Dr. Chandler is in private practice in Cleburne, Texas.
A 62-year-old moderately overweight white man with a longstanding history of insulin-dependent diabetes mellitus and comorbidity of decreased circulation presented initially on November 23, 2004. The patient had a longstanding history of ongoing diabetic peripheral neuropathy with previous failure of medications to relieve his symptoms. He had tried over-the-counter preparations, including capsation agents, which had not alleviated his symptoms. He described the sensation in his feet and legs as a burning and stinging sensation, which was worse in the evening. The patient was seen in the past for diabetic foot care as well as a left ankle sprain. Previously, the patient had been placed in diabetic shoes with molded accommodative inner soles.
The patient had no known drug allergies. His past surgical history was remarkable for bilateral total knee arthroplasty. In addition to insulin-dependent diabetes mellitus, his medical history was significant for osteoarthritis, headaches, decreased circulation, glaucoma, and hearing problems. The patient had a negative history of stomach ulcers, liver disease, lung disease, kidney disease, and cardiac problems. He reported that his blood sugars fluctuate, and his last hemoglobin A1c averaged 9. His past family history was noncontributory.
The patient’s medications included Altace 5 mg daily and Protonix 80 mg twice a day by mouth. His insulin regimen was a total of 120 units of NovoLog 70/30 daily with Humulin Regular 20 units on a sliding scale as needed.
The patient was married and denied alcohol consumption. He quit smoking in 2000, and prior to that time, he was a 1-pack-a-day smoker for approximately 20 years.
At presentation, the lower-extremity examination revealed decreased turgor, temperature, and texture and absence of hair growth of bilateral lower extremities. Nail plates were thickened, dystrophic, yellowish to yellowish brown, and lusterless in appearance in 1 through 5 of both feet. Pedal pulses were slightly palpable or diminished and rated at 1/4 for dorsalis pedis and posterior tibial arteries. Venous plexus filling time was less than 4 seconds bilaterally. The patient presented with telangiectasia as well as varicosities of bilateral lower extremities. Pedal edema was noted as 1+ on both lower extremities. The patient had no sign of lymphedema or lymphangitis of either lower extremity. Gait analysis revealed an antalgic type gait with increased pronation. He had decreased muscle group power and function for dorsiflexors, plantar flexors, invertors, and evertors in bilateral lower extremities. Hammertoe deformity of the fifth toe bilaterally was noted.
The patient’s skin was dry and scaly, and fissuring was noted on bilateral heels. He had a flexible pes cavus foot type.
The patient’s neurological evaluation revealed decreased vibratory and sharp/dull sensation of bilateral lower extremities. Mulder sign and Tinel sign were negative and Babinski reflex was absent for bilateral lower extremities. He reported altered sensation of both feet and described a stinging and burning sensation, which was worse in the evening. Deep tendon reflexes were palpable and rated at 2/4.
The patient was not at loss of protective sensation. Dyskinesia was noted on bilateral lower extremities. At presentation, the patient was in off-the-shelf extra-depth shoes with heat-molded inner soles. The patient was first placed on a trial of Metanx in June 2005. He was subsequently followed up on June 20, 2005, secondary to follow-up of a left ankle sprain. At that time, the patient reported that the burning and stinging sensation had improved and requested a prescription. At a follow-up office visit on August 10, 2005, the patient again reported that the condition of his bilateral lower-extremity peripheral neuropathy was greatly improved, and the burning and stinging sensation had decreased. The patient also reported decreased restless leg-type sensation in the evening. He had been placed on a 3-month prescription of Metanx on June 20 and had been taking the medication once daily by mouth as first instructed. He reported no problems with the medication, and no adverse effects were noted. On August 26, 2005, the patient again reported improvement of burning and stinging sensation of the balls of both feet. At an additional 2-month follow-up, he again reported improvement.
Commentary
David E. Allie, MD
This elderly patient has responded to Metanx therapy but by description also has significant lower-extremity PAD by exam with 1/4 distal pulses and would benefit from a vascular consultation. We must remember that the patient with diabetes is at 7–40 times greater risk for amputation in his or her lifetime than the patient without diabetes, and 1 of every 3 patients with diabetes will experience critical limb ischemia sometime in his or her lifetime.
Allen M. Jacobs, DPM
The nocturnal presentation of symptomatology in Dr. Chandler’s patient is common in association with diabetic neuropathy. One must be careful to establish and document the coexistence of adequate circulation in such a patient, as rest pain may also be associated with ischemia.
Dr. Chandler describes his patient as having dry, scaly skin with fissuring. He also noted pedal edema and nail dystrophy. These observed changes from normal may be reflective of a variety of disorders, including autonomic neuropathy with neurogenic edema and sudomotor and vasomotor alteration. I have always believed that the patient with evidence of autonomic neuropathy is at greater risk for harm than the patient with simple loss of protective sensation. Unfortunately, without referral of the patient for specific testing of such parameters as skin sweat function or skin conductivity, the presence of autonomic neuropathic changes in the foot is inferred but not proven, as such changes are not pathognomic.
Dr. Chandler also noted decreased muscle strength in his patient. Sarcopenia is a natural consequence of aging; however, it may also be a consequence of diabetes or diabetic neuropathy. Loss of muscle strength has been demonstrated in men as having a direct relationship to level of glycemia. This may be a direct metabolic effect or may be related to diabetic motor neuropathy. Decreased muscle mass results in less glucose utilization. Together with associated decreased activity with aging, sarcopenia is a factor contributing to hyperglycemia. Decreased muscle mass in the feet of patients with diabetes has been demonstrated by musculoskeletal imaging. The result of this is deformity of the foot, abnormal pressure distribution, and possibly ulceration and the sequelae of ulceration. The high arch foot observed by Dr. Chandler in this patient may represent such a deformity.
We tend to think about the effects of our treatment of diabetic neuropathy in terms of either restoration of sensation or the interdiction of disturbing parathesias and dysesthesias. However, the effects of autonomic neuropathy and motor neuropathy may be equally disruptive to the lives of our patients. The effects of methylcobalamin, L-methylfolate, and pyridoxal 5’-phosphate on motor or autonomic neuropathy may be as or more important than the effects of these vitamin B complexes on the sensory nerves. Again, from a personal clinical perspective, I initiate therapy with these agents when confronted with evolving signs or symptoms of sensory, motor, autonomic, or entrapment neuropathies.
Antidepressant and antiseizure medications have antinociceptive properties for diabetic neuropathy, but they also have more potentially significant side effects than agents like Metanx. In addition, Metanx offers a potential remittive action on diabetic neuropathy, which many alternative agents used for the management of diabetic neuropathy may not offer.
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