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Point-Counterpoint: Nerve Decompression In Diabetic Patients: Should It Be Done?

VOLUME: 18         PUBLICATION DATE: Jun 01, 2005

Issue Number: 6

Author(s): By Stephen L. Barrett, DPM, Patrick DeHeer, DPM, and Stephen Offutt, DPM

Yes. This author discusses the etiology of diabetic peripheral neuropathy, cites reports of efficacy for peripheral nerve decompression in the literature and shares insights from his experience in performing the procedure.

By Stephen L. Barrett, DPM

   Mainstream medical education is still teaching that the symptoms of diabetic peripheral neuropathy are progressive and irreversible. There is adequate and overwhelming basic and clinical medical science that contradicts this dogma.1-5 Indeed, one wonders how many additional outcome studies are needed in addition to those already reported before we achieve a better collective understanding of the etiology of symptoms in diabetic peripheral neuropathy.


    Additionally, we have also learned it is not safe to operate on patients with diabetes. However, that paradigm has recently shifted with the plethora of literature supporting Charcot reconstruction and other palliative procedures in patients with diabetes. It is interesting that we are still debating this issue when the basic medical science and clinical results have been available for many years. Prior to any discussion of this topic, it is imperative to stress that no one can surgically treat diabetic peripheral neuropathy.


    However, with proper selection criteria, peripheral nerve surgical decompression/neurolysis can be highly successful in patients who have superimposed chronic nerve entrapments that cause most of their symptoms of diabetic peripheral neuropathy.

What The Literature Reveals About The Etiology Of The Condition

   Volumes have been written on the metabolic pathways that are involved in the
development of diabetic peripheral neuropathy. In 1978, Jakobsen made rats diabetic with injections of streptozotocin. Their sciatic nerves developed endoneurial and subepineurial edema, resulting in a larger cross sectional area. The diabetic rats were heavier in comparison to the non-diabetic control group.6


    The concept of “double crush” or multiple crush syndrome is well established in peripheral nerve physiology.7 Diabetes is known to act as the first “crush” of peripheral nerve entrapment. Chronic nerve compression studies have conclusively documented a cascade of histological events, beginning with the loss of the blood nerve barrier and ending with severe demyelination and axonal degeneration.


    It is well known that the peripheral nerve in patients with diabetes is more susceptible to chronic nerve compression due to endoneurial edema, decreased axoplasmic flow, which impairs neural repair, and glycosylation of collagen that makes the nerve stiffer. For those who are contemplating peripheral nerve decompression surgery, it is imperative to understand the etiological difference between neuropathic conditions. There is neuropathy that begins with axonal degeneration from the actual metabolic nature of whatever neural disease is present. Then there are neuropathies in which chronic nerve compression, due to an edematous “swelling” of the neve, ultimately ends up leading to axonal damage. When the neuropathic disease process directly affects the neuron, there is usually no role for peripheral nerve decompression surgery.8

    Perhaps the most compelling argument from a basic medical science perspective comes from MacKinnon and Dellon’s Textbook of Peripheral Nerve Surgery.8 They clearly demonstrate astounding histological differences in a diabetic primate via photomicrographs of the ulnar nerve from two different anatomical sites. The authors compare a cross section of the ulnar nerve in the mid-upper arm, where there is no known site of anatomical compression, to a second photomicrograph of the same nerve (just several centimeters distal to the first photo) from the cubital tunnel, a known site of anatomical entrapment. The comparison of these photomicrographs reveal significant histological changes of nerve degeneration with loss of myelination.8

    Clearly, if diabetic peripheral neuropathy were solely a disease of the axon as so many believe and are still teaching, then how could that explanation account for this tremendous histological difference in the same nerve only centimeters apart?

Assessing Results From Different Studies

    Dellon’s important early critical observations in his hand surgery patients with diabetes indicated that many neuropathic patients demonstrated improvement in their sensation and reduction of their neuropathic pain after peripheral nerve decompression surgery in their upper extremity. He also made the point that “nerve compression develops from the inside out as well as outside in.”8


    By using walking track analysis studies of rats that became diabetic (which included a subsection of rats that had tarsal tunnel decompression surgery), Dellon, et. al., were able to show that those rats with prior surgical decompression did not develop a neuropathic walking track pattern.9 It is also well documented that the peripheral nerve in patients with diabetes can regenerate after decompression repair.10


    Chris Maloney, MD, a Clinical Assistant Professor of Plastic and Neurosurgery at the University of Arizona, recently reported his results for 200 consecutive peripheral nerve decompressions among patients with diabetic peripheral neuropathy at the 2005 American College of Foot and Ankle Surgeons Annual Scientific Meeting.11 An independent observer collected and analyzed his data. He reported that 87.3 percent of his patients had improved sensation and 83 percent had a mean pain improvement of greater than 7 points on the visual analog scale (VAS). More importantly, no patients reported a worsening of their pain symptoms.


    Another parameter that Maloney measured and reported was that of improved balance. In his series of 200 patients, 92.1 percent had improvement in balance. His presentation included a retrospective analysis of the other published papers dealing with diabetic peripheral nerve decompression. He found that out of 425 patients, employing peripheral nerve decompression had an overall success rate of 88 percent for reduction in pain and a 78 percent improvement in sensation.11

Other Key Points


    What does this data tell us? While there remains a need for more outcome studies, there is already enough compelling data from different surgeons throughout the nation that substantiate the benefits of peripheral nerve decompression in properly selected patients with diabetic peripheral neuropathy. There are now more than 200 surgeons throughout the United States and the world who have taken additional training in peripheral nerve surgery and are currently performing the techniques.


    In addition to the fact that different surgeons are seeing consistent outcomes, there is the huge global economic benefit of reducing healthcare spending for the management of diabetic ulcerations and amputations, not to mention the impact that improved balance will have in reducing the incidence of hip fractures in the elderly population. This does not take into account the fact that this procedure is life-changing and, in some cases, is life-saving surgery for that individual suffering with severe symptoms from diabetic peripheral neuropathy.

In Conclusion


    There has been much criticism leveled at this emerging surgical trend and concept in the management of superimposed chronic nerve entrapments in patients with diabetic peripheral neuropathy. This stems largely from a misunderstanding of what the surgeon is doing for the patient as well as a misunderstanding about the true source of the symptoms. These misunderstandings have been compounded by the long entrenched medical dogma of diabetic peripheral neuropathy.


    It is imperative to note that these patients must have adequate peripheral lower extremity circulation to heal. Indeed, when one ensures appropriate patient selection, meticulous surgical technique and proper postoperative management, podiatric surgeons can expect a high success rate with this procedure.


    I have been performing this type of surgery for more than four years now and have been astonished at the outcomes. Most patients return to have the procedure performed on their contralateral extremity. If these techniques did not have optimal outcomes, I doubt that many patients would return to have surgery on the other foot. Interestingly, many of these patients are reporting their successful outcomes back to their internists and endocrinologists, who are subsequently referring more patients for decompression.

    Dr. Barrett is a Fellow of the American College of Foot and Ankle Surgeons. He is an Associate Professor within the Arizona Podiatric Medicine Program at the Midwestern University College of Health Sciences.


1. Aszmann OC, Kress KM, Dellon AL. Results of decompression of peripheral nerves in diabetics: a prospective, blinded study. Plast Reconstr Surg, 2000. 106(4):816-22.

2. Dellon AL. Treatment of symptomatic diabetic neuropathy by surgical decompression of multiple peripheral nerves. Plast Reconstr Surg, 1992. 89(4):689-97; discussion 698-9.

3. Dellon AL. Diabetic neuropathy: review of a surgical approach to restore sensation, relieve pain, and prevent ulceration and amputation. Foot Ankle Int, 2004. 25(10):749-55.

4. Wood WA, Wood MA. Decompression of peripheral nerves for diabetic neuropathy in the lower extremity. J Foot Ankle Surg, 2003. 42(5):268-75.

5. Biddinger KR Amend KJ. The role of surgical decompression for diabetic neuropathy. Foot Ankle Clin, 2004. 9(2):239-54.

6. Jakobsen J. Peripheral nerves in early experimental diabetes: expansion of the endoneurial space as a cause of increased water content. Diabetologia, 1978. 14(2):113-9.

7. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet, 1973. 2(7825):359-62.

8. MacKinnon SE, Dellon AL. Surgery of the Peripheral Nerve. 1988.

9. Dellon AL, Dellon ES, Seiler WAT. Effect of tarsal tunnel decompression in the streptozotocin-induced diabetic rat. Microsurgery, 1994. 15(4):265-8.

10. Babovic S, et. al. Nerve regeneration in diabetic rats. Microsurgery, 1998. 18(1):9-11.

11. Maloney CT. Surgical Management of Diabetic Peripheral Neuropathy: 200 Consecutive Patients. Presented at the 2005 ACFAS Meeting, 2005.

    No. These authors raise questions about the procedure and say there are not enough evidence-based studies to support its use in this high-risk patient population.

By Patrick DeHeer, DPM, and Stephen Offutt, DPM


    When it comes to patients with diabetic neuropathy, lower extremity specialists know this particular patient group all too well. For some patients, it would be a blessing for the pain to go away but for others, the situation would be so much easier if they could only feel pain.


    Currently, the standards of treatment for diabetic neuropathy include tight glycemic control, exercise, narcotic and non-narcotic analgesics, antidepressants, anticonvulsants and vitamin therapy. More recent treatments include a selective serotonin and a norepinephrine reuptake inhibitor. Novel treatments will no doubt continue to surface in the near future. However, to date, not one of the aforementioned therapies reverses the effects of diabetic neuropathy, namely that of permanent nerve damage.


    Through years of intense concentrated effort and study, Dellon and co-workers have developed a surgical approach to decompress the afflicted nerves of the lower extremity. The nerves most commonly released are the common peroneal nerve at the level of the fibular neck, the deep peroneal nerve at the level of the extensor hallucis brevis tendonous slip and the tibial nerve (all four tunnels) at the level of the tarsal tunnel and plantar vault. A limited number of supporting studies demonstrate a significant reduction of pain and a restoration of sensation for some patients.

Why A Closer Look At Decompression Is Warranted


    While we understand and appreciate the excitement and promise of such a development, it is important to take a closer look at this treatment option. Premature and/or overzealous incorporation of surgical decompression for neuropathy is not without risks and possible disastrous consequences. There are areas that require more prospective research before podiatrists can consider nerve decompression a consistently viable modality for treating diabetic neuropathy.


    The premise behind decompression centers on just a few key ideas. With increased levels of hydrophilic sorbitol, the diabetic nerve swells and accordingly occupies more volume as it passes through tight anatomical tunnels throughout the body. These tunnels are increasingly tight in patients with diabetes due to the decrease in elastic properties of diabetic connective tissues. This entrapment scenario increases pressure on the nerve, causing relative local ischemia. Furthermore, the ischemic nerve is unable to repair itself due to the decreased axoplasmic flow, another metabolic occurrence in patients with diabetes.


    One thing that is somewhat puzzling with the above sequence of events is the disparity of symptomatic neuropathy in the lower extremities versus the upper extremities. Metabolic changes should not show anatomical variances and we know of tight passages in the upper extremity (i.e., the carpal tunnel and cubital tunnel). Then why do we see such a drastic incidence of changes in the lower extremity versus the upper extremity? Is part of the interneural edema gravity dependent?


    Another point that is somewhat unclear revolves around the decreased elasticity of diabetic connective tissues. We are by no means refuting this observation. We have all seen this with the incredible occurrence of equinus in this population but what about the perineurium and endoneurium? The peripheral nerve decompression procedures do describe the need to perform internal neurolysis of the perineurium in selected cases but not the endoneurium. Wouldn’t the endoneurial tissues be subject to the same metabolic changes as the perineurial tissues? It is understood that their release would be highly impractical if not impossible. However, it raises the question that perhaps the loss of connective tissue elasticity does not play the role we assume.

Why One Should Strongly Consider The Patient’s Diabetic Condition


    We also must step away from the procedure itself and not forget this patient population. No procedure is without risks and this is especially true in the diabetic population. One must perform judicious scrutiny of the patient’s preoperative state. Just because this is a soft tissue procedure is not a reason to let down one’s guard. Many of these patients will be at an increased surgical risk and could potentially develop serious wound complications, particularly at the tarsal tunnel site.


    One must also closely assess distal vascularity prior to any surgery and check to ensure that part of the pain is not ischemic in nature. Anecdotally, we have heard of iatrogenically induced Charcot changes after patients have undergone nerve decompression. This is by no means specific to the procedure but one must consider this potential complication nonetheless.


    We also cannot accept the mindset that the successful post-decompression patient with diabetes is no longer a high-risk patient. These patients will still need regimented podiatric monitoring, diabetic shoegear and/or orthotic management. Nerve decompression does not change the metabolic status of these patients and, as post surgical patients, they could be subject to re-entrapment as perineurial tissues and ligamentous restraints continue to lose elasticity and fibrotic tissue contracts.

Is More Research Necessary?


    Another contention stems from the published research to date. The overwhelming majority of research has stemmed from Dr. Dellon and his colleagues at the Institute for Peripheral Nerve Surgery. Research from a non-affiliated group would add significant validity to this technique and the surrounding ideology. Andrew Boulton, MD, a premier authority on diabetic peripheral neuropathy, who criticizes the possibility of diabetic neuropathy being an entrapment neuropathy, denounces surgical decompression for this condition.1


    We understand that individuals who are pioneering new approaches often find clinical and academic support in forming a collective, but we believe this pioneering work has progressed far enough to deserve and demand attention from outside investigators.

Final Thoughts


    There is strong optimism and promise in the field of neurosensory testing and peripheral nerve release for the treatment of diabetic neuropathy. While we also feel there is potential with this technique, the procedure is still relatively new and, in some medical circles, highly controversial. For many states, a release of the common peroneal nerve far exceeds our practice scope. It would be terrific to see long-term studies with prospective controlled data or perhaps even a long-term limb survivorship study between surgical decompression patients and those with sound appropriate diabetic foot care.


    Unfortunately, there has not been any published controlled trial data to date to support peripheral nerve decompression in patients with diabetes. In a time when we need to seek out good evidence-based medicine, it is simply not there yet for this technique.

    Dr. DeHeer (pictured) is a Fellow of the American

of Foot and Ankle Surgeons and is a Diplomate of the American Board of Podiatric Surgery. He is also a team podiatrist for the Indiana Pacers and the Indiana Fever. Dr. DeHeer is in private practice with various offices in Indianapolis.

    Dr. Offutt is a member of the American College of Foot and Ankle Surgeons. He is in private practice at various offices in Indianapolis.

Editor’s Note: For a related article, see “Current And Emerging Options For Treating Diabetic Neuropathy” in the March 2005 issue or check out the archives at www.podiatrytoday.com.


1. Boulton A. Expert insights on painful diabetic neuropathy. Podiatry Today. 16(3):30-36, 2003.