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9 Articles in Volume 16, Issue #3
CDC Issues Final Guidelines for Opioid Prescribing: PPM Editorial Board Responds
Don L. Goldenberg, MD, FACP
Don't Flinch From Prescribing Pain Medications!
Help Patients Achieve Diet/Weight Goals to Manage Pain
Hormone Testing and Replacement: Status Report 2016
Living With, and Managing, Chronic Pain: A Patient’s Story
Nerve Decompression Surgery Can Reverse Neuropathy of the Foot
Pulsed Electromagnetic Field Therapy: Innovative Treatment for Diabetic Neuropathy
Specialized Pharmacies Step Into Risk-Management Role

Nerve Decompression Surgery Can Reverse Neuropathy of the Foot

Similar to carpal tunnel syndrome surgery, nerve decompression surgery helps improve symptoms of diabetic peripheral neuropathy of the foot and prevents amputation.
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Nerve decompression surgery can be used effectively to treat the pain and complications of diabetic peripheral neuropathy (DPN), reversing the symptoms of numbness and tingling, and in most cases, preventing amputation.

This article will review the science behind DPN and explain how this surgical procedure may benefit your diabetic patients.

Etiology of DPN

While there are many hypotheses about what causes diabetic neuropathy, they all have one theme in common—that is, DPN is a systemic disease that is progressive and irreversible.1,2 The only way to prevent DPN is through proper glycemic control. It has been established that hyperglycemia is responsible for vascular complications, which have been linked to the development of neuropathies in diabetic patients. An accumulation of sorbitol and fructose within the nerve caused by unchecked hyperglycemia alters the aldose reductase biochemical pathway.

Additionally, an increase in blood glucose levels causes an increased binding of glucose to collagen resulting in advanced glycosylation end products (AGEs), which thicken the connective tissue of both the nerve and the tunnel and constrict the anatomical site it runs through.3

Like water flowing through a dam, nerve decompression surgery can reverse the symptoms of numbness and tingling (nerve compression and entrapment) associated with diabetic neuropathy.

In 1978, Jakobsen published a landmark study of the effect of hyperglycemia on the peripheral nerve—specifically, the expansion of the endoneurial space in the sciatic nerve of diabetic rats.4 Interestingly, he found significant changes in the sciatic nerve upon necropsy. The sciatic nerves were up to 50% larger in a cross-sectional area, had significant edema, but surprisingly, the large fibers (A-α, A-β) were still well myelinated for the most part. From his work some very important concepts have been proffered:

  • The peripheral nerve, which is subjected to hyperglycemia, becomes edematous, and therefore is larger in a cross-sectional area
  • The nerve has less ability to repair itself, because there is a slowing of anterograde and retrograde transport in the axon
  • The nerve is more susceptible to compression
  • The nerve remains relatively well myelinated in areas where there is no focal compression.

What does this mean clinically? First, we know that if the nerve is edematous, it is more likely to become entrapped in small, non-expandible anatomical tunnels or constrictive areas (Figures 1-7). This has been demonstrated in both the upper extremity and in the leg and foot. In fact, the incidence of carpal tunnel syndrome in the general population in the United States is 2%, while in the diabetic population it is estimated to be between 14% and 30%.5

Could this focal physical entrapment of a nerve caused by a systemic disease (diabetes) account for most of the symptoms attributed to DPN rather than a true axonopathy itself? Could this entrapment be the cause of the gamut of symptoms (pain, numbness, burning, loss of sensation, etc), which manifest as “diabetic symmetric polyneuropathy”?

The skeptic may ask how the patient with diabetes develops a “stocking” or “glove” distribution of their neuropathy from a focal entrapment. If there is only a focal entrapment, what is accounting for the majority of symptoms? Table 1 lists peripheral nerve compression pathology, illustrating that focal entrapment can cause widespread symptoms.

Surgical Treatment of Entrapment

It is well documented that the pain and symptoms of carpal tunnel syndrome can be relieved by peripheral nerve decompression in the diabetic patient.6-12 In the 1980s, MacKinnon and Dellon noted that most diabetic patients with carpal tunnel syndrome and symptoms of peripheral neuropathy—such as numbness and tingling in their hands—regained their sensation after carpal tunnel decompression surgery.6 The patients’ pain also improved, if it was not completely eliminated.

The researchers then went on to discover that if the ulnar nerve, and subsequently the radial sensory nerves, were surgically decompressed, most of these patients would then regain sensation in the remainder of their previously “gloved” distribution of “polyneuropathy sensory deficit.” It is easy to visualize how this combination of peripheral nerve compressions can produce a “glove” effect.6 These pleasantly surprised and satisfied patients had another question for the surgeons. “What can you do for my feet?” Why would the same concept not apply to the lower extremities? Certainly nothing metabolic has been changed by surgery!

Interestingly, when evaluating patients with diabetes after lower extremity peripheral nerve decompression, Maloney et al showed a predictive success rate of 88% for decompression of patients’ lower extremities.13 What occurred was that the focal nerve entrapment was relieved (the true pain generator), and their pain disappeared or was greatly diminished. Immediate sensory improvement with improved motor function is often seen in the postoperative acute care unit after nerve decompression.

There has been extensive research into the effects of peripheral nerve decompression done for the treatment of DPN symptoms, and in particular tarsal tunnel decompression.14,15 In more recent study, greater effects were seen when the common peroneal nerve was decompressed in addition to the tarsal tunnel.16 This not only means that symptomatic DPN can be effectively treated via surgical nerve decompression, but that surgical decompression can prevent the complications of DPN from developing.17

Preoperative Evaluation

While it is not within the scope of this article to discuss the specifics of the surgical techniques, there are some points that the reader might find helpful. First, in some provider groups there is a misperception that it is not safe to operate on a patient with diabetes. This is simply not true, and in fact, more foot surgery is performed on patients with diabetes than without.

It is imperative, however, that the vascular status of the patient is evaluated and determined to be adequate, usually with an ankle brachial index (ABI—the ratio of the blood pressure in the lower legs to the blood pressure in the arms)—of ≥0.7 (which is adequate perfusion to safely perform surgery, though normal ABI is 1.0 to 1.2) with palpable pulses and little trophic change to the skin.18 In fact, this surgery is now being implemented into limb salvage surgery regimens.19

The patient is ideally allowed to walk the same day as the procedure, and the complication rate has been very small with the most common complication being a partial wound dehiscence easily managed by local wound care.19

Last updated on: April 15, 2016
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