Charcot Foot: The Silent Emergency in Diabetic Neuropathy

What lies behind it

Diabetic neuro-osteoarthropathy, clinically referred to as Charcot foot, is a progressive destruction of bones and joints. The pathology is based on a combination of two main pathomechanisms, which are discussed in medical literature as the neurotraumatic and neurovascular theories. The neurotraumatic component is based on the loss of protective sensation. Due to diabetic polyneuropathy, affected individuals do not notice microscopic fractures or capsule tears in the tarsal and metatarsal areas. Everyday mechanical stress is continued without dampening compensatory movements, leading to cumulative destruction of the bone substance.

In parallel, the neurovascular theory describes autonomic neuropathy of the peripheral vessels. The sympathetic vasomotor control fails, leading to persistent vasodilation and increased blood flow to the skeletal system. This hyperaemia activates osteoclasts via the RANK/RANKL signalling pathway, causing bone resorption to drastically exceed bone formation. The bone loses its stability, gradually softens, and collapses under body weight.

In the clinical classification according to Eichenholtz, four phases of the disease are distinguished. Stage 0 describes the acute initial stage without radiologically visible bone destruction, but with clinical hyperthermia and swelling. Stage I is the developmental or destructive stage, in which bone fragments, joint dislocations, and collapse of the arches of the foot become visible on X-rays. The Lisfranc joint and the Chopart joint are particularly frequently affected. Stage II represents the repair phase, during which the body attempts to consolidate the debris zones. In Stage III, the consolidation phase, healing occurs, often resulting in an altered, deformed skeletal anatomy.

Typical signs

The most prominent key symptom of acute Charcot foot is sudden, often unilateral redness and swelling of the foot or ankle joint. The discolouration can range from pale pink to deep erythema and frequently decreases slightly when the leg is elevated. A central feature is local hyperthermia. During comparative palpation or measurement using an infrared thermometer, the affected foot demonstrates a temperature difference of more than two degrees Celsius compared to the healthy opposite side.

Due to existing neuropathy, patients rarely complain of pain that corresponds to the severity of the findings. Some merely report an indefinite feeling of pressure, tightness, or a dull, deep ache. This absence of pain frequently leads to a fatal misassessment by those affected. Full weight is continuously placed on the foot, even though microstructural fractures are already present inside.

Differentiation from other clinical conditions requires high clinical vigilance. Deep vein thrombosis is also accompanied by swelling, but usually affects the entire calf and shows no primary bone destruction. Erysipelas, a bacterial infection of the skin, also presents as red and warm, but is almost always accompanied by a high fever, chills, and significantly elevated inflammatory markers in the blood count. A gout attack or phlegmon must also be excluded as differential diagnoses. Differentiating Charcot foot from osteomyelitis is particularly complex when open skin defects are already present.

Everyday causes

In daily life, acute Charcot joint damage rarely arises without a specific trigger. However, a minor impact is usually sufficient to initiate the cascade. Spraining an ankle slightly on a kerb, tripping over the edge of a carpet, or taking a long walk in new, unsuitable footwear can cause microfractures. Because the body's internal warning system of pain perception remains silent, the body does not react with rest, but rather with continued impact loading.

Inadequate footwear plays a central role. Shoes with overly rigid soles, a lack of a roll-off aid, or an excessively narrow cut generate focal peak loads on the metatarsal bones. If foot deformities such as hallux valgus, splayfoot, or claw toes are already present, the centre of pressure shifts. This static maldistribution of pressure promotes structural changes in the skeleton. Furthermore, autonomic neuropathy leads to reduced sweat secretion, making the skin dry and cracked, which in turn creates entry points for minimal inflammation.

Consider a typical example from clinical practice. Mr K., a 62-year-old patient diagnosed with type 2 diabetes 14 years ago, went on a three-hour hike in the Unterallgäu region. He wore sturdy hiking boots that pinched slightly in the heel area. The next morning, his right midfoot was tightly swollen and noticeably warm. Since Mr K. felt no pain, he interpreted the swelling as ordinary strain and continued his usual work in the garden over the following days. It was only three weeks later, when the shape of his foot broadened visibly and the longitudinal arch flattened, that he sought medical help. By that time, the foot skeleton had already collapsed.

When medical evaluation is necessary

Any newly occurring unilateral swelling or warming of the foot in people with diabetes constitutes a medical emergency. One must not wait to see if symptoms resolve on their own. As soon as a temperature difference between both feet is detected or the skin appears noticeably tight and reddened, a specialized diabetic practice or a specialized foot clinic must be consulted immediately.

The primary goal of acute therapy is the immediate and complete offloading of the affected leg. Anyone who continues to bear weight on the foot despite redness and swelling risks the complete collapse of the bone architecture. At the clinic or specialist practice, following diagnostic imaging using magnetic resonance imaging or X-rays, a total contact cast is applied. This is a special, custom-made full-contact plaster cast or a removable orthosis such as the VACOped boot, which distributes pressure evenly and prevents any movement in the tarsal joints.

Warning signs requiring immediate referral include:

• A visible change in foot shape with collapse of the dorsum of the foot or broadening of the sole.
• A temperature difference of more than two degrees Celsius in side-to-side comparison.
• The emergence of open skin wounds, blisters, or ulcerative changes over prominent bony points.
• Signs of systemic infection such as chills or elevated body temperature.

What podiatric treatment can achieve

Podiatry plays a key role in the interdisciplinary network of diabetic care. In the phase of healed, chronic Charcot foot as well as in prevention, the focus is on preventing secondary damage. Following successful immobilization in the acute stage, irreversible deformities such as a rocker-bottom foot often remain. Extremely high pressure peaks occur at protruding bony points on the sole of the foot, which, if untreated, can rapidly lead to deep ulcerations.

In our practice, we perform a differentiated risk stratification. We check protective sensation using a Semmes-Weinstein monofilament with a testing force of ten grams and test vibration sensation at the ankles using a Rydel-Seiffer tuning fork at 128 Hertz. Regular podologische Komplexbehandlung (comprehensive podiatric treatment) includes the gentle removal of hyperkeratoses and calluses using sterile scalpel blades and rotating diamond burrs. Pressure points are thus relieved in a targeted manner before a subkeratotic haematoma or an ulcer forms underneath.

Once the foot is stable after consolidation, our practice, operating as a practice with a sektoralen Heilpraktikerin für Podologie (sectoral practitioner in podiatry), can independently establish podiatric diagnoses and initiate treatment pathways. If renewed warmth or swelling is noticed during a follow-up treatment, we refer the patient without delay to the treating diabetologists and orthopaedic shoe technicians. Treatment intervals for patients with a history of Charcot foot are typically three to four weeks in order to detect skin changes at an early stage.

What you can do yourself

Patients contribute significantly to the protection of their feet through consistent daily self-checks. Because pain perception is reduced, the eyes must take over the warning function of the nerves. A fixed evening routine helps to notice changes early.

The most important measures for daily self-checks include:

• A thorough visual inspection of the entire surface of the foot, the heels, and between the toes using a hand mirror or a telescopic mirror.
• Manual palpation of skin temperature with the back of the hand or precise measurement with a non-contact infrared thermometer at several defined points on both feet.
• Checking the inside of footwear with the hand before putting shoes on, to detect foreign objects, small stones, or folded lining seams.
• Daily application of urea-containing care lotions to the feet, avoiding the spaces between the toes to prevent fungal infections.

When purchasing shoes, people with diabetes should look for a wide toe box, soft upper material, and an absence of pressure-causing internal seams. Walking without footwear must be strictly avoided. Even on carpets in one's own home, small objects such as pins or toy parts can unexpectedly penetrate the sole of the foot. Walking barefoot increases the risk of injury manifold and is one of the most common causes of secondary wounds in diabetic neuropathy.

Common mistakes

In clinical practice, we regularly encounter misbehaviours and misconceptions that can dramatically worsen the course of Charcot foot. The most severe mistake is treating detected redness and swelling with cold packs or ice bags. Because microcirculation is frequently impaired by diabetes and cold sensation is absent, direct contact with ice leads extremely rapidly to tissue toxicity, frostbite, and irreversible skin necrosis.

Another widespread misconception is continuing to walk in the belief that without pain, no serious injury can be present. Many affected individuals interpret the swelling as harmless insect bites or mild sprains and attempt to make the foot supple again by walking. However, every single step taken on an unstable Charcot foot shatters further bone trabeculae in the skeleton.

Hot foot baths are equally dangerous. Diminished temperature perception prevents the timely detection of scalding, while water softens the calloused skin and facilitates the entry of microorganisms. Attempts to remove calluses or corns independently using rasps, planes, or over-the-counter corn plasters also frequently end in hard-to-heal wounds. The salicylic acid contained in plasters burns healthy tissue and creates deep lesions.

Current evidence and classification

Scientific research on Charcot foot has made significant progress over the past two decades. International guidelines from the International Working Group on the Diabetic Foot [1] emphasize the critical importance of early offloading in stages 0 and I. Studies show that delaying immobilization by just a few weeks increases the rate of permanent foot deformities from 15 percent to over 65 percent.

The S3 guideline of the German Diabetes Society (Deutsche Diabetes Gesellschaft) [2] emphasizes interdisciplinary cooperation between diabetologists, surgeons, podiatrists, and orthopaedic shoe technicians. Structured care pathways have significantly reduced amputation rates in diabetic foot syndrome within specialized centres. Investigations by Rogers et al. [3] further highlight the role of procalcitonin and CRP screening in reliably differentiating between purely aseptic neuro-arthropathic inflammation and bacterial osteomyelitis.

Recent work by Chantelau et al. [4] demonstrates that consistent application of total contact casts or rigidly set orthoses over a period of at least three to six months successfully achieves bone consolidation in the majority of cases. Supplementary studies on biomarker analysis [5] are currently investigating the influence of bisphosphonates and the RANKL inhibitor denosumab on inhibiting osteoclast activity in the acute stage, although evidence for routine pharmacological therapy is not yet established as standard in all guidelines.

Treatment in Memmingen

For patients in the Memmingen region, Unterallgäu, Upper Swabia, and the entire Allgäu, our practice is a reliable point of contact for preventive and follow-up foot health. At FREITAG® Podologie GmbH at Kempterstr. 25, 87700 Memmingen, we work closely with regional specialist physicians and diabetologists to offer comprehensive care for individuals with diabetic foot syndrome.

Owner Helga Maria Freitag brings her years of expertise as a state-recognised podiatrist and sectoral practitioner in podiatry to every treatment. We support you with professional precision, low-pain removal of pressure points, and comprehensive advice on suitable footwear. If you have questions about foot health in diabetes or wish to have a finding evaluated, please reach out through our contact page or find out more on our practice page.

Orthopaedic shoe technology care after consolidation

Following completion of the consolidation stage, restoring mobility without renewed tissue damage is the primary focus. Standard off-the-shelf footwear no longer offers sufficient protection for deformed feet with a collapsed arch or bony prominences. To protect delicate tissue from ulceration, orthopaedic shoe technology plays a central role.

Dynamic pedobarography forms the measurement-based foundation for any orthopaedic fitting. In this process, capacitive pressure-measuring insoles inside the shoe measure pressure distribution under the sole during the roll-off motion. Peak loads exceeding fifty kilopascals are considered a critical threshold for the development of pressure ulcers. Based on these biomechanical data, orthopaedic technicians manufacture custom-fitted insoles using a sandwich technique composed of synthetic materials and foams of varying hardness.

In cases of pronounced deformities, such as the collapse of the Lisfranc or Chopart joints, mere insole provision in off-the-shelf shoes is insufficient. In such cases, the fabrication of custom orthopaedic footwear is required. This features a rigid stiffening frame, a widened ground-contact surface, and an individually positioned butterfly pad or metatarsal rocker sole. This special sole construction shortens the stance phase of the foot and gently rolls pressure over the midfoot without causing the affected joints to bend again. Regular inspection of footwear every six months ensures that material fatigue is detected in good time.

Surgical procedures for progressive deformity

Although conservative therapy with immobilization and pressure relief represents the gold standard, certain disease courses require surgical intervention. If bony prominences on the sole of the foot repeatedly lead to chronic wounds despite custom-made orthoses, corrective surgery is indicated. A surgical measure is always carefully weighed, as any operative stimulus can trigger renewed inflammatory hyperaemia.

A frequently performed procedure is exostosectomy. In this procedure, the surgeon minimally invasively removes the troubling bone spur on the sole of the foot to permanently eliminate the mechanical pressure peak. If, on the other hand, there is a severe deformity or marked instability, bone removal alone is usually insufficient. In such cases, reconstructive arthrodeses are employed. In this procedure, destroyed joint surfaces of the tarsus are resliced or excised, anatomically aligned, and stabilized using angle-stable plates, intramedullary nails, or an external ring fixator.

An accompanying problem in Charcot foot is frequently a shortened Achilles tendon, which significantly increases pressure on the midfoot. Percutaneous Achilles tendon lengthening or a gastrocnemius tenotomy can effectively reduce tension on the hindfoot. Postoperative care again requires a strict offloading phase in a cast or specialized boot over a period of twelve to sixteen weeks. Only when radiologic consolidation of the arthrodesis is confirmed can gradual reloading begin.

Interdisciplinary wound management in complex ulcerations

The occurrence of a skin defect over a collapsed bone structure abruptly alters the prognosis of Charcot foot. Once the barrier function of the skin is broken, pathogens can penetrate freely into deep tissue layers and softened bone tissue. Threatening osteomyelitis or ascending phlegmon in this phase requires highly specialized, stage-appropriate wound management.

Surgical wound debridement thoroughly removes necrotic tissue and fibrinous coatings using a scalpel or sharp curette. Subsequently, modern wound dressings are applied to maintain a moist wound environment and promote granulation. For heavily exuding wounds or deep wound pockets, practitioners frequently utilize negative pressure wound therapy. Here, an electric pump generates continuous negative pressure, typically minus one hundred and twenty-five millimetres of mercury, over a specialized foam dressing. This method enhances local blood circulation, reduces oedema, and draws wound edges together.

Parallel to local wound treatment, microbiological diagnostic workup must be performed. Deep tissue samples from the wound bed identify pathogens such as Staphylococcus aureus or Pseudomonas aeruginosa in order to initiate targeted systemic antibiotic therapy. Blood glucose levels must be monitored and regulated extremely closely during this inflammatory phase, as hyperglycaemia inhibits white blood cell defense function. Only when the wound is completely closed and inflammation has subsided can the transition to definitive orthopaedic shoe fitting take place.