What is Charcot foot in a patient with diabetes (Diabetes Mellitus) and peripheral neuropathy?

What is Charcot Foot?

Charcot foot (Charcot neuro-osteoarthropathy) is an inflammatory process occurring in patients with peripheral neuropathy—most commonly from diabetes—that causes progressive destruction of bones, joints, and soft tissues of the foot and ankle, leading to fractures, dislocations, and severe deformity if left untreated. 1, 2

Pathophysiology

The disease involves an inflammatory cascade in neuropathic patients where trauma triggers disproportionate cytokine release, activating osteoclastogenesis through the RANKL pathway, resulting in accelerated bone resorption. 3 This inflammatory process, combined with continued mechanical forces during ambulation on an insensate foot, causes ligament disruption, joint dislocations, and fractures. 3 The impaired pain perception from peripheral neuropathy prevents patients from recognizing the ongoing destruction, allowing the disease to progress silently. 1, 4

Epidemiology

• Charcot foot affects approximately 0.3% of patients with diabetes mellitus, representing roughly 1.6 million people worldwide with an annual incidence of 160,000 new cases. 2, 3
• The true prevalence is likely underestimated because the absence of pain from neuropathy delays presentation to healthcare providers. 1

Clinical Presentation

The hallmark presentation is a unilateral red, warm, swollen foot with intact skin in a patient with diabetes and peripheral neuropathy. 1, 2, 5 Key clinical features include:

• Increased temperature compared to the contralateral foot (this is the most reliable early sign) 1
• Erythema and edema of the affected foot 2, 5
• Minimal or absent pain despite significant inflammation, due to sensory neuropathy 1
• Progressive deformity if untreated, leading to altered weight-bearing patterns 2

Critical Diagnostic Pitfall

This presentation is frequently misdiagnosed as cellulitis, gout, deep venous thrombosis, or inflammatory arthropathy by untrained clinicians, leading to catastrophic delays in treatment. 4, 6 You must exclude infection, gout, and DVT before diagnosing Charcot foot, but if Charcot is suspected, begin treatment immediately while completing the workup. 1

Diagnostic Approach

Clinical Diagnosis

Always suspect active Charcot neuro-osteoarthropathy in any diabetic patient with neuropathy presenting with a warm, swollen, erythematous foot compared to the contralateral side. 1, 5 This is a Best Practice Statement from the IWGDF 2023 guidelines. 1

Temperature Monitoring

• Use infrared thermometry to measure skin temperature differences between feet using a standardized approach. 1
• Calculate the temperature difference by comparing the highest temperature on the affected foot with the same anatomic point on the contralateral extremity. 1
• A temperature gradient between affected and unaffected limbs supports the diagnosis and helps monitor disease activity. 2, 5
• For bilateral Charcot or absence of contralateral limb, use ascending temperature gradients (toe-to-knee) for comparison over time. 1

Imaging Studies

Obtain bilateral weight-bearing plain radiographs (AP, medial oblique, and lateral projections) as the initial imaging study, even when the diagnosis is clinically suspected. 1, 5 If the patient cannot bear weight, non-weight-bearing films are acceptable but may miss malalignments. 1

Perform MRI when plain radiographs appear normal but clinical suspicion remains high—this is a strong recommendation as MRI can detect bone marrow edema characteristic of early Charcot (stage 0) before structural changes appear on X-ray. 1, 2, 5 This is critical for early diagnosis when treatment is most effective. 7

If MRI is unavailable or contraindicated, consider nuclear imaging (scintigraphy), CT scan, or SPECT-CT to support the diagnosis. 1

Laboratory Testing

Do not use C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), white blood count, alkaline phosphatase, or other blood tests to diagnose or exclude Charcot neuro-osteoarthropathy. 1, 2 These tests lack diagnostic accuracy for this condition.

Treatment Algorithm

Immediate Management

Initiate a non-removable knee-high offloading device (total contact cast) immediately when Charcot is suspected—do not wait for imaging confirmation, as delays allow continued bone and joint destruction. 1, 5 This is a strong recommendation from the IWGDF 2023 guidelines. 1

Treatment Hierarchy

1. First-line: Total contact cast (TCC) for active Charcot with intact skin—this is the gold standard providing optimal immobilization and offloading to promote disease remission and prevent deformity progression. 1, 5

2. Second-line: Non-removable knee-high walker if TCC is not feasible. 1

3. Third-line: Removable knee-high device worn at all times, only when non-removable options are contraindicated or not tolerated. 1

4. Never use below-ankle offloading devices (surgical shoe, postoperative sandal, custom molded shoe, or slipper cast) as they provide inadequate immobilization of diseased bone and joints. 1, 2

Adjunctive Measures

• Use assistive devices (crutches, walker, wheelchair) to reduce weight-bearing on the affected limb. 1, 2
• Consider vitamin D and calcium supplementation during fracture healing according to national guidelines for those at risk of deficiency. 1, 2

Pharmacological Interventions

Do not use alendronate, pamidronate, zoledronate, calcitonin, PTH, methylprednisolone, or denosumab as treatment for active Charcot neuro-osteoarthropathy. 1, 2 This is a strong recommendation based on moderate-quality evidence showing no benefit. 1

Surgical Intervention

Consider surgery when: 1, 2, 5

• Joint instability persists despite conservative treatment
• Deformity creates high risk of ulceration within the offloading device
• Pain cannot be adequately controlled in TCC or non-removable device

Monitoring Disease Activity and Remission

• Use serial temperature measurements comparing affected and unaffected limbs to monitor disease activity. 2, 5
• Consider temperature normalization, clinical edema resolution, and imaging findings together before concluding remission. 5
• The acute phase typically requires 3-6 months of immobilization, though duration varies by individual. 7

Post-Remission Management

After remission, prescribe customized footwear and orthoses that accommodate and support the altered foot architecture—this is essential to prevent reactivation. 1, 2, 5 This is a strong recommendation based on moderate-quality evidence. 1

When deformity or joint instability is present, use below-knee customized devices to optimize plantar pressure distribution. 1, 2, 5 This provides additional protection against reactivation. 1

Consequences of Untreated or Delayed Treatment

• Severe deformity from fractures and dislocations that permanently alters foot architecture 1, 2
• Ulceration from altered weight-bearing patterns on deformed foot 2, 4
• Infection secondary to ulceration 2, 4
• Amputation risk increases 6-12 times in individuals with foot ulcers resulting from Charcot deformity 2
• Mortality: pooled 5-year mortality rate of 29% 2
• Severe impact on quality of life 2

Common Clinical Pitfalls

• Misdiagnosing as infection or inflammatory arthritis due to the warm, red, swollen appearance—always consider Charcot in diabetic patients with neuropathy. 4, 6
• Using inadequate offloading such as removable devices or below-ankle devices when non-removable knee-high devices are indicated. 1, 2
• Delaying treatment while waiting for imaging confirmation—begin immobilization immediately when diagnosis is suspected. 1
• Failing to monitor disease activity with regular temperature measurements during treatment. 2, 5
• Inadequate post-remission footwear, leading to reactivation of the disease. 1, 2
• Attempting pharmacological treatment with bisphosphonates or other agents that have no proven benefit. 1, 2