Charcot Foot in Diabetes | Diabetes Textbook

Charcot neuropathic osteoarthropathy, commonly referred to as Charcot foot, is a severe and progressive degenerative condition affecting the bones, joints, and soft tissues of the foot and ankle. It is most frequently seen in individuals with diabetes mellitus (DM), particularly those with peripheral neuropathy. The disease leads to bone destruction, joint dislocations, and deformities, significantly increasing the risk of ulcerations, infections, and amputations if not managed promptly.

Charcot foot was first described by Jean-Martin Charcot in 1868 in patients with tertiary syphilis, but today, diabetes is the leading cause due to its association with neuropathy. Early diagnosis and intervention are critical to preventing irreversible damage.

Pathophysiology of Charcot Foot

The exact mechanism of Charcot foot is not fully understood, but it is believed to result from a combination of neurotraumatic and neurovascular factors in the presence of peripheral neuropathy.

1. Neurotraumatic Theory (Mechanical Insult)

Diabetic peripheral neuropathy leads to loss of protective sensation, meaning patients do not perceive pain from repetitive microtrauma or fractures.
Continuous weight-bearing on an injured foot causes bone and joint destruction due to unperceived stress.

2. Neurovascular Theory (Autonomic Dysfunction)

Autonomic neuropathy causes increased blood flow to the foot due to abnormal arteriovenous shunting.
This leads to bone resorption (osteolysis) and weakening of bone structure, making the foot more susceptible to fractures.

3. Inflammatory Component

Some researchers suggest that pro-inflammatory cytokines (e.g., TNF-α, IL-1β) contribute to bone destruction.
A localized inflammatory response may trigger osteoclast activation, accelerating bone breakdown.

Stages of Charcot Foot (Eichenholtz Classification)

Stage 1 (Fragmentation/Development) – Acute inflammation, swelling, erythema, bone fragmentation.
Stage 2 (Coalescence) – Decreased swelling, early bone healing, and fusion.
Stage 3 (Consolidation/Remodeling) – Stable but deformed foot architecture.

Clinical Presentation

Charcot foot is often misdiagnosed initially because its symptoms mimic other conditions like cellulitis, gout, or deep vein thrombosis (DVT). Key clinical features include:

Acute Phase (Stage 1)

Significant swelling (unilateral, warm, red foot)
Increased skin temperature (2-5°C warmer than contralateral foot)
Minimal or no pain (due to neuropathy)
Possible joint instability (subluxation/dislocation)

Chronic Phase (Stages 2 & 3)

Deformities (rocker-bottom foot, midfoot collapse)
Callus formation (high-pressure points leading to ulcers)
Chronic instability (difficulty walking)

“Red Flags” for Charcot Foot

A diabetic patient with warm, swollen foot but no open wound or infection.
History of minor trauma (e.g., twisting ankle, stepping wrong).
Rapid progression of deformity.

Diagnosis

Early diagnosis is crucial to prevent permanent deformity. Diagnostic approaches include:

1. Clinical Examination

Monofilament test (assesses neuropathy)
Temperature difference (compared to the other foot)
Palpable bone crepitus (in advanced cases)

2. Imaging Studies

X-rays – Initial imaging, may show:
Bone fragmentation (early stage)
Joint subluxation, fractures, or disorganization (later stages)
MRI – More sensitive for early bone marrow edema, soft tissue involvement.
Bone Scan (SPECT/CT) – Detects early inflammation before radiographic changes.

3. Laboratory Tests

Rule out infection (e.g., elevated ESR, CRP, leukocytosis).
Blood glucose/HbA1c to assess diabetes control.

Management Strategies

The primary goals of Charcot foot management are:

Stabilizing the foot to prevent further damage.
Preventing ulcers and infections.
Restoring functional mobility.

1. Acute Phase Management (Stage 1)

Immediate Offloading:
Total contact cast (TCC) – Gold standard, redistributes pressure.
Removable cast walker (RCW) with a rigid sole.
Strict non-weight-bearing (NWB) for 8-12 weeks.
Pharmacological Therapy:
Bisphosphonates (e.g., zoledronic acid) – May reduce bone resorption.
Anti-inflammatory drugs (short-term NSAIDs for pain/swelling).
Monitoring:
Weekly follow-ups to assess temperature changes, swelling reduction.

2. Chronic Phase Management (Stages 2 & 3)

Custom Orthotics & Bracing:
Charcot Restraint Orthotic Walker (CROW) – Provides stability.
Custom-molded shoes with rocker-bottom soles.
Surgical Intervention (if severe deformity):
Exostectomy (removal of bony prominences causing ulcers).
Arthrodesis (fusion) – Stabilizes unstable joints.
Reconstructive surgery (in cases of severe collapse).

3. Long-Term Prevention Strategies

Regular foot exams (every 3-6 months).
Glycemic control (HbA1c <7% to slow neuropathy progression).
Patient education on foot care, avoiding trauma.

Complications of Untreated Charcot Foot

If not managed properly, Charcot foot can lead to:

Chronic foot ulcers (due to abnormal pressure points).
Osteomyelitis (bone infection, often requiring amputation).
Severe deformities (e.g., rocker-bottom foot, leading to disability).
Increased amputation risk (5-year mortality post-amputation is ~50%).

Conclusion

Charcot foot is a devastating complication of diabetic neuropathy, leading to progressive bone and joint destruction. Early recognition and aggressive offloading are critical to preventing irreversible deformities and amputations. A multidisciplinary approach involving endocrinologists, podiatrists, orthopedic surgeons, and physical therapists is essential for optimal outcomes.

Future research should focus on biomarkers for early detection and advanced surgical techniques to improve long-term prognosis. For now, patient education, strict offloading, and glycemic control remain the cornerstone of Charcot foot management in diabetes.

References

Rogers, L.C., et al. (2011). “The Charcot Foot in Diabetes.” Diabetes Care.
Jeffcoate, W.J., et al. (2008). “Charcot Neuroarthropathy in Diabetes Mellitus.” Diabetologia.
Armstrong, D.G., et al. (2017). “Offloading the Diabetic Foot for Ulcer Prevention and Healing.” Journal of the American Podiatric Medical Association.