Can Diabetic Nerve Decompression Have An Impact?

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The treatment of patients with diabetes and associated complications has been extensively studied. Over the past several decades, the treatment of foot and ankle ailments in patients with diabetes has dramatically shifted from conservative measures of “do not perform surgery” to the present day thinking that has taught us that diabetic feet are not very different from normal feet.
The most common misconception with diabetic foot ailments has been that the loss of limbs is due to severe vascular problems. However, with time, we have found that vascular issues in the diabetic foot are less problematic than previously suggested and less common than suspected. Often, the ulcer formation is the result of neuropathy and a lack of sensation.
What has been of interest is that the major cause of peripheral limb loss among patients with diabetes is due to peripheral neuropathy and loss of protective sensation. In the past, the prevailing thinking on protective sensation loss in patients with diabetes was that it was irreversible, symmetrical and progressive. With time, there has been an increased interest in the surgical decompression of diabetic limbs in order to decrease pain and increase sensation. Although much controversy still exists, more and more doctors are beginning to understand the philosophy and potential for a chronic nerve compression of the diabetic limb.
During my residency, I spent a great deal of time with several hand surgeons. The surgeons performed a very large number of carpal tunnel releases in diabetic patients and never doubted the fact that carpal tunnel may be possible in a patient with diabetes. Now when I think back to the nerves, they were often flattened and swollen beyond normal levels with internal scarring. The diabetic nerves often were far larger and more swollen than the nerves of patients who did not have diabetes. I believe surgical decompression is a revolutionary treatment with excellent potential. However, it is essential to look at each case and weigh the benefits and risks of surgery versus conservative care.
In regard to surgical decompression, the largest study group to date is part of the Neuropathy Foundation of the Southwest with 200 or so surgeons, and over 2,000 cases logged to date. Overall, they have achieved, on average, an 80 percent improvement in pain and a 70 percent improvement in sensation among the study group patients with a positive Tinel sign over the involved nerve release sites. The results for pain relief and sensation restoration dip to 50 and 55 percent, respectively, in the groups with no Tinel sign noted.

What The Studies Have Revealed About The Etiology Of Diabetic Peripheral Nerve Compression

In 1973, Upton and McComas initiated the theory of a double crush hypothesis, suggesting that a nerve with serial limitations of axoplasmic flow may cause a more distal entrapment.¹ In theory, diabetes is considered one cause of crush with a secondary local entrapment being the second cause. Although each of the crush factors may cause pain, the summation of multiple factors causes a far more symptomatic outcome than the parts. As a result, the local compression is a combination of a double crush due to a local entrapment in combination with a second crush factor, which, in this case, is diabetes. However, the issue is far more involved when one looks at it in more detail.
Researchers have performed many studies on diabetic animal models. In 1980, Jakobsen and Sidenius showed a decrease in axoplasmic flow with diabetes.² Further studies by Tomlinson and Maher, Fink, et al., and Dahlin, et al., have confirmed the finding of decreased axoplasmic flow in diabetes.^3-5
Many of the studies have involved the use of rats and primates with streptozotocin-induced diabetes mellitus.^6-8 In such studies, researchers have utilized nerve biopsies and observed gait pattern changes to analyze the effect of diabetes on the peripheral nerves. Several rat studies have shown that the theory of a double crush phenomenon involving decreased axoplasmic flow as one crush and diabetes as a second crush involves a chronic nerve compression of peripheral nerves at locations of possible impingement.⁹
Researchers have also suggested that the increased water content of the diabetic nerve may potentially contribute to peripheral nerve compression in patients with diabetes.^10,11 Several studies have shown that the increased size of the peripheral nerve, as a result of increased water content, may have caused chronic nerve compression at sites of anatomic narrowing in the upper and lower extremity.^12-14
The metabolic factors of diabetic neuropathy have been related to excess glucose conversion into intracellular sorbitol. The prevailing thinking is that the sorbitol subsequently blocks the uptake of myoinositol, leading to reduced sodium and potassium activity thought to be necessary for proper nerve conduction.
Researchers have also suggested that the increase of intracellular sodium results in paramodal demyelination.¹⁵ With time, there is a decrease in axoplasmic flow, eventually leading to axonal degeneration.¹⁶
The vascular causes of diabetic neuropathy are still being extensively researched. It is clear to us that there is no small or large vessel disease associated with diabetic neuropathy.^17-19 However, there is a chance that axonal swelling may cause extraneural compression, leading to axonal degeneration, demyelination and nerve fiber loss.^20-22
A possible secondary cause of diabetic peripheral neuropathy may be biomechanical factors contributing to nerve entrapment at local compression regions. In the upper extremity, these sites would include the common peroneal nerve at the fibular head region, the tarsal tunnel and distal medial plantar, lateral plantar and calcaneal tunnels at the medial ankle, and the deep peroneal nerve on the dorsum of the foot. [4]
Two causes have been associated with diabetic nerve compression syndrome. The first is compression at the aforementioned sites due to increased water content in the nerve resulting in axonal swelling, neural ischemia and neuropathic symptoms.²³ Several studies have noted changes in the size and weight of the sciatic nerve in streptozotocin induced rats.
The second potential biomechanical cause of peripheral nerve pain is the loss of tissue elasticity and possible localized nerve impingement. [5]Non-enzymatic binding of glucose to collagen in the epineurium of the nerve may be a cause of decreased elasticity in the nerve.²⁴ With advanced glycosylation of the nerve, there is a loss of peripheral nerve gliding and increased tension about and along the nerve. This increase in tension may also cause a decrease in neural blood flow.²⁵

A Guide To The Patient History And Physical Examination

The physical examination of peripheral nerve entrapment in patients with diabetes is quite straightforward. The first and foremost point of importance is that the patient has pain and/or difficulty with ambulation and daily activity. In cases of numbness without pain or in cases in which patients respond well to oral neuropathy medications, surgery is not suggested as the risks may outweigh the potential positives.
In the history taking process, the most common findings are a symmetrical numbness and pain that is debilitating. Often, the patient has tried several types of compounded foot creams and has also been on multiple medications for neuropathy pain. Patients will often suggest that they have pain at night and have a difficult time with balance in the foot and ankle. They often have to take narcotic medication to calm the pain. Often they feel that elevation and rest do not help the pain very much.
The physical examination should show good peripheral pulses including the femoral, popliteal, dorsalis pedis and posterior tibial pulses. If there is any question of peripheral circulation, one may use transcutaneous oximetry or vascular Doppler testing with the toe brachial index (TBI) and segmental pressures for additional information. Patients with questionable circulation should not have surgery until there is a complete check of their circulation and appropriate clearance from a vascular surgeon.
Foot musculature should be mature without severe weakness of all regions. Often, the common peroneal nerve entrapment results in weakness of the dorsiflexors, including the anterior tibial and extensors. This may result in a shuffling gait pattern and weakness of the ankle and great toe to dorsiflexion strength. Podiatrists should treat any existing wound infection and strive for wound closure prior to surgery.
Nerve testing is quite simple to perform. We avoid surgery on patients without a Tinel’s sign of the tibial and deep peroneal nerve, and pain in the common peroneal nerve region. This is not to say that results cannot be positive in cases of a negative Tinel sign but the overall outcome is far better when there are positive Tinel signs.
Physicians should perform nerve testing by tapping the local nerve entrapment sites. Ask the patient if he or she feels tingling with the tapping. A positive Tinel sign would suggest a proximal or distal tingling with tapping of the nerve. If a patient suggests that a different region is tingling than the site of sensory output for the local nerve, the test is not positive. If the Tinel sign is negative but there is a high index of suspicion and all other testing is positive, discuss the possible surgical outcomes with the patient. Explain that there may be a 50 percent positive outcome when there is a negative Tinel sign as opposed to an 80 to 85 percent positive outcome with a positive Tinel finding.

Inside Insights On Diagnostic Modalities For Diabetic Nerve Testing

Magnetic resonance imaging (MRI) and computerized tomography (CT) are of little help in the diagnosis and treatment of peripheral neuropathy. A recent study used ultrasonography of the peripheral nerves at sites of potential compression such as the tarsal tunnel to show reduction in the width of the nerve at the compression site and swelling of the nerve distal to the compression site.²⁶ [6]This study provides hope for the potential establishment of ultrasound guidelines for assessment of peripheral nerve entrapment locations and the measurement of the nerve as a potential sign of entrapment syndrome.
In regard to testing of the nerve for signs of peripheral neuropathy versus local compression, physicians have often relied on nerve conduction velocity (NCV) and electromyelogram (EMG) testing. This sequence of testing potentially shows a decrease in the conduction velocity of the nerve along its course, especially at locations of potential compression. Furthermore, the supply of nerve impulse to local musculature may be potentiated with possible impingement resulting in slow to no muscle impulse.
However, the testing has had severe limitations with lower extremity uses. The rate of false negative data has been fairly inconsistent in the lower extremity. However, in a properly done test, the ideal test data will show distal axonopathy with decreased amplitude and decreased velocity and latency of the associated nerves with demyelination. In our hands, the main use for EMG and NCV testing is to rule out potential lower back pain as a source of extremity pain. In cases of lower back pain with or without distal sciatic radiation, one may use EMG and NCV testing to evaluate radiculopathy.
A fairly new testing option is the Pressure Specified Sensory Device (PSSD, Sensory Management Services). [8]Studies comparing electrodiagnostic testing to PSSD testing have shown that the PSSD is at least as sensitive as electrodiagnostic testing studies.²⁷
With an increase in nerve compression, there is a loss of one- and two-point sensation threshold. This is similar to the Semmes Weinstein testing threshold but the PSSD is far more sensitive. Semmes Weinstein testing has shown that a one point loss of protective threshold at 11.8 g would be similar to 90g/mm² on the PSSD testing threshold.^28-29 Researchers have found the ulcer formation threshold to be at 30g/mm².³⁰ Therefore, by the time the Semmes Weinstein testing of protective threshold is positive, there is severe nerve damage and axonal loss.
The essential improvement with the PSSD testing is that one can perform one- and two-point static and motion testing under controlled computer driven settings. This allows better control of the amount of pressure and space between the two points needed to induce a sensation potential.
With an increase in one- and two-point static pressure findings, one should consider a deduction of possible nerve irritation versus mild entrapment. If there is an increase in the width between the two points prior to sensation potential, consider axonal degeneration of the associated nerve.
When it comes to the patient with diabetes, the most common testing sites include:
• the first web space representing the deep peroneal nerve region.
• the great toe pulp representing the tibial/medial plantar nerve region;
• the medial heel representing the tibial/calcaneal nerve region; and
• the lateral calf region representing the sciatic termination and common peroneal nerve region.
Our current diagnostic workup entails a neurosensory PSSD test in combination with local nerve ultrasound. The point of the ultrasound testing is to make sure there is no foreign mass in the region and check for the amount of compression on the nerve and the size of the nerve. One can also check gliding of the nerve but this is far more difficult. After ultrasound testing, the physician can perform a peripheral PSSD test. Often when it comes to patients with diabetes, there are very poor results with preoperative testing but one can detail the level of neuropathy and nerve compression.
In regard to our current requirements for surgical consideration, we prefer a healthy patient who has no vascular issues, well controlled diabetes levels, no gross infection, a positive Tinel sign and positive PSSD testing. We may consider surgery on a patient with a negative Tinel test but we will explain that the results of surgery are not as successful in comparison to a patient with a positive Tinel sign.

Essential Surgical Insights

When it comes to nerve decompression, the surgeon may proceed with local anesthesia, with or without monitored anesthesia, or general anesthesia. As there is a need for thigh tourniquet use, general anesthesia is preferred for patient comfort.
The first site for surgical decompression is the terminal sciatic nerve/common peroneal nerve. Bend the leg at the knee to a 90-degree angle. Have an assistant hold the leg at this position or use a bolster. One can easily palpate the nerve posterior and lateral to the fibular neck region.
Make an incision along the lateral fibular neck extending from the posterior edge of the neck to the anterior peroneus longus region. The incision is transverse in nature and measures 3 inches in length. Carry blunt dissection through the soft tissue to the level of the covering fascia of the common peroneal nerve. Release the deep fascia over the common peroneal nerve, taking care to avoid damage to the nerve.
Divide the lateral bands of the peroneus longus along the course of the nerve and make a small window at this region. This facilitates dorsal and plantar release of the fascia fibers. If the nerve is irritated by the lateral muscle branches of the peroneus longus muscle, cauterize and release these branches. Then release the deep fascia of the peroneus longus below the level of the common peroneal nerve.
At this point, the index finger of the surgeon should easily glide along the released nerve and into the dorsum of the anterior shin. Use caution when feeling the opening of the nerve and the more distal release of the tunnel as the nerve will begin to give off muscular branches in this region, which one must protect. We prefer to close the wound with an absorbable deep skin closure and skin staples. This allows for a more rapid movement of the region.
Proceed to focus on the tarsal tunnel region. Start by marking common important landmarks. Make a linear to curvilinear incision, centering the incision between the medial malleolus and the Achilles tendon. Bring the incision distally to the level of the medial abductor muscle belly at the point at which the deep fascia covering the medial and lateral plantar nerve branches should be present. Often, the fascia over the tibial nerve is not the site of greatest tightness. Make a small incision into the tibial retinacular fascia and perform a careful scissor release of the tibial nerve. Free the nerve proximally to the point at which the index finger can easily glide along the nerve in a proximal fashion. Perform bipolar cautery of the edges of the fascia.
Take care to identify the lateral cutaneous calcaneal nerve branch of the tibial nerve. Protect this nerve for lateral release. Release the superficial fascia of the abductor muscle belly and protect the muscle distally and plantarly. Doing so exposes the deep fascial tunnels of the medial, lateral and calcaneal nerve branches. Identify the tunnels with a straight hemostat and also identify the dividing fascial branch for release. Release the fascial tunnels along the line of each nerve branch.
Following the release of the medial plantar and lateral plantar tunnels, release the dividing fascial band between the two tunnels. There now should be one large tunnel that allows the pinky or index finger to enter the arch easily and reach close to the level of the navicular tuberosity. [7]
Proceed to release the calcaneal branch tunnel, taking care not to injure the nerve as it traverses below the calcaneus. Perform bipolar cautery of the fascial tunnel edges as far along the tunnel as is visible and easily accessible. Also release and cauterize any venous branches crossing and placing pressure on the tibial nerve or its distal branches. Check the tibial nerve for any endoneural thickening. If this thickening exists, perform a microdissection release of the endoneurium of the nerve. Again, we prefer a non-absorbable deep skin closure and staple skin closure.
Proceed to direct your attention to the deep peroneal nerve region. The deep peroneal nerve entrapment site is on the dorsum of the foot in the region of the first and second metatarsal base/ cuneiform region. The main culprit of entrapment in this region is the tendon of the extensor hallucis brevis, which has been shown to cross over the deep peroneal nerve and is a source of potential irritation.²⁴ The deep peroneal nerve may also be pressured by the dorsal extensor retinaculum.
Place a dorsal linear incision over the region of the deep peroneal nerve, centering the incision about the first and second metatarsocuneiform joint. Angle the incision slightly lateral to medial from proximal to distal. Carry blunt dissection through the deep tissues to the level of the extensor brevis tendon and retincular layer.
Remove a section of the extensor tendon located over the nerve. This section is commonly 2 cm long. Then free the retinaculum over the dorsal aspect of the nerve along its entire course. The retinaculum is usually 3 to 4 cm long and the surgeon can easily free it with a scissor. Once the nerve is free dorsally, check the actual nerve. Often there is a dell over the dorsum of the nerve at the region of the extensor tendon crossing with bulbous enlargement distal to this site. Close the skin with your choice of material. Again, I prefer to use staples as they offer additional strength and allow for more rapid weightbearing.

Key Post-Op Considerations

Dress the region with a bulky dressing that will allow slight movement but will prohibit extreme motion. Take care not to make the dressings very tight so you can avoid severe compression across the nerve sites. Using a soft wrap cotton padding is an excellent option. Podiatrists often use this for Jones compression style dressings. Place a mild compression Ace wrap over the bulky soft padding for slight compression. Do not perform casting.
Patients are allowed to touch their heels to the ground and one should teach them to use either crutches or a walker for balance and limited weightbearing. Remove the initial dressings at five days and check the wound. Utilize a light dressing and stabilize the ankle with an Aircast type brace. One should still emphasize limited weightbearing but you can allow the patient to move the foot in a dorsal and plantar manner for five minutes per day with very slow motion.
You should see the patient for a follow-up visit three weeks after the surgery. At this time, one can remove the staples or stitches, and have the patient start physical therapy. Wound healing should be complete prior to the removal of staples and initiation of physical therapy. Allow the patient to return to normal shoes and walking without exercise walking for an additional month.
Physical therapy has multiple goals. Initially, the goal is to calm swelling and prevent scar formation. Physical therapy should start with cross-fiber and deep tissue massage, ultrasound and laser therapy. Emphasize gentle and guarded motion at first. Over time, one can proceed to emphasize balance improvement and proper proprioception, balance and comfortable ambulation. Overall, the period of physical therapy is often one to two months.
One may clear the patient for a return to full activity at two to three months post-surgery. Often, the patient will feel less pain immediately after surgery and may or may not require pain medication or neuropathy medication for a period of two to six months post-surgery. Often, the neuropathy medication tapers off in the initial two to three months post-surgery. It is not unusual to have patients feel complete relief of severe pain within days of surgery. However, in most cases, there is continued pain and tenderness for two to six months post-surgery. At this point, the nerve begins normal axonal transport and pain subsides.

What Are The Results Of Nerve Decompression?
Dellon initially presented his results in 1991 on 51 upper extremities and 31 lower extremity surgeries.³¹ He performed electrodiagnostic testing for the preoperative testing. Patients with positive local compression syndrome on testing showed 100 percent relief with surgery. Those with preoperative electrodiagnostic testing suggestive of neuropathy had 50 percent relief. When there was a finding of neuropathy and local compression, the results showed an improvement in 80 percent of patients.
Diabetic neuropathy cases have been less commonly reported than general nerve compression studies. Wieman and Patel reported on 26 patients with diabetic neuropathy.³² They performed an isolated tarsal tunnel release on 33 legs. A significant improvement in pain was present in 92 percent of patients while 72 percent showed an improvement in sensation. Two patients with a negative Tinel test preoperatively did not have any improvement after surgery. This lead the authors to conclude that a positive Tinel test is essential for good outcomes. The authors of the study noted that diagnostic testing did not seem to convey any form of optimal outcome potential.
Aszmann, et al., presented their results of nerve decompression on 31 nerves with 20 diabetic patients.³³ They performed both upper and lower extremity decompression. A therapist was blinded to the site of surgery and patients underwent PSSD testing for sensibility of the surgical versus the non-surgical limb. Improvement in PSSD testing was present on 69 percent of lower extremities and 88 percent of upper extremities with worsening of neuropathy on the non-surgical limb.
Dellon, et al., also presented results showing the importance of a Tinel sign in determining sensation restoration results in diabetic and non-diabetic neuropathy.³⁴ In patients with diabetes, the presence of a positive Tinel sign had a sensitivity of 88 percent and specificity of 50 percent. There was also a positive predictive value of 88 percent in showing good to excellent results in outcome prediction.
Caffee has also reported on diabetic nerve release in the lower extremity involving patients with diabetes.³⁵ Thirty-six patients with 58 tibial nerve release procedures were included in the study. Eighty-six percent of patients had significant pain relief after surgery. In patients who had a main complaint of numbness, only 60 percent had improvement from the initial complaint findings. Finally, none of the patients developed a foot ulcer after surgery.
Biddinger, et al., presented results of lower extremity triple site release of 18 patients involving 25 operative lower extremities.²⁴ Fifteen of the patients had diabetic neuropathy while three had idiopathic neuropathy. The researchers achieved satisfactory outcomes for eighty percent of patients and 88 percent of the legs with triple release. The pain improved by an average of four points while numbness improved by an average of 4.6 points. The study noted that when one utilizes proper patient selection criteria, including the presence of a positive Tinel’s sign over the entrapment sites, patients can attain pain relief and restored sensation.
Rader reported results of diabetic nerve release in 39 patients and 49 limbs in 2005.³⁶ A technician, who was blinded to the surgical site in order to prevent adjusted judgment, performed preoperative and postoperative testing. In all but six patients with bilateral nerve decompression, neuropathy medication was discontinued. Patients exhibited a significant improvement of average one- and two-point sensation postoperatively at three and six months with improvement of average levels at six months in comparison to three months. The visual analog scale (VAS) score also improved from a preoperative average of 8.72 to less than an average of 1 postoperatively. Patients had a very high level of satisfaction.
Valdevia, et al., also reported on 100 consecutive nerve decompression cases.³⁷ Sixty of the patients had diabetes while 40 had idiopathic neuropathy. At the follow-up, which occurred at least one year after the surgery, 87 percent of patients with preoperative numbness reported improved sensation, 92 percent with preoperative balance problems reported improved balance, and 86 percent with a pain level of 5 or greater on the VAS scale prior to surgery reported an improved pain level.

In Conclusion
There is a definite learning curve to the diabetic nerve decompression surgery and recovery process. However, the surgery itself is not very complex and one can master it over time. While the idea of nerve decompression in the patient with diabetes continues to be swirled in controversy, the results speak of a far different outcome.
The results for pain relief and return to activity have been excellent. Overall, the surgical decompression patients fare better in regard to ulcer formation and amputation risk than those without decompression.
Diabetic nerve decompression is not for every patient. It is essential to select patients carefully and to make sure that the aforementioned testing and examination findings are present prior to surgery. When one emphasizes proper patient selection and has appropriate training in this procedure, diabetic nerve decompression can be an excellent treatment option for patients with painful neuropathy and nerve compression.
Dr. Baravarian is an Assistant Clinical Professor at UCLA School of Medicine. He is the Chief of Foot and Ankle Surgery at Santa Monica UCLA Medical Center and Orthopedic Hospital. Dr. Baravarian is also the Director of the University Foot and Ankle Institute in Los Angeles.

References:

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