Neuropathic & Dysvascular Arthropathy

Joseph S. Pongratz, CPO, FAAOP
President – Director of Clinical Services
Pongratz Orthotics and Prosthetics, Inc.

Diabetics who suffer from symptoms of peripheral neuropathy are susceptible to chronic ulcers, Charcot deformities, fractures and ultimately amputations. Neuropathic and dysvascular arthropathy secondary to diabetic complications has successfully been managed using the Chronic Relief Orthotic Walker (C.R.O.W). This orthosis is comprised of a solid ankle foot orthosis with a pre-tibial shell extended over the dorsum to enclose the forefoot. It is lined with a soft liner and has a custom multidensity insert with SACH (Solid Ankle Cushioned Heel) and forefoot rocker bottom. The Chronic Relief Orthotic Walker is designed with features that specifically address each level of Tri-Neuropathy (sensory, motor, and autonomic), the location of Charcot deformity (Type 1,2 or 3), and chronic ulceration (Hindfoot, Midfoot or Forefoot). Along with conservation of extremity the Chronic Relief Orthotic Walker has also been utilized as a weight bearing postoperative amputation dressing from lisfranc to symes levels.

Neuropathy is defined as an altered nerve metabolism caused by chronic hyperglycemia (1) and is said to be a true result of diabetes mellitus (8). 50% of diabetic patients will develop neuropathy within twenty years; more importantly 90% of long term diabetics will develop some form of neuropathy in their liftime (9). There is no clinical test for neuropathy, however, medical professionals do know that it is more debilitating in patients with poorly monitored glucose levels (1) and the onset can be gradual or sudden (8). When treating a patient with neuropathy a practitioner must be aware that there are many levels of severity within the three phases (sensory, motor and autonomic) that occur simultaneously and are referred to as Tri-Neuropathy (8).

Sensory neuropathy is the loss of protective sensation to pain, pressure and temperature (1) and with advanced cases patients lose the sense of identity with their feet (8). A commonly used test to determine the level of sensory deficit is the Semmes-Weinstein Filament set (2). This test contains three filaments of different durometer that detects sensory thresholds. It is very important to manage sensory neuropathy correctly because of its association with chronic ulcerations and Charcot collapse deformities.

Motor Neuropathy is the loss of (1) intrinsic musculature, which can result in claw toe deformity, and (2) extrinsic musculature resulting in drop foot and an unstable ankle compartment (8). Muscles function as force producers that move an extremity, they also play a major role in supporting the structural integrity of bones and their articulations. Therefore motor neuropathy results in the loss of these important functions and causes the extremity to be more susceptible to fractures, dislocations, and Charcot collapse. (8).

Autonomic Neuropathy affects the (1) blood flow, as well as (2) sweat and oil secretions in the body. The loss or minor disruption in either of these two systems has significant ramifications that can lead to further complications. Sympathetic denervation results in arterial dilation, which increases blood flow to the foot. In response to the excessive arteriole capacity the blood is shunted to the venous side of circulation bypassing the nutrient vessels that absorb the minerals and promote tissue healing and ectoblastic activity (1). The increase in blood and the loss of the venivasomotor reflex together cause increased venous pressure, blood pooling and promote tissue edema, an unfavorable factor when dealing with would healing (1, 10).

At the onset of diabetes when there are early sign of increased blood sugar levels and body reacts by localized profuse sweating. Fungus and keratin build up in the glands and prevent sweats and oil secretions from nurturing the skin. As a result, skin elasticity is lost and hardened cracked skin permits infection and bacterial growth.

Charcot deformities have been studied by many dating back to 1831 when Mitchell and Charcot first described the condition as a progressive destruction of the insensate joint (10). Later a German surgeon, Volkman, also agreed the deformities were due to progressive micro trauma to the unfeeling joint (4). Along with sensory Neuropathy as a cause of Charcot deformities, increased evidence suggests that autonomic changes that control the nutrients to the bones and joints cause the breakdown of these structures (6,7).

As the population of diabetics increases so does the need to recognize, understand and effectively treat Charcot deformities. Following plain radiographs Charcot deformities must be identified and classified as to the area of the foot involved. Type 1 is the most common form because of its location in the tarsometarsal and naviculo-cunieform joints as 70% of reported cases are in this classification (3). Plantar bony prominences and pronated deformities caused by medial displacement of the talo-navicular joint and calcaneo-cuboid dislocation are typical symptoms that cause the “rocker bottom” appearance (3). Type 2 involves more proximal articulations in the talo-calcaneal, talo-navicular and calcaneal-cuboid joints and Type 3 involving the most proximal articulations, the tibio-talar joint. Type 3 deformities present with either a varus or valgus ankle deviation with accompanying forefoot inversion or eversion. The length of time a patient must unweight the involved joint usually correlates with the osteoblastic activity that is needed to strengthen the bones and joints preparing them for weight bearing forces. Type 3 deformities are clinically the most challenging to orthotically manage because of the weight bearing function of the tibio-talar joint. These forces must be transferred proximally onto the posterior gastrocnemius of patellar tendon area so that further destruction does not occur (5).

The Chronic Relief Orthotic Walker is designed to address each phase of Tri-Neuropathy, each classification of Charcot Deformity, and each location of associated chronic ulcer. A multidensity insert custom made to a positive mold of the patient’s foot is a common modality in treating an insensate foot. If plantar bony prominences exist due to Type1 Charcot deformities extra relief is necessary to ensure proper weight distribution and prevent further ulcer complications. A rigid copolymer bi-valved shell that locks the ankle compartment and prevents further bone displacement also maintains the structural integrity of the Charcot joint. To ensure efficient ambulation a rocker forefoot and SACH are included. The function of the bi-valved shell also minimizes volume changes that result from chronic edema by applying circumferential compression to the extremity. Closing and locking the bi-valved system in the morning when edema is low achieve this. The only removal of the orthosis should occur when the patients need to change a sock due to excessive sweating or when they need to add a sock to maintain volume control and prevent pistoning while weight bearing. The use of compression stockings with low pressure has been used in conjunction with the Chronic Relief Orthotic Walker; however, patient compliance due to retinopathy and limited joint mobility prevented proper donning so the use continued to only certain patients.

Diabetics are faced with a host of complications in their lives, each ranging in its degree of severity. Each phase of Tri-Neuropathy causes debilitating problems that most diabetics will encounter at some point. The Chronic Relief Orthotic Walker can be used to manage a wide variety of complications that help patients maintain or return to a more functional life style and increase their quality of life.

References:

  1. Birke JA Novick A. Hawkins ES. Patout C. A review of Causes of Foot Ulcerations in Patients With Diabetes Mellitus. Journal of Prosthetics and Orthotics 1991; 4:1:13-22
  2. Bowker JII. Neurological Aspects of Prosthetic/Orthotic Practice. Journal of Prosthetics and Orthotics 1993; 5:2:52-54
  3. Brodsky JW, Negrine JI. Orthotic Solutions for Recalcitrant Charcot Deformity. Biomechanics. May 1995,65-68
  4. Brower AC, Allman RM. Pathogenesis of the Neurotrophic Joint; Neurotraumatic vs. Neurovascular Radiology 1981;139-349-354
  5. Carlson JM, Hollerback F. Day B. A Calf Corset Weightbearing Ankle Foot Orthosis Design. Journal of Prosthetics and Orthotics 1991;4:1:41-44
  6. Delano PJ. The Pathogenesis of Charcot Joints. American Journal of Roentgenology 1946; 56:189-200
  7. Edmonds ME: The Diabetic Foot: Pathophysiology and Treatment Clinics in Endocrinology and Metabolism 1986; 15:4:889-916
  8. Elftman N. Clinical Management of The Neuropathic Limb. Journal of Prosthetics and Orthotics 1991; 4:1:1-12
  9. Kay AS Black E. STATS Biomechanics. Feb 1995. 61-64
  10. Michael JW Isbell MA, Harrelson JM. Orthotic Management of Diabetic Neuropathic Arthropathy. Journal of Prosthetics and Orthotics 1991; 4:1:45-55