Foot and ankle OA patterns and ankle sprains: when to treat, when to refer

Foot and ankle surgeon (Otter: “Dr Vegan”) — OA patterns talk

About five years as a Gold Coast consultant after a Sydney fellowship (overseas travel restricted in the peri-COVID period). Splits time between public work at Gold Coast University Hospital (elective foot and ankle plus some general trauma) and private practice at Coast Foot Ankle Clinic with Simon Platt. Otter’s surname is badly garbled — this write-up does not invent a corrected name.

Dr Sonia Simon (Otter also: “Dr Simon” / host “Dr Sean”, “Dr Slammer”, “Dr Shawn”) — ankle sprains and hormones

Foot and ankle surgeon on the Gold Coast for about nine years. Operates at Gold Coast Private; retains a public appointment including shared paediatric foot and ankle. Introduces herself clearly as “Sonia Simon.” Host introductions in the recording are garbled; where unclear we say Dr Simon / Dr Sonia Simon rather than guessing another surname.

Who was speaking — and what Otter mangled

The first talk is a foot and ankle surgeon Otter labels “Dr Vegan”. He has been back on the Gold Coast about five years as a consultant, completed fellowship training in Sydney when overseas travel was restricted, and splits public (GCUH) and private time at Coast Foot Ankle Clinic with Simon Platt. He asks the room not to confuse that clinic with another similarly named Gold Coast foot service. We keep Otter’s name as-is and do not invent a surname.

After a short thank-you interlude (and a brief osteoporosis fact-sheet reminder for an endocrinology colleague), the host introduces the second speaker with heavily garbled audio — Otter hears “Dr Sean,” “Dr Slammer,” then later “Dr Shawn.” The surgeon herself says clearly: “I’m Sonia Simon”, a foot and ankle surgeon about nine years on the Gold Coast, mum of two active daughters, adult foot and ankle with some paediatric public work. This write-up uses Dr Sonia Simon / Dr Simon and notes the host garble.

Why foot and ankle OA matters

Without workable feet and ankles, hip and knee replacements do not help people mobilise. The foot alone has about 28 bones and many joints; add tibia, fibula, talus, and calcaneus for the hindfoot, then muscles and ligaments, and pattern recognition becomes essential in general practice.

Pathoanatomy in brief: initiating factors (often post-traumatic or recurrent instability for the ankle, rather than purely primary OA as in hip/knee) → early molecular cartilage breakdown → synovial thickening → instability → a painful, inflamed, sometimes deformed joint.

Four common OA patterns

The first speaker focuses on the four patterns he sees most often.

1. First MTP (big toe) osteoarthritis

• Pain with dorsiflexion and plantarflexion; progressive loss of range.
• Often younger adults (40s–50s); frequently after forgotten trauma in teens/twenties.
• May look “bunion-like”; straighten the digit and recreate motion — end-stage disease is stiff and painful.
• Early disease: less stiffness, more impingement pinch at extremes of motion (running, yoga).

2. Midfoot arthritis

• Dull aching pain, often 2nd and 3rd tarsometatarsal joints (TMTJs).
• Post-traumatic Lisfranc-type injury, high arch or planus morphology; associated inflammatory disease (rheumatoid, gout) also relevant.
• Can be mistaken for posterior tibial tendon dysfunction / flat-foot; weight-bearing X-ray helps separate them.
• Much midfoot OA is tolerable — midfoot joints are relatively stiff across life — but when painful, pick the culprit joint before fusing.

3. Subtalar and Chopart joints

• Pain on uneven ground; inversion/eversion irritability.
• After talus injury (subtalar, tibiotalar, or talonavicular OA) or end-stage adult-acquired flat foot.
• On imaging, parallel reference lines through the midfoot/hindfoot fall out of parallel as the arch collapses (Otter: “show part” = Chopart — talonavicular and calcaneocuboid).

4. Ankle joint osteoarthritis

• Deep joint pain, restricted range, gait change, sometimes instability or deformity.
• Often post-traumatic or after years of “stable” arthritis that suddenly decompensates after a minor twist.

History, examination, imaging, red flags

History

• Previous trauma? Current or chronic instability (especially ankle)?
• Activity-related pain? Classic starter pain — first steps agony, then warms up?
• Stiffness versus the other side; systemic disease (lupus, rheumatoid, gout).

Examination

• Gait and limb alignment; can they recreate an arch? Toe motion through gait? External rotation moment?
• Localise tenderness: hindfoot / midfoot / forefoot.
• Range and stability compared with the contralateral side.
• Tendon and muscle function — local problem versus driven from spine, hip, or knee.
• Neurovascular exam — several patients referred for surgery had no palpable pedal pulses; that is a contraindication until vascular status is sorted.

Imaging

• Start with weight-bearing plain films: AP, lateral, mortise; hindfoot alignment views show where deformity is driven.
• Early disease / osteochondral lesions: MRI (the first speaker deliberately leaves OCLs to Dr Simon’s territory).
• CT for three-dimensional surgical planning (e.g. ankle replacement planning) and to decide which midfoot joint to fuse; targeted local anaesthetic / steroid injections can confirm the pain generator when CT is equivocal.

Conservative care first

• Diagnosis and education first — degenerative disease tends to worsen over time, not spontaneously reverse.
• Activity modification; weight — roughly every kilo above the waist ≈ eight kilos through the ankle.
• Analgesia without opioids preferred: paracetamol and NSAIDs if cardiac/BP meds allow; topical NSAIDs. Opioids are hard to walk back from.
• Physio and podiatry together when possible — physios keep people moving and strong; podiatrists offload and align. Patients do best when both camps cooperate.
• Footwear: rocker / cam sole with thicker cushion (brand named in talk as an example, not an endorsement) to propel forward without demanding painful joint motion. Gold Coast thongs are common — not ideal for symptomatic OA.
• Orthotics: start cheap off-the-shelf ($5–$20) before $400 customs that end up in the cupboard.
• Shockwave and acupuncture: framed as optional patient-trial options with some pain-relief evidence, not cures. “If Reiki helped — do it again” — whatever safely manages pain.
• Injections: limited evidence for PRP in foot/ankle; hyaluronic acid or steroid can help but effects may be short-lived in end-stage disease.

When to refer

• After a genuine trial (speaker: often three months-plus) of the measures above — many referred patients improve and never return to surgery (quoted 70–80% redirected to conservative care).
• Functional limitation they cannot or will not live with; inability to fit shoes; ulceration or callosities from deformity.
• Diagnostic uncertainty — “lots of bones, lots of joints”; surgeons are happy to advise.

Surgical options

• Ankle: fusion remains a very good operation for end-stage OA — pain-free activity with locked, united bones. Ankle replacement preserves motion and needs patient-specific planning (CT-based plans matching X-rays); outcome data still catching fusion in some domains.
• Subtalar / Chopart / end-stage flat foot: triple arthrodesis (fuse the three involved joints).
• Midfoot: fuse the painful TMTJ(s) only — CT ± diagnostic injection to choose correctly.
• 1st MTP: many joint-preserving operations exist before fusion; when many operations exist for one pathology, none is perfect — fusion is reliable for pain relief (anecdote: a high-level tennis player returned after bilateral fusions). Early disease may still suit joint-preserving surgery.

Ankle sprains: high vs low, don’t miss the deltoid

Dr Sonia Simon’s talk: ankle sprain is the most common ankle injury. Keep classification simple for registrars — mild (walk off), severe (may need surgery), everything else in the middle — and remember the “chair with four legs” model: cut the chair in half and the parts no longer work together.

• High ankle sprain = syndesmosis. Missed injuries historically labelled “just a sprain” can present with post-traumatic arthritis and deformity 10–15 years later, with fewer good surgical options left.
• Low ankle sprain = lateral ligaments (ATFL/CFL) more common given foot posture and gait; medial deltoid (superficial vs deep) — many superficial; deep disruption is more serious (~“half the chair gone”). Missed deltoid laxity can contribute to post-traumatic pes planus.
• Ask about one big trauma versus repeated low-grade rolls.
• Mechanism videos from sport can show what is old versus new on MRI.

Exam, imaging, boot then functional rehab

Presentation

Swollen, sore ankle; ecchymosis often day 2–3 and may track to the toes by gravity. Patients may report a crack; osteochondral injury may feel like a pop. Recurrent sprains can happen on flat ground when peroneals (dynamic stabilisers) and static ligaments fail together. Swelling may last 6–12 months, especially with comorbidities.

Exam (hard when acutely sore)

• Exclude fracture first; Ottawa-oriented thinking, then X-ray.
• Anterior drawer: patient relaxes; one hand behind calf just above the joint, other draws the foot forward — look for soft endpoint / talus translating (ATFL ± PTFL context). Compare sides — hypermobile patients can look “positive” bilaterally; overtightening them surgically makes them miserable.
• Inversion stress for CFL, again compared contralaterally.

Imaging

• X-ray first if worried — look for fracture, arthritis, old injury.
• Ultrasound vs MRI: ultrasound is operator-dependent; MRI preferred for ligament/complex injury unless you need a dynamic study (e.g. Achilles rupture, peroneal subluxation).
• Acute MRI is “all blown up” — interpret carefully. Inversion injuries often show medial bone contusion / “kissing” deltoid signal reported as partial tear even when the deltoid is structurally intact — correlate with mechanism (true in–out injury vs pure inversion).

Initial management

• Chemist-warehouse short boots often fail to immobilise the ankle and can worsen pain. Prefer a long walker boot that actually controls the ankle — patients usually feel better after the swap. Available via many after-hours centres / orthotic suppliers.
• Avoid leaving the ankle in plantarflexion with only tubigrip — getting back to plantigrade is slower and more painful.
• PRICE / ice (frozen peas still work; dedicated ice packs help post-op swelling).
• Unless fractured: functional rehab — early gentle dorsiflexion/plantarflexion and progressive weight-bearing beat prolonged rest. Use crutches if needed for a short period.
• Typical ATFL/CFL pathway quoted: ~2–4 weeks in boot, then a comfortable functional ankle brace (modern non-lace designs preferred over fiddly ASO lace-ups; grade options exist) for ~2 weeks then wean with physio. First four weeks: ROM and balance/proprioception (e.g. single-leg stand after shower). Progress loading once pain settles after ~four weeks.
• Patients may legally drive in a brace that fits a normal shoe — check local advice and the individual.

Chronic instability vs impingement — and surgery

• Instability: recurrent giving-way, even after small incidents, after prior trauma.
• Impingement: pain without true instability after recurrent injuries — common in young dancers; treatment differs.
• Connective tissue disorders: ligaments heal poorly; repairs using native tissue may fail — plan alternatives.
• Most sprains need good rehab, not surgery. When operating: ankle arthroscopy (camera + shaver portals) to clear scar, assess cartilage/OCLs, probe syndesmosis (e.g. “drive-through” type assessment), check ligaments; then open mini-incision lateral repair rather than all-arthroscopic lateral repair (nerve risk). Prefer repair of patient tissue; moved away from sacrificing peroneals (dynamic stabilisers). Internal brace (synthetic augmentation over the repair, often knotless anchors) for poor tissue, connective-tissue patients, or high-demand sport — body does not stretch it out the same way.
• Post-op sketch: moon boot with early DF/PF as pain allows (~4 weeks), then functional brace, wean from ~6 weeks. Share protocols freely with the physio/osteopath the patient trusts — “allied health is a bit like a hairdresser.”

Hormones, ligaments, and tendons

• Estrogen (and relaxin): influences collagen stiffness and failure load. Female athletes may be more ligament-injury prone around ovulation — “more klutzy.” Some use the pill to steady the hormonal environment; AIS-style thinking also looks at training periodisation across the cycle. Pregnancy/postpartum: nasty ankle or Lisfranc-type injuries after seemingly minimal trauma.
• HRT: many middle-aged women feel better; some notice more pain (e.g. plantar fasciitis) — correlation flagged, evidence evolving.
• Testosterone / TRT / anabolic steroids: more muscle bulk but relative weakness at the musculotendinous junction — Achilles, biceps, severe ligament injury, and signals of higher ACL risk in the early months of TRT (including discussion of use beyond classic male hypogonadism). Tendons may repair poorly. Patients may not realise the mismatch.
• Peptides: colleagues split — some hope for tendon healing, other evidence raises opposite concerns; works in dogs in some models. Watch this space; not a GP endorsement.
• Q&A: ACL concern with hormone therapy was discussed in the context of raising testosterone above physiological support levels — not a simple “all HRT” message.

Take-home messages for clinic

1. Pattern-recognise OA: forefoot (1st MTP), midfoot, hindfoot (subtalar/Chopart), ankle — history, contralateral exam, weight-bearing X-ray.
2. Simple treatments first for months: education, load, non-opioid analgesia, physio + podiatry, rocker soles, cheap orthotic trial; opioids last resort.
3. Refer for failed conservative care, deformity/ulcers, or diagnostic uncertainty — many never need surgery; healing is slow when they do.
4. Sprains: exclude fracture; don’t miss syndesmosis or deltoid; long boot then functional rehab beats short useless boots and prolonged rest.
5. Separate chronic instability from impingement; surgery is arthroscopy ± repair ± internal brace when rehab fails or tissue is poor.
6. Ask about cycle, pregnancy, TRT/steroids in soft-tissue presentations — hormones change the story.

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