Eichenholtz Staging

1. Why Stage Charcot?

Staging matters because it drives treatment decisions:

• Stage 0–I — absolute non-weight-bearing in a total contact cast. The window in which deformity can still be prevented.
• Stage II — transition cast to CROW boot; protected weight-bearing.
• Stage III — definitive footwear / accommodative shoe; surgical reconstruction if there is unstable or ulcerogenic deformity.

The staging system also organises communication and audit: every published trial of casting, bisphosphonates, surgery, or footwear stratifies its outcomes by Eichenholtz stage. Understanding the system is therefore essential to reading the literature.

Two classification axes coexist: chronological / radiographic (Eichenholtz, Sella & Barrette) describes when the disease is in its course; anatomic (Brodsky, Sanders, Frykberg) describes where in the foot the disease is. A complete chart entry mentions both: e.g., “Eichenholtz stage I, Brodsky type 1 (midfoot/Lisfranc) Charcot.”

2. The Eichenholtz System (1966)

Sidney N. Eichenholtz, in his 1966 monograph Charcot Joints (Charles C Thomas, Springfield), proposed a three-stage radiographic system based on a series of 68 patients followed for years through the natural history. Each stage represents a dominant biological process with characteristic radiographic signs and a characteristic clinical correlate:

The original Eichenholtz scheme had only stages I–III, but the recognition that MRI detects an earlier inflammatory phase with normal plain radiographs led Sella and Barrette (J Foot Ankle Surg 1999) to add Stage 0: the pre-radiographic acute Charcot. This addition is now universal.

Stages 0 and I together constitute “active” Charcot. Stages II and III are the “quiescent” phases. The transition from active to quiescent is signalled by resolution of skin temperature differential (\(\Delta T < 2\,^\circ\text{C}\) for ≥1 week) and by radiographic evidence of coalescence rather than continuing fragmentation.

3. Stage 0 — Pre-radiographic / Acute Inflammatory

The pre-radiographic stage is the critical diagnostic window. The patient presents with a warm, swollen, erythematous foot in the setting of neuropathy. Plain radiographs are normal or near-normal. MRI shows bone marrow oedema, subchondral microfracture, joint effusion, and ligamentous oedema.

• Clinical: \(\Delta T \ge 2\,^\circ\text{C}\), swelling, mild pain, often a recognisable precipitant.
• Plain X-ray: Normal or only soft-tissue swelling.
• MRI: Marrow oedema in periarticular bone; subchondral “ghost fractures”; effusion.
• Bone scan: Tc-MDP markedly positive; In-WBC negative.
• Lab: CRP/ESR variably elevated, often only mildly.

This is the foot that can still be saved from deformity. Casting at Stage 0 frequently produces complete radiographic normalisation within 8–12 weeks, with no residual rocker-bottom and no need for surgery in many cases. Failure to recognise Stage 0 lets the foot move into Stage I and accumulate irreversible architectural change.

4. Stage I — Development / Fragmentation

The developmental phase is the active, destructive stage. The foot is still warm and swollen; radiographs now show the visible consequences of the cascade described in Part II:

• Periarticular fragmentation — small avulsion fragments at joint margins.
• Subluxation / dislocation — especially Lisfranc, naviculocuneiform, or talonavicular.
• Osteopenia — juxta-articular bone loss from hyperaemic resorption.
• Joint effusion / soft-tissue swelling.
• Loss of joint architecture — the “5 Ds” in evolution.

On MRI, marrow oedema is now confluent across multiple bones and joints; T1 hypointensity and STIR/T2 hyperintensity pattern. Bone marrow oedema and fragmentation may extend across an entire foot region (e.g., the entire tarsometatarsal complex).

Clinically the foot remains warm (\(\Delta T\) often 4–8°C), swollen, and dependently erythematous. Pain, when present, is mild. The patient often continues to walk on the foot until restrained.

Treatment in Stage I: total contact cast (TCC), strict non-weight-bearing initially, contralateral footwear adjustment, weekly clinical assessment. Cast change every 1–2 weeks initially, then every 2–4 weeks as the foot cools. Expect 2–4 months in Stage I before transition to Stage II. See Part VI.

5. Stage II — Coalescence

The coalescence phase is the early healing response. The fracture / fragmentation cascade is no longer progressing; the body now repairs:

• Absorption of fine debris — small fragments resorb.
• Periosteal new-bone formation — visible at fragment margins; sclerotic.
• Sclerosis of larger fragments.
• Reduction of soft-tissue swelling.
• Decreased temperature differential — \(\Delta T\) decreases; classic threshold for Stage II is \(\Delta T < 2\,^\circ\text{C}\) sustained.

On MRI, marrow oedema diminishes. T1 returns toward fat signal in non-fragmented bone. Soft-tissue oedema fades.

Stage II is also the transition phase in management. The patient may be transitioned from TCC to a removable CROW boot (Charcot Restraint Orthotic Walker) or commercial Walker boot, and gradual partial weight-bearing is permitted. Strict serial monitoring of skin temperature continues; any re-warming signals failure of Stage II and a return to TCC.

Typical duration: 2–6 months. The foot looks better radiographically than at Stage I — smoother margins, increased bony continuity — but the underlying architecture is now permanently altered.

6. Stage III — Consolidation / Reconstruction

The consolidation phase is the quiescent, “burnt-out” foot. Bony ankylosis is established, the architecture is remodelled to whatever shape the cascade has left, and the foot is mechanically stable albeit deformed.

• Bony ankylosis — fragments fuse into a single mass.
• Sclerosis — mature trabecular pattern in fused bone.
• Residual deformity — rocker-bottom, varus/valgus hindfoot, talar collapse, etc.
• Cool foot — \(\Delta T \approx 0\)
• Risk concentrated at bony prominences — which create skin pressure and ulcer risk.

MRI shows marrow signal returning toward fat (T1 intermediate-to-high), no residual oedema, deformed but stable architecture.

Stage III is the long-term residual state the patient lives in. Management is footwear, custom insoles, lifelong foot surveillance. Roughly two-thirds of well-managed Stage III feet remain ulcer-free with appropriate footwear. The remainder — especially those with rocker-bottom plantar prominences in the midfoot — ulcerate repeatedly and become the candidates for surgical reconstruction (Part VII).

Importantly, an “old” Stage III foot can reactivate after new injury (or revascularisation, or contralateral amputation requiring weight-shift). Patients should be educated to recognise the warm-foot warning sign and to seek care immediately. The Eichenholtz stages are not a one-way street.

7. Brodsky Anatomic Classification (1990)

James W. Brodsky (Foot & Ankle Clinics 1990) introduced the most widely-used anatomic classification, based on the foot region affected:

The Brodsky type carries significant prognostic and surgical weight:

• Type 1 (Lisfranc midfoot) is the most ulcerogenic but the most amenable to plantar exostectomy.
• Type 2 (hindfoot Chopart) often requires hindfoot arthrodesis; instability tends to recur.
• Type 3A (ankle) is the most limb-threatening pattern. Tibiotalocalcaneal arthrodesis with retrograde IM nail is the typical reconstruction; failure rates and amputation rates are higher than for other patterns.
• Type 3B (calcaneal avulsion) is a distinct entity — an Achilles avulsion fragment from osteopenic bone, producing a pes calcaneus deformity. Often missed.

The two-axis classification (Eichenholtz stage + Brodsky type) is the standard chart entry. Surgical literature universally reports outcomes stratified by Brodsky type.

8. Sanders & Frykberg / Other Anatomic Systems

The Sanders & Frykberg classification (1991) divides the foot into five anatomic levels of involvement, slightly different from Brodsky’s in numbering convention:

The two systems describe broadly the same anatomy with different numbering. In a busy foot & ankle clinic, “midfoot” (Brodsky 1 / Sanders II and III) and “ankle/hindfoot” (Brodsky 2–3A / Sanders IV) are the binary that drives most management decisions.

Other classifications occasionally cited:

• Schon classification — a midfoot-focused system that grades the severity of midfoot deformity into types I–IV (alpha/beta subtypes), useful for surgical planning.
• Trepman, Nihal & Pinzur staging — integrates “active vs inactive” with anatomic location, attempting to bridge Eichenholtz and Brodsky.
• Rogers Charcot Index — a clinical/radiographic combined severity score for trial standardisation (Diabetes Care 2011).

No single classification is perfect; the working pair in 2026 remains Eichenholtz (chronological) + Brodsky (anatomic), augmented by Schon when midfoot surgery is being considered.

9. Choosing & Using Classifications — A Clinical Synthesis

In daily practice the staging system answers four sequential questions:

1. Is the foot active? — \(\Delta T \ge 2\,^\circ\text{C}\), MRI marrow oedema, or radiographic fragmentation indicate Stage 0 or I.
2. Has it cooled? — \(\Delta T < 2\,^\circ\text{C}\) sustained, oedema resolving, fragments coalescing → Stage II.
3. Is it consolidated? — bony fusion, deformity stable, no oedema, cool foot → Stage III.
4. Where is the deformity? — Brodsky 1 / Sanders II–III, Brodsky 2–3A / Sanders IV, etc., to plan surgery.

The activity criterion drives non-operative management (continue casting in Stages 0–I; transition in II; definitive footwear in III). The anatomic criterion drives surgical planning (exostectomy for midfoot prominence; arthrodesis for instability or non-correctable deformity).

An example chart entry:“58-year-old man with 18-yr T2DM, Eichenholtz Stage I Brodsky type 1 (midfoot/Lisfranc) Charcot, \(\Delta T = 5.2\,^\circ\text{C}\), MRI shows periarticular bone-marrow oedema across the tarsometatarsal complex with early dorsolateral subluxation. TCC, NWB, weekly review.”

Such a note unambiguously communicates stage, location, severity, and management. The next two parts dive into the conservative (Part VI) and surgical (Part VII) management of those stages and patterns.