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12 Articles in Volume 13, Issue #1
A Modest Proposal (Thanks to Jonathan Swift—1667-1745)
Chronic Pain: Study of Complementary and Alternative Treatments
Decompression Surgery to Reduce Diabetic Peripheral Neuropathy
Extracorporeal Shock Wave Therapy—Application for Trigger Points
Improving a Practice Model for Prescribing Opioids
Interpretations and Actions Following Cytochrome P450 Testing
Is It Safe to Restart an NSAID Following an Endoscopically Confirmed NSAID-Induced GI Bleed?
January/February 2013 Pain Research Updates
Massage Therapy in an Ambulatory Pain Clinic
Practical Tips in the Treatment of Osteoarthritis of the Hip
Quantum Theory Underpins Electromagnetic Therapies for Pain Management
When a Pain Patient Insists on Alternative Treatments Alone

Decompression Surgery to Reduce Diabetic Peripheral Neuropathy

Similar to carpel tunnel syndrome surgery, nerve decompression surgery helps improve symptoms of DPN of the foot and prevents amputation.

It has been entrenched in medical training that the symptoms of diabetic peripheral neuropathy (DPN) are irreversible. Once a patient develops DPN, the best clinicians can offer is palliative treatment to mask or ameliorate symptoms—a notion that is repeatedly supported by articles in the medical literature.1,2 However, recent study and clinical practice has demonstrated that decompression surgery can be used effectively to treat DPN of the foot, and in most cases, prevent 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 can only be treated with medications. 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 poly-biochemical pathway. Additionally, an increase in blood glucose levels causes an increase 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

In 1978, Jakobsen published a landmark in vivo 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 anatomical tunnels or constrictive areas (Figures 1-7). This has been demonstrated in the upper extremity and in the 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 entrapment of a nerve caused by a systemic disease (diabetes) account for most of the symptoms attributed to DPN rather than the true axonopathy itself? Could this entrapment be the cause of the gambit of symptoms (pain, numbness, burning, loss of sensation, etc), which manifest as “diabetic systemic polyneuropathy”? The skeptic may ask how the patient with diabetes develops a “stocking” or “glove” distribution of their neuropathy from a focal entrapment. If it is 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.

Table 1Table 1

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. Dellon et al 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 their previously “gloved” distribution of “polyneuropathy sensory deficit.”

These pleasantly surprised and satisfied patients had another question for him. “What can you do for my feet?” Why would the same concept not apply to the lower extremities? Certainly nothing metabolic has changed! Interestingly, when evaluating patients for 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 improvement is often seen in the postoperative acute care unit after nerve decompression with improved motor function.

There has been extensive research into the effects of peripheral nerve decompression for the prevention of symptoms caused by DPN, and in particular tarsal tunnel decompression.14,15 In a 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 symptoms of DPN from developing.17

Figure 1Figure 1

Figure 2 Decompression Surgery for DPNFigure 2

Figure 3 Decompression Surgery to Reduce DPNFigure 3

Figure 4 Decompression Surgery for DPNFigure 4

Figure 5 Decompression Surgery for DPNFigure 5

Figure 6 Decompression Surgery for DPNFigure 6

Figure 7 Decompression Surgery for DPNFigure 7






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 usually allowed to walk the same day as the procedure, and the complication rate has been very small with the most common complication being a wound dehiscence.19

How do complication rates of foot surgery compare to conventional care in patients with diabetes? In other words, can decompression surgery prevent ulcers and amputations? In a 2-year study of infection rates in 1,666 diabetic patients in a managed-care setting, Lavery et al reported that 151 patients (9.1%) developed 199 foot infections (ulcers), with an overall hospitalization rate of 3.7%.20 The development of deep-seated ulcers significantly increased rates of amputation (P<0.001). By comparison, a study of 1,322 decompression surgeries performed on 1,025 diabetic patients by 36 different surgeons showed only a 0.8% admission rate.21 Data for infection was not included in this registry, but in over 12 years of performing more than 500 of these surgeries in my private practice, there have been no hospital admissions for infection, and fewer than 10 patients who developed minor cellulitis.

Accurate diagnosis and assessment is imperative, preoperative patient education mandatory, and formalized training in peripheral nerve surgery is a prerequisite for patient safety and excellence of outcomes. It is also imperative to stress the point that not all diabetic patients with neuropathic symptoms are candidates for this type of surgery, and that a highly predictive factor is a positive Tinel’s sign at the known sites of compression.

Assessing Decompression Surgery

The reviews of the efficacy of decompression surgery as a treatment for symptomatic diabetic neuropathy have been mixed. In 2006, the American Academy of Neurology (AAN) conducted a literature review of surgical decompression and concluded that “the literature revealed only Class IV studies concerning the utility of this therapeutic approach. Given the current evidence available, this treatment alternative should be considered unproven.”22 However, the literature also reveals very positive studies of decompression surgery. One small study by Aszmann et al compared the impact of surgery on the development of ulcers and amputations in an operated and nonoperated limb of 50 patients with diabetes. The authors reported no ulcers or amputations in the decompressed leg, compared to 12 ulcers and 3 amputations in the contralateral limb.23 Dellon wrote that “…there have been 15 peer-reviewed studies that used the inclusion criteria of:
1) presence of symptomatic neuropathy, 2) positive Tinel’s sign over the tarsal tunnel demonstrating a site of compression, 3) no previous history of ulcer or amputation, and 4) used the Dellon Triple Decompression technique. These studies demonstrated relief of pain in 88% and restoration of sensation in 79% of patients.”

A more recent study by Nickerson in 2010 showed similarly compelling findings.25 Certainly, while not randomized, these patients served as their own controls with similar diets, lifestyles, and glycemic control. There are a plethora of studies that refute this assertion by the AAN, albeit they may not be Class I studies.18,19,24,26-36 The most recent study of 560 decompression patients by Zhang et al showed significant improvement in nerve conduction velocity, quantitative sensory testing, and the Toronto Clinical Scoring System. Even more impressive was what investigators found after 18 months of follow up: 37% of these patients (208) had a Wagner Classification 1 ulcer before surgery. At 18 months there were no ulcers present in these 208 patients.37

It is likely that semantics played a role in these subcommittees’ conclusions, in that as we know it, it is impossible to operate on DPN, but it is completely reasonable to decompress a focal nerve entrapment superimposed on DPN. I would propose that AAN consider the same question for carpal tunnel surgery in the patient with DPN. Would their conclusion be that it is “unproven” to decompress a focal entrapment of the medial nerve? I don’t think so.

There is no argument that more robust studies are needed to quash the “evidence-based medicine” argument, but with more than a decade of experience with this surgery, I can think of nothing more “evidenced based” than an 85% return rate of the patients seeking decompression of their second extremity.


Surgical decompression for the patient with DPN and superimposed focal nerve entrapment are life-changing surgeries—and have saved patients’ lives from the sequelae of ulcer and subsequent amputations, but also suicide. The reader is urged to consider the wide-ranging ramifications of what this surgery means for the reduction or elimination of pain for the patient, the prevention of diabetic ulcers and amputations, the improvement in the quality of life, and reduction in healthcare costs. It is easy to put this into perspective when performing this type of surgery for the patient, and receiving daily positive feedback from these patients who suffer with horrible symptoms. I would urge any provider who frequently encounters patients with DPN, regardless of surgical specialty, to look further into this. A good resource is the Association of Extremity Nerve Surgeons (www. AENS.us). Finally, the reader must recognize the fact that no surgeon is able to operate on DPN but is clearly able to decompress superimposed nerve entrapments, which are more prevalent in patients with diabetes, and relieve symptoms that are caused by the nerve compression.

Last updated on: March 11, 2013
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