Department Editor: Tania J. Phillips, MD, FRCPC

Overall Learning Objective: The physician or podiatrist participant will develop a rational approach to the evaluation and treatment of a variety of uncommon wounds and will have an increased awareness of the differential diagnosis of cutaneous wounds and the systemic diseases associated with these wounds.

Submissions: To submit a case for consideration in Diagnostic Dilemmas, e-mail or write to: Executive Editor, WOUNDS, 83 General Warren Blvd., Suite 100, Malvern, PA 19355, eklumpp@hmpcommunications.com

Completion Time: The estimated time to completion for this
activity is 1 hour.

Target Audience: This CME/CPME activity is intended for dermatologists, surgeons, podiatrists, internists, and other physicians who treat wounds.

At the conclusion of this activity, the participant should be able to:
1. Describe and discuss the relationship between neuropathy and painful insensitive feet
2. Describe and discuss the superimposed nerve compressions that can occur in the patient with neuropathy in the lower extremity
3. Describe the relationship and roles of electrodiagnostic testing and neurosensory testing in documenting the presence of neuropathy
4. Describe how to identify the neuropathic patient with a good prognosis to recover sensation and relieve pain by surgical decompression of a nerve.

Disclosure: All faculty participating in Continuing Medical Education programs sponsored by HMP Communications, LLC, are expected to disclose to the program audience any real or apparent conflict(s) of interest related to the content of their presentation. Dr. Dellon discloses he has no conflicts of interest relevant to the content of this article.

Accreditation: HMP Communications, LLC, is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. HMP Communications, LLC, is approved by the Council on Podiatric Medical Education as a sponsor of continuing education in podiatric medicine.

Designation: HMP Communications, LLC designates this continuing medical education activity for a maximum of 1 credit hour in category 1 credit toward the AMA Physician’s Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity. HMP Communications designates this continuing medical activity for .1 CEUs available to participating podiatrists.

Method of Participation: Read the article, take, submit, and pass post-test by December 10, 2004.

This activity has been planned and produced in accordance with the ACCME Essential Areas and Policies.

Release date: 12/10/03
Expiration date: 12/10/04

Presentation

A 65-year-old African American man with diabetes presented by ambulance to the emergency room in February of 1993 for the treatment of frostbite to the toes of his right foot. He had been requiring insulin for 15 years. The frostbite occurred while the patient was outdoors shoveling snow. He could not feel either of his feet at the time of presentation. The physical examination demonstrated a superficial degree of frostbite, excellent posterior tibial and dorsalis pedis pulses, and positive Tinel signs over the tibial nerve in the tarsal tunnel, the deep peroneal nerve at the dorsum of the foot, and a tender common peroneal nerve at the fibular neck.

Diagnosis

The patient was diagnosed with diabetic neuropathy complicated by frostbite.

Discussion

Diabetic neuropathy. In the patient with diabetes, the diagnosis of symptoms of pain in the feet must first differentiate a vascular from a neurologic etiology. A history of symptoms with walking or a worsening of symptoms can occur in both etiologies, but coldness in the feet and aching in the calves are more suggestive of large vessel disease. There is a false negative rate approaching 40 percent, assuming a palpable pulse implies good tissue perfusion.[1] If the physical examination suggests poor blood flow, segmental arterial pressures and imaging of the vessels are required. Symptoms of burning pain alone may suggest the rare small fiber neuropathy of diabetes, which can be identified by demonstrating abnormal thermal threshold or abnormal sudomotor function. With small fiber neuropathy, the results of electrodiagnostic testing and measurement of cutaneous vibratory and pressure thresholds are normal. Biopsy of the skin will show reduction of intra-epithelial nerve fibers.[2] The most common source of pain in the feet of diabetic patients is the symmetrical distal polyneuropathy. This is a distal axonopathy and can be identified with electrodiagnostic testing, which demonstrates axonal loss as a decrease in amplitude and later a decrease in conduction velocity and distal latency as demyelination occurs. If there are associated complaints of back pain or pain that radiates down the leg to the feet, electromyography is indicated to evaluate a radiculopathy. However, in the most common situation, the patient will complain of pain with associated numbness or tingling paresthesia that indicates there is a large fiber component to the neuropathy.[3] The pattern of the pain and numbness is that of a stocking with both the top and bottom of the foot being symptomatic and the area of symptoms slowly progressing proximally above the ankle. The clinical examination will show decreased perception of vibratory stimulus, using either a tuning fork or a vibrometer, and decreased perception of pressure, using either a nylon monofilament or the pressure-specified sensory device.[4,5] Axonal loss in the sensory system is manifested by a decrease in the ability to discriminate one from two static touch points. The earliest finding is an increase in the pressure threshold required to discriminate one from two static points.[6] Using this information the degree of neuropathy can be staged and the progression of the neuropathy documented.[7]

In diabetes, the peripheral nerve is susceptible to chronic compression. The pathophysiology that causes the nerve to be susceptible is due to the following: 1) the increased endoneurial water content of the nerve, related to the increased aldose reductase activity of the polyol pathway; 2) the decreased slow anterograde component of axoplasmic transport, which delivers large protein molecules to distal sites needing repair; and 3) the increased stiffness of the nerve, which prevents gliding and is related to nonenzymatic binding of glucose to the collagen within the connective tissues of the nerve.[8] Electrodiagnostic testing often cannot identify a superimposed nerve compression in the setting of diabetic neuropathy, even for the most common peripheral nerve entrapment, carpal tunnel syndrome.[9] The clinician must rely on Tinel’s sign, the traditional physical examination technique of gentle percussion along the course of the peripheral nerve at known sites of anatomic narrowing, such as the common peroneal nerve at the fibular neck, the deep peroneal nerve over the dorsum of the foot, and the tibial nerve in tarsal tunnel.[10,11] A positive Tinel sign results in the patient’s perception of distal radiation into the territory of that nerve’s cutaneous distribution. The common peroneal nerve, when entrapped, will more often just exhibit tenderness, rather than produce radiation into the dorsum of the foot. The deep peroneal nerve radiates into the dorsal first web space. The tibial nerve in the tarsal tunnel may radiate to the heel, the arch, the ball of the foot, or the toes, representing the possibility of its branches being compressed in the medial and lateral plantar tunnels and the calcaneal tunnel. The successful approach to restoration of sensation to the feet in diabetic patients must involve decompression of all four of these medial plantar tunnels.

Frostbite. Frostbite results from exposure of tissue to temperatures that result in the formation of ice crystals in the interstitial space. Just as the diabetic patient is at risk for developing neuropathic ulceration on the feet due to loss of protective sensation, the diabetic patient is at risk for frostbite due to the loss of normal sensibility in the fingers and toes. Awareness of this risk from cold exposure is the best preventive approach, just as protection of the insensitive foot is critical for the daily routine of the patient with diabetic neuropathy.

In the emergency setting, rapid rewarming of the affected tissue with water that is about 104 degrees F is required. Water at this temperature will thaw the ice crystals and prevent them from reforming and causing further damage to cell membranes. Temperatures above 105 degrees F risk creating a thermal burn. Antiprostaglandins will decrease viscosity of the blood, minimizing clotting of the dermal vessels that precedes gangrene.[12]

Neuropathic pain medication can relieve pain in patients with diabetic neuropathy,[13,14] but cannot restore the sensibility that is critical in preventing soft-tissue injury related to either frostbite or neuropathic ulceration.

Nerve compression in the diabetic patient can be treated successfully by surgical decompression of the peripheral nerve at known sites of anatomic narrowing, such as decompression of the carpal tunnel in the upper extremity. Over the past decade this approach increasingly has been reported to be performed in lower extremity nerves, in experimental models of diabetes,[15,16] and in prospective clinical series.[17–20] In the clinical studies, there has been relief of pain in up to 90 percent of the patients, and restoration of some two-point discrimination in up to 70 percent of the patients. The most recent reports indicate a positive predictive value of positive Tinel sign to be 92 percent in the diabetic patient.[21] Furthermore, restoration of sensation to the painful insensitive foot in the diabetic patient is successful at preventing ulceration and amputation.[22]

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.

Figure 1

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.

Figure 2

Figure 2. 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.

Conclusion

Neuropathy in the patient with diabetes not only may contribute to the risk of ulceration but also may contribute to the risk of frostbite in cold weather conditions due to loss of normal sensibilities in the fingers and toes. Education for the patient with diabetes should include awareness of proper protection of extremities in extreme weather conditions.

How to obtain educational credits by reading this article

Learning Assessment: Successful completion entails scoring at least 70 percent on the questions, printing off the evaluation form (below), filling it out completely, and faxing or mailing it to the correct address listed below. Certificates will be mailed to those who successfully complete the learning assessment by December 10, 2004.

Fax the completed form to: (610) 560-0501 or mail the completed form to: Trish Levy, CME Director, HMP Communications, LLC, 83 General Warren Blvd., Suite 100, Malvern, PA 19355

Questions

1. Which of the following is not present in diabetic small fiber neuropathy?
A. Abnormal thermal threshold
B. Abnormal intra-epithelial nerve fibers
C. Abnormal electrodiagnostic testing
D. Abnormal sudomotor testing

2. Which of the following is not present in diabetic symmetrical polyneuropathy?
A. Abnormal intra-epithelial nerve fibers
B. Abnormal cutaneous pressure threshold
C. Abnormal cutaneous vibratory threshold
D. Abnormal nerve conduction velocity
E. Abnormal sensory nerve amplitude

3. The mechanism of cell death in frostbite is:
A. Slow ionic flux
B. Increased cell adhesion molecule activity
C. Intracellular ice crystal formation
D. Interstitial ice crystal formation
E. Loss of conductivity

4. The diabetic patient with symmetrical distal polyneuropathy is at risk for frostbite because:
A. Impaired temperature regulation in the dermis
B. Loss of protective sensibility
C. Decreased arterial blood flow
D. Decreased soft tissue perfusion
E. Autonomic instability

5. Frostbite should be treated by placing the frostbitten extremity in:
A. Snow
B. Luke warm water
C. Boiling water
D. Hot water
E. Cool water

6. Increased susceptibility to chronic nerve compression in diabetes is due to:
A. Increased endoneurial water
B. Decreased axoplasmic flow
C. Increased glycoselated collagen within the nerve
D. Narrowed anatomic passages in the extremity
E. All of the above

7. Sites of chronic nerve compression in the lower extremity do not include:
A.The vertebral foramen for the spinal nerve
B.Fibular neck for the common peroneal nerve
C.Dorsum of foot for deep peroneal nerve
D.Tarsal tunnel for the tibial nerve
E. Medial and lateral plantar and calcaneal tunnels

8. A technique useful to identify nerve compression in the diabetic patient with neuropathy is:
A. Semmes-Weinstein’s monofilament
B. Wartenberg’s Wheel
C. Tinel’s Sign
D. Spurling’s Maneuver
E. Lasegue’s Sign

Frostbite and Diabetic Neuropathy Answer Form and Evaluation

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This activity avoided commercial bias or influence YES NO

Now that you have read this article, can you:

1. Describe and discuss the relationship between neuropathy and painful insensitive feet? YES NO
2. Describe and discuss the superimposed nerve compressions that can occur in the patient
with neuropathy in the lower extremity? YES NO
3. Describe the relationship and roles of electrodiagnostic testing and neurosensory
testing in documenting the presence of neuropathy? YES NO
4. Describe how to identify the neuropathy patient with a good prognosis to recover
sensation and relieve pain by surgical decompression of a nerve? YES NO

What questions do you still have?_______________________________________________

How will you use what you have learned from this activity?____________________________

All tests must be received by 12/10/04.