A neuropathic foot - a management scheme: a case report.

The Neuropathic Foot--A Management Scheme: A Case Report Lower extremity neuropathies associated with diabetes mellitus present serious problems that frequently lead to chronic foot ulcers. Plantar sensory loss increases the risk of ulcer development because patients lack the appropriate pain warning and positional feedback systems that signal the need to shift gait patterns, rest, or remove shoes to allow the traumatized foot to heal. [1] When an ulcer has formed, continued walking may lead to infection that could spread into bones and joints, resulting in severe tissue destruction and often amputation. [2]

Neuropathic changes may also affect the motor system and result in muscle imbalances, joint stiffness, and bony deformities. These abnormalities will not result in skin breakdown in a foot with normal sensation. Continuous, concentrated, or repetitive moderate stress to an insensitive foot with deformities, however, greatly increases the risk of injury. [3, 4] A neuropathic fracture (Charcot fracture) may result in deformities secondary to the bony destruction and collapse of the normal architecture of the foot. These deformities frequently become sites of high pressure loading and subsequent ulceration. [5, 6] Although the signs of a Charcot fracture are painless ankle and foot swelling, with redness and warmth, these fractures are often not recognized and treated appropriately by clinicians. [7]

Management of plantar ulcers has included bed rest, whirlpool treatment, electrical stimulation, dressings with or without medication, and hyperbaric oxygen treatment. [8] The results of these regimens are often poor or require lengthy periods of treatment time. Recent studies have demonstrated successful management of ulcers (defined as the length of time needed for complete wound closure with no evidence of drainage or sinus formation) through use of the total contact walking cast (TCC) and molded double-rocker plaster shoe. [1, 9-11]

The concept of the TCC was first introduced by Brand for the treatment of chronic ulcers in patients with Hansen's disease. [12] By increasing the weight-bearing area over the entire surface of the foot, the TCC promotes healing and relieves unperceived, excessive plantar surface pressures on the ulcerated regions of the foot. In addition, the TCC immobilizes the tissues, thereby reducing the chance of spreading the infection through soft tissue movement. It also protects the wound site from outside contaminants and still allows for a maintained patient activity level. [13-15] By addressing one of the primary causes of skin breakdown, the TCC has been incorporated successfully into treatment programs for management of the diabetic foot.

Successful management of the plantar ulcer, as previously defined, is only the initial step in the treatment regimen. To be truly successful, the treatment approach must also prevent reulceration by incorporating techniques designed to protect the foot and reduce foot pressures for the rest of the patient's life.

The purpose of this case report is to present an effective management approach for the healing and long-term care of a neuropathic plantar ulcer in a patient with diabetes and an accompanying Charcot fracture.

Patient History

The patient was a 46-year-old man who was initially seen at the Gillis W Long Hansen's Disease Center on April 27, 1987, for evaluation of a plantar lesion unresponsive to a treatment program of local wound care and hyperbaric oxygen. The patient's height was 5 ft (*1) 8 in, (*2) his weight was 320 lb, (*3) and he had a 10-year history of diabetes mellitus. For the two years preceding the evaluation, he had been insulin dependent. In 1985, the patient underwent surgery for a below-knee amputation secondary to an eight-year history of chronic foot swelling and redness, including a two-year history of plantar ulceration. On April 1, 1987, he developed a fever and chills and became aware of an ulcerative site over the fifth metatarsal head of his intact left extremity. Prior to this visit, the patient was ambulating with a below-knee prosthesis, using a cane, and was independent in all activities of daily-living.

Assessment

In the intact extremity, the patient demonstrated Fair to Good (3/4) muscle strength in all muscle groups except for a muscle test grade of Zero (0) in the extensor hallucis longus muscle and the intrinsic muscles of the foot. The neurological examination revealed loss of protective sensation throughout the plantar surface of the foot, confirmed by the inability to perceive nylon monofilaments calibrated to bend at 75 g of force. [16]

Active range of motion showed gross restrictions in all motions with the exception of plantar flexion. The foot demonstrated an equinus deformity, mild forefoot varus, hallux limitus, and bony prominences at the base and head of the fifth metatarsal.

The ulcer was located over the left fifth metatarsal head and was 1.9 cm in diameter (Fig. 1). A tract communicating with the ulcer probed to a depth of 1.5 cm (Grade 2 on the Wagner scale) and revealed joint fluid. Although there was no evidence of infection, the midfoot and forefoot had temperature increases of 3[degrees]C relative to the ankle. [7] A vascular examination using Doppler pressures indicated an ankle-brachial index of 0.89. (An absolute value of [is greater than or equal to] 55 mm Hg of pressure at the ankle or an ankle-brachial index of [is greater than or equal to] 0.45 are considered adequate for healing [18,19]). The patient's footwear could not be assessed because he could fit only a slipper onto his edematous foot at the time of the initial examination. Roentgenograms of the patient's foot indicated previously undiagnosed neuropathic fractures of the left navicular and first cuneiform bones, as well as bony absorption of the fifth metatarsal (Fig. 2).

Treatment

The goals of treatment were to heal the ulcer and Charcot fracture and to implement a course of management to protect the foot and prevent recurrent ulceration. The ulcer was cleaned, debrided of necrotic and calloused tissue, and dressed with antiseptic and a light gauze pad. A TCC was applied in the manner described by Coleman et al. [13] The first cast was changed after one week. Thereafter, the casts were changed at one- to two-week intervals. During the casting period, the patient continued to work at his office job. He was instructed to use his cane and restrict ambulation as much as possible.

By June 9, 1987, the ulcer was completely closed, but follow-up roentgenograms showed that the fracture sites were still not healed. A 3-D orthopedic walker (*4) was ordered for the patient. This orthopedic device was selected because it has been shown to be effective in reducing plantar foot pressures and provide immobilization of fractures, while still allowing the patient to ambulate. [20] Further pressure reduction was achieved by the fabrication of a molded footbed of Plastazote [R], (*5) which was placed inside the 3-D device (Fig. 3). Skin temperatures were used as an indicator of fracture healing.

The patient's status continued to improve during the time of fracture healing with the exception of recurrent foot swelling. A Jobst custom-made garment (*6) was ordered, and the swelling resolved with wearing the garment. By September 28, 1987, the foot temperatures and swelling had stabilized, and the roentgenograms showed that the Charcot fracture was healed.

At this time, the patient was fitted with molded Plastazote [R] sandals (Fig. 4), which were worn until a newly purchased pair of extra-depth oxford shoes could be modified. [21] The sandals were molded to the shape of the sole of the foot and provided relief under the bony prominences as well as cushioning for shock absorption. [22]

Modifications were made on the definitive footwear and included an outsole modification with a rigid rocker sole. The rocker outsole design has been shown to significantly reduce pressure and shear stresses on the forefoot during ambulation. [21,23] The greatest reductions in forefoot pressures have been found in shoe designs that have a take-off point of the rocker at a location of 50% of the sole length (Fig. 5). [24] Further modifications were made to the insole of the shoe from positive models of the patient's foot. An insole was made with a combination of PPT [TM] (Poron) (*7) and Pe-Lite [TM] (*8) with added relief provided under the areas of bony prominences at the fifth metatarsal. The patient progressively increased wearing time of the shoes, alternating with sandal wear throughout the day.

Patient education was ongoing throughout treatment and consisted of instruction in daily foot inspection, foot care, and routine shoe inspection. As of August 22, 1988, the patient has exhibited no evidence of recurrent ulceration or progression of the Charcot foot deformity.

Discussion

Tissue breakdown in the foot of the diabetic patient is commonly caused by a combination of neuropathy and infection, with or without vascular impairment. [4] The physical therapist's responsibilities for the care of the person with loss of sensation of the foot must include a thorough evaluation, appropriate selection of treatment, and patient education with an approach that strongly focuses on the causes of tissue breakdown. The more common manifestations of peripheral neuropathy are appreciated by most clinicians; however, a manifestation that frequently is not recognized is the neuropathic (Charcot) fracture. This fracture may result in potentially unstable deformities leading to high-pressure areas and devastating ulceration.

The treatment approach used in this case study was successful in wound healing and also accounted for the mechanical stresses that continue to exist in the insensitive foot, even after the wound was healed. This case study demonstrated the need for a program of ulcer management that emphasizes interim footwear (eg, 3-D orthopedic walker, molded Plastazote [R] sandals) to allow time for tissue maturation of an extremely fragile, newly headed ulcer. The 3-D orthopedic walker also provided the necessary immobilization for the lengthy healing time of the patient's Charcot fracture. Any delay in providing protective footwear to the patient would likely result in reulceration. [21]

Definitive footwear is the final level in the management scheme. Extra-depth shoes were recommended to provide adequate space to accommodate the molded insert. A rigid rocker sole has been shown to reduce shear stresses on the foot as well as minimize the damage to toes that have limited motion at the metatarsophalangeal joint. A curved-sole design was incorporated into this patient's shoe to allow smooth transition from heel-strike to push-off and still reduce metatarsal head pressure by providing a fulcrum or take-off point at 50% of the shoe sole length.

The symptoms of this patient's intact foot closely resembled those that led to the unfortunate outcome of ulceration and amputation of his opposite foot. Frequently, clinicians feel that the remaining extremity of an individual with a lower extremity amputation must withstand excessive stresses, and they are not optimistic about the healing capabilities of ulcerated limbs. This patient's symptoms of foot swelling, redness, increased temperatures, ulceration, and Charcot fractures, however, were recognized and successfully managed by a noninvasive, progressive treatment approach.

(*1) 1 ft = 0.3048 m.

(*2) 1 in = 2.54 cm.

(*3) 1 lb = 0.4536 kg.

(*4) 3-D Orthopedic, Inc, 10520 Olympic Dr, Dallas, TX 75220.

(*5) Bakelite Xylonite Ltd, London, England, distributed by AliMed Inc, 297 High St, Dedham, MA 02026.

(*6) The Jobst Institute Inc, 653 Miami St, PO Box 653, Toledo, OH 43694.

(*7) Professional Protective Technology, 21 E Industry Ct, Deer Park, NY 11729.

(*8) Durr-Fillauer Medical Inc, 2710 Amnicola Hwy, Chattanooga, TN 37406, distributed by Apex Foot Products Corp, 200 Forest Ave, Englewood, NY 07631.

References

[1] Walker SC, Helm PA, Pullium G: Total contact casting and chronic diabetic neuropathic foot ulcerations: Healing rates by wound location. Arch Phys Med Rehabil 68:217-221, 1987

[2] Brand PW: Management of the insensitive limb. Phys Ther 59:8-12, 1979

[3] Birke JA, Sims DS: The insensitive foot. In Hunt G (ed): Physical Therapy of the Foot and Ankle. New York, NY, Churchill Livingstone Inc, 1988, pp 133-168

[4] Brand PW: The diabetic foot. In Ellenberg M, Rifkin H (eds): Diabetes Mellitus: Theory and Practice, ed 3. New Hyde Park, NY, Medical Examination Publishing Co Inc, 1983, pp 829-849

[5] Harris JR, BRand PW: Patterns of disintegration of the tarsus in the anaesthetic foot. J Bone Joint Surg [Br] 48:4-9, 1966

[6] Warren AG: Tarsal bone disintegration in leprosy. J Bone Joint Surg [Br] 53:688-692, 1971

[7] Goldman F: Identification, treatment, and prognosis of Charcot joint in diabetes mellitus. J Am Podiatr Assoc 72:485-490, 1982

[8] Gault WR, Gatens PF Jr: Use of low intensity direct current in management of ischemic skin ulcers. Phys Ther 56:265-269, 1976

[9] Helm PA, Walker SC, Pullium G: Total contact casting in diabetic patients with neuropathic foot ulcerations. Arch Phys Med Rehabil 65:691-693, 1984

[10] Sinacore DR, Mueller MJ, Diamond JE, et al: Diabetic plantar ulcers treated by total contact casting: A clinical report. Phys Ther 67:1543-1549, 1987

[11] Diamond JE, Sinacore DR, Mueller MJ: Molded double-rocker plaster shoe for healing a diabetic plantar ulcer: A case report. Phys Ther 67:1550-1552, 1987

[12] Brand PW: The insensitive foot. In Jahss MH (ed): Disorders of the Foot. Philadelphia, PA, W B Saunders Co, 1982, vol 2, pp 1266-1286

[13] Colemann WC, Brand PW, Birke JA: The total contact cast: A therapy for plantar ulceration on insensitive feet. J Am Podiatr Med Assoc 74:548-552, 1984

[14] Birke JA, Sims DS, Buford WL: Walking casts: Effect on plantar foot pressures. J Rehabil Res Dev 22(3):18-22, 1985

[15] Pollard JP, LeQuesne LP: Method of healing diabetic forefoot ulcers. Br Med J 286:436-437, 1983

[16] Birke JA, Sims DS: Sensory threshold in the ulcerative foot. Lepr Rev 57:1-9, 1986

[17] Bergtholdt HT: Temperature assessment of the insensitive foot. Phys Ther 59:18-22, 1979

[18] Wagner W: A Classification and Treatment Program for Diabetic, Neuropathic, and Dysvascular Foot Problems. American Academy of Orthopedic Surgeons Instructional Course Lecture, vol 28, 1979, pp 1-46

[19] Raines JK, Darling RC, Buth J, et al: Vascular laboratory criteria for the management of PVD of the lower extremities. Surgery 79:21-29, 1976

[20] Birke JA, Nawoczenski DA: Orthopedic walkers: Effect on plantar foot pressures. Clinical Prosthetics and Orthotics 12:2,74-80, 1988

[21] Coleman WC: Footwear in a management program of injury prevention. In Levin ME, O'Neil LW (eds): The Diabetic Foot. St Louis, MO, CA Mosby Co, 1988, pp 293-309

[22] Hampton GH: Therapeutic footwear for the insensitive foot. Phys Ther 59:23-29, 1979

[23] Pollard JP, LeQuesne LP, Tappin JW: Forces under the foot. J Biomed Eng 5:37-40, 1983

[24] Nawoczenski DA, Birke JA, Coleman WC: The effect of rocker sole design on plantar forefoot pressures. J Am Podiatr Med Assoc 78:455-460, 1988

D Nawoczenski, Med, PT, is Assistant Professor, Department of Physical Therapy, College of Allied Health Professions, Temple University, 3307 N Broad St, Philadelphia, PA 19140 (USA).

J Birke, MS, LPT, is Chief of Physical Therapy, Gillis W Long Hansen's Disease Center, River Rd, Carville, LA 70721.

S Graham, MS, LPT, is Staff Physical Therapist, Gillis W Long Hansen's Disease Center.

E Koziatek, RPT, is Deputy Chief Physical Therapist, Gillis W Long Hansen's Disease Center.

This article was submitted February 25, 1988; was with the authors for revision for 13 weeks; and was accepted October 12, 1988.