Charcot Foot (T/F)

• Charcot foot refers to a chronic, progressive degeneration of the weight-bearing portion of a joint.
• It involves hypertrophic or atrophic changes at the periphery.
• Charcot foot is associated with neurologic disorders resulting in a loss of joint sensation.

History

• Joint changes in patients with spinal cord disease were first reported in 1831 by Mitchell.
• In 1868, Jean Martin Charcot first defined the disease, initially associating it with tabes dorsalis.
• Though commonly linked to diabetes mellitus since William Jordan's findings in 1936, it can occur in other conditions causing neuropathy in the lower extremities.

Epidemiology

• Neuropathy is a requirement for Charcot foot.
• Risk factors include long-standing diabetes, immunosuppressive therapies, osteoporosis, and metabolic abnormalities.
• Diabetics represent the primary population affected today.
• The incidence in the diabetic population with neuropathy ranges from 0.1% to nearly 30%.
• 91% of cases are unilateral.
• The condition is generally considered to be underdiagnosed.

Jean-Martin Charcot (1825-1893)

• Charcot studied over 5000 chronically ill patients at Salpetriere (France).
• He began working with Tabes Dorsalis in 1868.
• Charcot developed the "French Theory" defining the condition.
• Charcot's theory was opposed by the "German Theory" proposed by Virchow and Volkman.

Pathophysiology: Traditional Theories

• The French Theory suggests that Neurovascular issues, where the denervation of sympathetics causes vasodilation and increased blood flow to the foot lead to "washing out" of the bone. This results in osteopenia, bone resorption, and weakening.
• The German Theory posits that neurotraumatic occurrences and the loss of sensation lead to abnormal plantar pressures. The result is repetitive trauma, microfractures, destabilization, and joint dislocation.

Peripheral Neuropathy

• Autonomic neuropathy can weaken bone and lead to breakdown through loss of vasomotor control, increased AV shunting, and increased peripheral flow.
• Sensory-motor neuropathy causes deformity, loss of protective sensation, absent DTRs, diminished vibratory sense, muscle weakness, and ankle equinus.

Modern Theory

• The modern theory includes inflammation, and incorporates elements of both other theories.
• Sensory neuropathy may lead to abnormal loading, and increased force on areas of the foot resulting in fracture.
• This may result in acute inflammation, osteopenia, osteolysis and osteodastogenesis.

Clinical Presentation

• The classic presentation of Charcot foot is a red, hot, painful, and swollen foot
• Onset is typically in individuals over 50 years old with a DM diagnosis of over 10 years
• There is often a report of minor injury
• Swelling is often unilateral with warmth, at least 2-4 degrees C warmer than the contralateral side
• The pain is usually mild, not out of proportion to the presentation
• Clinicians obtain bilateral weight-bearing x-rays to assess joint instability, looking for subtle subluxations or avulsion fractures
• Lab results for WBC, CRP, and ESR are usually within normal limits
• Pulses may be bounding
• Late findings can include equinus and "rocker-bottom" deformity, and ulceration

Differential Diagnoses

• Infection, including cellulitis, osteomyelitis, and septic arthritis.
• Trauma.
• Arthritis, including crystal and inflammatory types.
• Compartment syndrome.
• Deep vein thrombosis (DVT).
• Complex regional pain syndrome.

Classification of Charcot Foot

• Eichenholtz (1966) created a classification system based on radiographic and clinical findings.
• Stage 0 (Subacute): Primarily clinical symptoms with subtle radiographic findings, added on by Shibata 1990.
• Stage I (Destruction/Acute): Capsular distension, osseous fragmentation, peri-articular debris formation, subluxations/dislocation, fracture.
• Stage II (Coalescence): Osseous resorption, evidence of consolidation, and repair of large fracture fragments.
• Stage III (Reconstructive/Remodeling): Maturation of bone consolidation, ankylosis, and hypertrophic proliferation.

Radiographic Findings

• Radiographic evidence displays subluxation, dislocation, and fracture.
• Eichenholz classification uses radiographs to identify Charcot stages.
• A subacute stage may present as a nonpainful traumatic event in a diabetic neuropathic patient.
• Stage I can present as a hot, edematous, and sometimes painful foot, along with subluxations and fractures.
• Stage II exhibits decreased inflammation, warmth, pain, healing fractures, and sclerosis.
• Stage III shows stable, remodeled bone with ankylosis and no pain.
• Sanders classification is based on anatomic location.
  • I Forefoot: 3%
  • II Lisfranc's: 48%
  • III Chopart's: 34%
  • IV Ankle: 13%
  • V Calcaneus: 2%

Diagnosis

• Diagnosis remains primarily clinical, and can be difficult.
• Misdiagnosis is common, with an estimated average delay of 29 weeks.
• The acute phase presents as a red, hot, swollen, and painful foot, but can be painless approximately 24% of the time.
• Pedal pulses are usually bounding.
• Systemic symptoms of infection are absent.
• X-rays may not show anything in very acute cases.

Early Diagnosis

• Diagnosing Charcot foot within 1 month of symptoms leads to better outcomes; a 2005 study found:
  • 11 patients were diagnosed within 1 month.
  • Weight bearing in a total contact cast (TCC) averaged 3 months.
  • 1/11 developed fracture and midfoot breakdown, attributed to noncompliance.
• Diagnosing Charcot foot after 3 months of symptoms leads to worse outcomes; the 2005 study found: -13 patients were diagnosed after 3 months. -Weight bearing in TCC averaged 5 months. -All developed fracture and eventual rocker bottom deformity.
• A 2011 study showed early diagnosis is beneficial: -Diagnosed at 4.1 weeks from onset of symptoms: 7 patients, NWB TCC, no one developed any stage I Eichenholz at 1 year follow up. -Diagnosed at 6.8 weeks from onset of symptoms: 15 patients, NWB TCC, developed stage I Eichenholz at average 11 weeks.

Progression

• Charcot leads to foot deformity, which leads to peak plantar pressures.
• Peak plantar pressures lead to ulceration.
• Ulceration can causes infection and amputation.
• Charcot can recur and occur in the contralateral foot in 15-30% of cases.

Imaging

• Plain film findings include focal demineralization, subchondral or periarticular changes with polyarticular distribution.
• MRI findings include:
  • Soft tissue edema.
  • Disruption of the Lisfranc's ligament
  • Arch collapse.
  • Joint effusion
  • Subchondral bone marrow edema (low signal T1, high T2).
• MRI has high sensitivity and specificity for diagnosing osteomyelitis (>90%) in the absence of neuropathic disease.
• To differentiation of neuroarthropathy from acute osteomyelitis, location is key.
  • Charcot is primarily periarticular.
  • Osteomyelitis develops from ulceration, sinus tract etc.
• Be wary of marrow replacement with low signal intensity on T1 and high signal intensity on T2, which is characteristic of osteomyelitis.
• A T2 hyperintensity (normally sensitive for osteomyelitis) without low signal intensity on T1 could just be osteitis secondary to soft tissue inflammation.

Osteomyelitis vs Charcot

• Differentiating between the two can be difficult, particularly with chronic ulcers.
• Frequent concomitant disease between osteomyelitis and Charcot can further complicate diagnosis.
• Factors for differentiating osteomyelitis from Charcot include: -Large ulcers (>2cm) are common for osteomyelitis, absence of an ulcer signifies towards Charcot. -Warm (>2 degrees C than contralateral) signifies towards Charcot. -History of trauma signifies towards Sharco whereas peri-ulcer inflammation signifies towards osteomyelitis. -Midfoot presentation signifies Charcot, whereas tose and forefoot presentation signifies osteomyelitis.
• Further laboratory results differentiate the conditions.
  • ESR >70 signifies osteomyelitis.
  • WBC and CRP elevation signals osteomyelitis.
  • Elevated bone-specific alkaline phosphatase (bone formation) and urinary deoxypyridinoline (bone resorption) signifies Charcot;
• Bone biopsy; -Osteomyelitis has a positive culture and histopathology. (+)(+) culture is 92% sensitive, 60% specific. Histopathology has aggregates of inflammatory cells, erosion of trabecular bone, marrow changes, loss of normal fat, fibrosis, and reactive bone formation. -Charcot has histopathology, where osteoclasts > osteoblasts.

Conservative Treatment

• Immobilization with a total contact cast (TCC).
  • The cast may need to be changed in 3 days to accommodate reduced edema.
  • Subsequently change the cast every 2 weeks for 2-12 months, with an average of 6 months.
• Supportive shoes can be used on the contralateral foot.
• An irremovable walker is as effective as a TCC
• The use of casts and walkers suggests patient noncompliance as a factor.
• Standard of care remains non weight bearing.
• Some studies suggest weight bearing, if immobilized, does not affect outcomes.
• Different protocols have been described in literature; partial weight bearing, heel weight bearing, all small studies.
• Weight bearing is forbidden if ulceration exists.

Pharmacological Treatment

• Bisphosphonate usage has been suggested, particularly in early diagnosis.
• A 2005 study on Alendronate by Pitocco examined: -20 randomized cases of new acute Charcot. -11 patients received 70mg alendronate po 1/week. -9 control patients were examined. -TCC for all was administered for 2 months, walker for 4 months= total 6 month tx, pain improved at 6 months, and decreased bone resorption markers.
• Other small studies have looked at zoledronic acid and calcitonin.
• While pharmacologic treatment is sometimes utilized, it is not the standard of care.
• Larger clinical trials are needed for FDA approval for Charcot treatment.

Surgical Treatment

• Surgical treatment aims for a stable, plantigrade weightbearing surface.
• Many techniques have been described with success- ex fix, internal fixation, intermedullary rods, plaining procedures.
• Arthrodesis is generally only indicated in Eichenholz stage II.
• Charcot plaining is generally best for Eichenholz stage III.
• Universal complications with surgery include wound healing difficulties, infection, and hardware failure.

Evidence Based Approach

• Localized unilateral swelling and warmth in a neuropathic patient with or without pain or deformity points to a potential case.
• A multi-disciplinary high risk food service should be consulted, with subsequent clinical testing including neuropathy, long standing diabetes, bounding pulses, and infrared dermal thermometry being tested.
• Clinical management means immediate immobilization using a TCC or irremovable walker, and any definitive diagnosis is made.
• Tests for acute Charcot diagnosis include: continue immobilization, edema control, at follow up visits reassess dermal temperatures, reapply TCC frequently, serial x-rays, optimize DM control, OT referral for home safety assessment, average management 2-12 months.
• If conservative treatment fails: refer to multidisciplinary high risk foot service for surgical evaluation, consider bisphosphonates.
• Tests for acute negative Charcot diagnosis include: continue immobilization until definitive diagnosis is made, work up DDx: osteomyelitis, cellulitis, deep space infection, DVT, gout, fracture, inflammatory arthritis.
• Tests of Chronic Charcot diagnosis, include confirmed clinical signs/symptoms resolved, no temperature gradient, weight bearing xrays show remodeling: gradual step down to partial weight bearing in aircast walker, offloading custom boots, shoes and orthotics depending on severity of deformity, patient education, frequent follow ups with podiatrist.

Conclusions

• Charcot Neuroarthropathy is a serious diabetic foot complication leading to high amputation risk.
• While diagnosis can be difficult, early diagnosis is key for preventing worsening conditions.
• Treatment standards include non weight bearing in an offloading boot such as a total contact cast.
• If there is need for surgery, focus should be placed upon a plantigrade foot.
• There is still level IV or expert opinion of evidence in most treatments, indicating that knowledge on treating the condition has not changed since research began.