Decompression Surgery to Reduce Diabetic Peripheral Neuropathy
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.
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