Frostbite and Diabetic Neuropathy

A. Lee Dellon, MD

Disclosures

Wounds. 2003;15(12) 

In This Article

Diagnosis and Discussion

The patient was diagnosed with diabetic neuropathy complicated by frostbite.

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°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°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.[17,18,19,20] 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]

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