amputated after it ulcerated, and now osteomyelitis was present in his second metatarsal head (Figure 1). He had excellent pulses in the left foot, and neurosensory testing confirmed excellent sensibility in his right foot. There was, however, severe axonal loss in his left foot. His left foot had positive Tinel signs over the known sites of anatomic narrowing, as his right foot had demonstrated seven years earlier. After several debridements of his left foot in the operating room, he underwent neurolysis of the same three nerves in the left foot to which he had neurolysis performed in his right foot. The wound on his left foot closed over the next four weeks with appropriate wound care. At six months after this surgery, repeat neurosensory testing documented neural regeneration occurring in the left peroneal and tibial nerves.

Shown here are both feet seven years after original treatment of frostbite in the right foot, decompression of the peroneal nerve at the knee and dorsum of foot, and neurolysis of the tibial nerve in the tarsal tunnel. Note preservation of tissue in the right foot. In contrast, the left foot, subjected to the same glycemic control as the right foot, has not had surgical decompression and now has amputation of two toes and osteomyelitis of the second metatarsal head.

In this patient, appropriate emergency treatment of frostbite in one foot prevented soft tissue loss, while decompression of the peroneal and tibial nerves in that same leg restored sufficient sensibility to prevent ulceration or amputation over the next decade. In contrast, the contralateral leg, which did not have nerve decompression, had progressive neuropathy, resulting in ulceration, osteomyelitis, hospitalization for infection, and ultimately the loss of two toes. The presence of a positive Tinel sign in this contralateral foot suggested, however, that there was still optimism to restore sensibility by decompression of peripheral nerves at known sites of entrapment. This was done after treatment of the foot wound, resulting in improvement in sensibility and three years of soft-tissue preservation.

Finally, three years later, the patient presented with an ulceration that had progessed to dry gangrene of his right ring finger, which has resulted from frostbite after shoveling snow (Figure 2). In the absence of infection, the first approach to the hand was to decompress the carpal tunnel and transpose the ulnar nerve at the elbow to restore sensibility to the hand. One month later, this late stage of frostbite was treated with debridement of the eschar and reconstruction of the ring finger to preserve length with a thenar flap.

Ten years after the patient first presented with frostbite of his right foot, he developed frostbite in the right ring finger. At three months following the frostbite injury, dry gangrene is present.


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