Charcot foot
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Charcot foot, also known as Charcot neuro-osteoarthropathy, is a severe complication of peripheral neuropathy, most commonly associated with diabetes. The disease involves the bones, joints, and soft tissues of the foot or ankle. Its essence is a rapid inflammatory response combined with the weakening of the bone structure, microfractures, ligament damage, and progressive joint destabilization. Impaired pain perception allows the patient to continue weight-bearing on the affected limb, which accelerates the development of deformities. Early diagnosis and immediate offloading of the foot help limit tissue destruction. Care should be managed by an interdisciplinary team including a diabetologist, orthopedist, surgeon, wound care specialist, physiotherapist, and podiatrist.
Charcot foot - who does it affect
Charcot neuro-osteoarthropathy develops primarily in people with advanced peripheral neuropathy, which is damage to the nerves responsible for sensing pain, temperature, touch, and limb position. The most important risk group consists of patients with long-standing type 1 or type 2 diabetes, especially with coexisting other microangiopathic complications.
The risk is increased by:
- long duration of diabetes,
- persistent hyperglycemia and high glycemic variability,
- loss of protective sensation in the feet,
- autonomic neuropathy affecting blood flow regulation and skin sweating,
- chronic kidney disease, especially requiring dialysis therapy,
- a history of ulceration or amputation within the lower limb,
- foot deformities and gait biomechanics disorders,
- excess body weight,
- trauma, sprain, fracture, or surgical procedure within the foot,
- a sudden increase in physical activity with impaired sensation.
Less frequently, Charcot arthropathy accompanies other causes of neuropathy, including spinal cord diseases, alcohol abuse, nutritional deficiencies, leprosy, and selected neurological diseases.
The disease usually affects one foot, although in some patients changes also appear on the opposite side over time. Particular observation is required for all individuals with neuropathy who present with unilateral warmth, redness, or swelling of the foot.
Charcot foot - how it develops
The development of Charcot foot results from the interplay of neuropathy, intensified inflammation, abnormal bone remodeling, and repetitive mechanical stress. The loss of protective sensation limits the ability to recognize microtrauma. The patient continues to walk, and subsequent overloading worsens damage to bones, cartilage, joint capsules, and ligaments.
In the active phase of the disease, excessive activation of the RANKL pathway occurs, which is the system regulating the formation and activity of osteoclasts. Osteoclasts are the cells responsible for bone resorption. The predominance of resorption over the formation of new bone tissue leads to a reduction in its strength and susceptibility to fractures.
The course typically includes three overlapping stages:
- the active phase, with intense inflammation, swelling, warmth, and progressive osteoarticular damage;
- the coalescence phase, in which the inflammatory response gradually subsides, and bone fragments undergo resorption and organization;
- the remission and remodeling phase, with the consolidation of the new foot architecture.
Advanced midfoot damage can lead to the collapse of the longitudinal arch and the development of the characteristic rocker-bottom deformity, a foot with a rocker-like plantar profile. Protruding bone fragments create high-pressure areas that are particularly prone to calluses, subkeratotic hematomas, and ulcerations.
Charcot foot - how to recognize it
Active Charcot foot should be suspected in a person with peripheral neuropathy when one foot becomes noticeably warmer, swollen, and red. The onset may be sudden, and the medical history sometimes includes minor trauma or increased activity. Pain varies in intensity. Preserved deep sensation or partial neuropathy may cause pain, whereas advanced nerve damage promotes minimal pain symptoms despite extensive destruction.
Diagnostic evaluation includes:
- examination of both feet, their shape, stability, blood supply, and skin condition,
- assessment of protective sensation with a monofilament and vibration sensation with a tuning fork,
- measurement of skin temperature at corresponding points on both feet,
- X-rays of the foot and ankle, preferably weight-bearing views, if the clinical condition permits,
- magnetic resonance imaging in the case of normal or inconclusive radiological findings,
- computed tomography when precise visualization of bone architecture is needed,
- laboratory tests helpful in evaluating infection and other causes of inflammation.
The early phase may present with normal radiological findings. Magnetic resonance imaging then reveals bone marrow edema, microfractures, and soft tissue damage.
Differential diagnosis includes skin and subcutaneous tissue infection, osteomyelitis, deep vein thrombosis, gout, trauma, arthritis, and acute venous insufficiency. The presence of an ulcer increases the likelihood of concomitant bone infection.
Charcot foot - why is it dangerous
The most serious consequence of the disease is permanent foot deformity, causing abnormal pressure distribution during standing and walking. Particularly high pressure develops over bony prominences, where the skin undergoes overload, hyperkeratosis, and gradual breakdown.
The chain of complications may include:
- callus and subkeratotic hematoma,
- skin defect and chronic ulceration,
- soft tissue infection,
- osteomyelitis,
- abscess, necrosis, or systemic infection,
- hospitalization and surgical treatment,
- amputation of part of the foot or limb.
Joint destruction also leads to instability, reduced independent mobility, and overloading of the other limb. Decreased activity contributes to muscle weakness, deterioration of cardiorespiratory fitness, and loss of independence.
Suspected active Charcot foot is an indication for urgent specialist evaluation. The cornerstone of management is prompt immobilization and offloading of the limb in a knee-high device, most commonly a total contact cast or an appropriately fitted orthosis. Treatment continues until clinical activity resolves and stabilization of the changes is achieved. Advanced instability, deformity threatening ulceration, or failure of conservative treatment may require surgical reconstruction.
Charcot foot - how to prevent
Prevention focuses on early detection of neuropathy, protecting the foot from overload, and systematic control of systemic diseases. A person with diabetes should undergo a comprehensive foot examination at least once a year, and in the presence of loss of protective sensation, deformity, or a history of ulceration, check-ups should take place more frequently, according to the individual risk category.
The most important preventive measures include:
- daily inspection of the soles, heels, interdigital spaces, and nails,
- monitoring the temperature, color, and volume of both feet,
- prompt reduction of weight-bearing on the limb upon the appearance of unilateral swelling or warmth,
- stable glycemic control and treatment of hypertension, lipid disorders, and kidney disease,
- using footwear of appropriate depth, width, and protective construction,
- using custom insoles and orthoses that distribute plantar pressure,
- gradually increasing activity after the active phase has ended,
- checking the inside of footwear before putting it on,
- protecting the skin from burns, cuts, and excessive dryness,
- regular professional care of calluses and nails.
After achieving remission, long-term monitoring is necessary, as reactivation of the process can occur in the same or the opposite foot. The return to weight-bearing should proceed gradually, using therapeutic footwear, insoles, and stabilizing devices tailored to the established shape of the foot.
Charcot foot care at the podiatrist
A podologist is primarily involved in the prevention of skin and nail damage, monitoring areas of increased pressure, and patient education. Active neuro-osteoarthropathy primarily requires protecting the limb and urgent medical care. Podiatric procedures are implemented to the extent determined by the current condition of the tissues, blood supply, the presence of ulcers, and the recommendations of the attending medical team.
Ambasada Urody's offer includes procedures that, following individual qualification, can support the care of a foot with neuropathy or a fixed deformity:
- basic medical pedicure, including the assessment of the skin and nails, treatment of mild hyperkeratosis, calluses, and periungual keratosis;
- extended medical pedicure, intended for the treatment of more numerous keratoses, extensive calluses, minor superficial corns, and initial cracks;
- specialist removal of deep corns, performed precisely and conservatively after a risk assessment;
- cracked heel therapy, including the treatment of fissure edges, skin protection, and the selection of regenerative preparations;
- cleansing of diseased nails;
- trimming of ingrown toenails and orthonyxia brace therapy, if vascular and local conditions allow for the safe performance of the procedure;
- reconstruction of a damaged nail plate, used exclusively on a properly prepared, healthy nail bed;
- custom offloading of areas exposed to excessive pressure.
The treatment of lesions should preserve as much healthy tissue as possible. Calluses on a neuropathic foot can be a marker of high plantar pressure; therefore, their removal requires a simultaneous load correction through footwear, insoles, or an orthosis. Foot massages, acid treatments, and cosmetic procedures require particularly cautious qualification. An active phase, ulceration, infection, significant ischemia, or foot instability directs management toward medical care and securing the limb.
