Neuropathic osteoarthropathy is a debilitating condition that affects diabetic patients with peripheral neuropathy. This distinct pathologic entity, commonly known as Charcot’s arthropathy or Charcot’s joint disease, is characterized by pathologic fractures, joint dislocation and deformity, resulting in a foot at high risk for ulceration and amputation in severe cases. Armstrong, et. al., found the prevalence of Charcot’s arthropathy ranges between 0.16 percent in the general diabetic population of patients to 13 percent of patients presenting to a high-risk diabetic foot clinic.1 Although several theories of this joint destructive process have emerged, the etiology is largely unknown and is probably multifactorial. Neuropathy and trauma are believed to be the two primary components in the development of Charcot’s joint disease. Nerve dysfunction may be autonomic in nature as well, thus exhibiting abnormal vasomotor regulation. Autonomic neuropathy is central to the development of the Charcot’s foot, leading to hyperemia, increased bone resorption and osteopenia. Increased blood flow promotes resorption of debris with a concomitant resorption and weakening of healthy bone. Increased lower limb blood flow in diabetes, likely a result of sympathetic denervation, is also associated with arteriovenous shunting. This increased blood flow in neuropathic limbs has been proven by studies such as plethysmography and venous pO2. Often, you may notice that the veins on the dorsum of the Charcot foot are mildly distended with increased skin temperatures as opposed to the contralateral non-affected side. Pedal pulses in patients with neuropathic osteoarthropathy are usually palpable. What The Literature Suggests One study involving over 100 patients with Charcot’s disease and quoted by Jeffcoate, et. al., showed the ankle/brachial index was greater than 1.0 in every case.2 Neuropathic patients also have a loss of pain perception, sympathetic functioning and proprioceptive function. With these sensory losses, joints are subjected to stresses that would otherwise not take place with intact protective mechanisms. Continued ambulation results in capsular and ligamentous attenuation and joint laxity, which then lead to distension and subluxation of joints. The process then continues with cartilage fibrillation, osteochondral fragmentation and pathologic fractures. Further joint destruction precedes a natural hyperemic response to injury, causing additional resorption and destruction of the joints.3 Although there’s been much discussion on causative factors, the etiology still lies somewhere between neurovascular and neurotraumatic theories. An article from The Journal of Bone and Joint Surgery revealed elevated peak plantar pressure in patients who have Charcot’s foot.4 This increased pressure, when combined with a tight Achilles tendon secondary to glycosylation, creates significant strain in the midtarsal joint region, which leads to collapse. The most common anatomical location of Charcot’s joint disease is at Lisfranc’s (tarsometatarsal) and Chopart’s (talonavicular/calcaneocuboid) joints in more than 80 percent of foot and ankle occurrences.1,4 Diagnostic Essentials For Detecting Charcot’s Arthropathy The disease process can be divided into three stages based on pathologic radiographic findings, which Eichenholtz described in 1966.5 The developmental stage, which is destructive in nature, is characterized by joint laxity, subluxation, osteochondral fragmentation and debris formation. A positive synovial biopsy showing osseous debris in thickened synovium is pathognomonic of Charcot’s foot at this stage. The coalescence stage of the process is marked by absorption of much of the fine debris and fusion of larger fragments of bone. Reconstruction is the final stage of the Charcot’s process and is marked by remodeling of joint architecture, revascularization and remodeling of bone fragments. The prognosis and outcome of any patient with neuropathic osteoarthropathy is highly dependent upon the amount of destruction taking place during the developmental phase. This destruction is directly proportional to the amount of trauma or weightbearing and stresses the joints are put under during the active process of the disease. Perpetuation of the destructive cycle is highly dependent upon continually introduced stress to the neuropathic joints, leading to a poor prognosis.3 The diagnosis of acute Charcot’s arthropathy relies on your awareness of the condition and having a high index of suspicion in susceptible patients. Often, patients present with comorbid states (obesity, poor blood glucose control, coronary artery disease, peripheral vascular disease, infection) along with impaired immunity. Within your armament of treatment modalities, it is imperative for you to utilize a thorough internal medicine, endocrinology, vascular and pedorthist work-up in order to provide the best possible outcome and prognosis for the patient. Early diagnosis of acute Charcot’s arthropathy results from clinical signs of unilateral swelling, elevated skin temperature, erythema, joint effusion and bone resorption in an insensate foot. These clinical entities, absent any skin lesions or ulcerations, are often pathognomonic of the disease. Often times, if the sensory loss is not complete, patients will present with some degree of pain despite an epicritic lack of sensation.6 This situation should definitely raise your clinical suspicion of Charcot’s foot. Caputo, et. al., discussed several critical aspects regarding diagnosis of the Charcot’s foot that will minimize the risk of limb loss in this relatively common complication.7 (See “Essential Tips On Minimizing Limb Loss Caused By Charcot” on page 34.) Insights On Appropriate Wound Care Regimens Preventing amputation in complicated diabetic patients with ulcer and arthropathy requires patience, a thorough knowledge and understanding of the disease process and, sometimes, creativity. You can use several techniques to treat diabetic ulcerations and Charcot’s arthropathy. At our institution, the majority of neuropathic patients are diabetic with a small percentage resulting from alcohol abuse, spina bifida, spinal cord injuries, syphilis and work-related toxin exposure. While sharp debridement remains the hallmark of wound care in our foot and ankle clinic, we commonly use wound gels and have done so even more in recent years, given the continuing advances in wound care biochemistry. In regard to the wound care regimen at our clinic, we use cadexomer iodine (Iodosorb gel) for heavily draining wounds and commonly employ gentian violet to fight wound maceration in a total contact cast. For granulating wounds, we’ll use wet-to-dry dressings and occasionally becaplermin. We use papain-urea to treat mild to moderately fibrotic wounds. We’ve also been able to achieve good clinical results in using papain-urea and chlorophyll combinations to treat granulating wounds. How To Ensure The Success Of Total Contact Casting Total contact casting (TCC) remains the gold standard to offweight the insensate foot and plantar ulcerations. Wound location plays a role in determining the effectiveness of the cast. You can significantly reduce forefoot pressures and, more importantly, impulse (force x time) via total contact casting. This modality provides somewhat less reduction for midfoot pressures. Rearfoot ulcerations do not respond as well to total contact casting and the modality actually increases the impluse in this area so it is usually better to use other treatment options for these ulcerations. A majority of patients develop Charcot’s arthropathy in the midfoot arch area. This makes the arch and entire midfoot susceptible to collapse and chronic ulcer formation. You need to be aggressive in applying a TCC, paying particular attention to the patient with Charcot’s foot. Keep in mind that those who are suffering from acute Charcot’s arthropathy are usually very edematous initially. Therefore, you should watch for loosening and pistoning of the cast. This is particularly true for the initial cast, which you should check for fit within three to four days of initial casting and change it if necessary. Change total contact casts in Charcot patients with associated ulcerations at least weekly, depending on drainage amount. For those patients without open wounds, change casts every one to two weeks. We apply eight to 12 TCCs per week in our clinics for both acute Charcot and plantar ulcerations. At each visit, be sure to take skin temperatures (via dermal thermography) on both feet and ankles so you can measure pedal temperature differences objectively. This allows you to monitor the progress of consolidation and extremity cooling. When You Should Consider External Fixation Surgical treatment of Charcot’s deformity can be divided into two indications: those patients with an acute/ emergency need basis and those with prophylactic need due to failed conservative measures or who are beyond the scope of conservative measures (such as custom bracing and other custom devices). More specifically, the patients in the first category may be cellulitic with abscess, with or without osteomyelitis and/or sepsis. Charcot patients with osteomyelitis undergo staged surgical correction, with incision and drainage, removal of infected bone and packing with antibiotic beads in preparation for later arthrodesis. A relatively common example of this is performing a tibial-calcaneal arthrodesis after resecting an osteomyelitic talus secondary to Charcot’s deformity. This is a great indication for an external fixator ring frame. By using this modality, you can avoid the direct area of resected infected bone, provide exceptional strength and stability, and it gives you the opportunity to dynamize during the healing process. You can also use the external fixator frame for midfoot/ tarso-metatarsal Charcot correction. You would bend the smooth wires adjacent to the site of arthrodesis toward each other before attaching them to the footplate portion of the frame. This facilitates compression of the arthrodesis site once the wires are tensioned. Should You Combine Simple Resection With Arthrodesis? You can perform Charcot planing or simple resection of the bony deformity by itself or in conjunction with arthrodesis. You may also perform simple resection of prominent bone without reconstructive arthrodesis if there is no major gross deformity of the foot that custom shoes or bracing could not control (it’s only the portion you are resecting) and the resection of bone (planing) must not cause joint instability in the area of resection. Otherwise, it is probably necessary to perform joint resection and deformity correction with arthrodesis in order to obtain a functionally stable foot. Regardless of the surgical treatment, we do perform a tendo-Achilles lengthening on our diabetic Charcot patients who undergo surgery. Tendon shortening is a consistent clinical observation we see among patients with diabetic neuropathy. This shortening causes severe equinus, which can contribute to Charcot collapse of the foot. Indeed, Achilles tendon lengthening should help reduce a major contributing force to Charcot development. What About Platelet Concentrates And Bisphosphonates? In our practice, we are using Symphony (DePuy) autologous platelet concentrate without exception on all Charcot reconstructive arthrodesis procedures. This system allows you to rapidly prepare platelet rich plasma from a small volume of patient blood. When activated, platelets release granules that contain a plethora of growth factors. Place the platelet concentrate into the site of arthrodesis prior to fixation and closure. Additionally, if bone grafting (autograft or allograft) is required, you should soak the graft material in the platelet concentrate material prior to implantation. We have employed bisphosphonates, such as Alendronate (Fosamax), to supplement the treatment of Charcot arthropathy in our practice. According to a 2001 United Kingdom study, this class of medications has been shown to reduce the amount of calcium lost from bone and increase bone density via inhibition of osteoclastic bone resorption.8 You can easily appreciate the potential benefits for the non-weightbearing patient who is recovering from acute Charcot’s arthropathy. Indeed, you can emphasize these easily dosed medications throughout the Charcot treatment course. Final Notes It is essential to continually educate patients on the pathology of Charcot’s deformity via detailed radiographic explanation and the use of foot and ankle models. We repetitively emphasize the importance of tight glycemic control, urge patients to stop smoking and stress the importance of patient compliance, emphasizing non- or partial weightbearing, extremity elevation and follow-up evaluation. Although continued research will most likely produce additional and promising treatment modalities, the standard of care for Charcot’s foot remains the same. A high index of clinical suspicion along with early diagnosis, aggressive treatment, consistent patient care and a team approach are essential and will lead to the most acceptable results and optimistic prognosis for the patient. Dr. Pupp is the Clinical Director of Kern Hospital and Medical Center Foot and Ankle Clinic in Warren, Mich. He is a Fellow of the American College of Foot and Ankle Surgeons and is also the Clinic Director at the Sinai Grace Diabetic Foot Center in Detroit. Dr. Hellmann and Dr. Savage are Fellows in Rearfoot/Charcot Reconstructive Surgery at the Kern Hospital & Medical Center.
References 1. Armstrong DG, Peters E: Charcot’s Arthropathy of the Foot. Journal of the Am Pod Med Assoc 92: 390, 2002. 2. Jeffcoate W, Lima J, et. al.: The Charcot Foot. Diabetic Medicine 17: 253, 2000. 3. Kozak GP, Hoar CS, Rowbotham JL, et. al.: “The Diabetic Charcot Foot,” in Management of Diabetic Foot Problems, p 103 WB Saunders, Philadelphia, 1984. 4. Armstrong DG, Lavery LA: Elevated peak plantar pressures in patients who have Charcot arthropathy. J Bone Jt Surg Am 80: 365, 1998. 5. Eichenholtz, SN: Charcot Joints, Charles B. Thomas, 1966, Springfield, Ill. 6. Armstrong DG, Lavery LA: Acute Charcot’s arthropathy of the foot and ankle. Phys Ther 78: 74, 1998. 7. Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P: The Charcot foot in diabetes: six key points. Am Fam Physician 57: 2705, 1998. 8. Jude EB, Selby PL, et. al.: Bisphosphonates in the treatment of Charcot neuroarthropathy: a double-blind randomized trial. Diabetologia 44: 2032-2037, 2001.