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6002 Ankle & Foot Cheat Sheet by

Conditions of the foot & ankle

Achilles Tendin­opathy

- The achilles tendon (aka triceps surae) is the strongest & largest tendon in the body
- Connects aponeu­roses of the gastroc, soleus, & plantaris m. to the calcaneus bone
- Crucial foe enabling calf muscles to exert force on the heel, necessary for walking & running
- Various factors can contribute to achilles tendon injuries, affecting specific locations such as insert­ional (damage at insertion on the post calcaneus) & non-in­ser­tional (inv. "­wat­ershed area", 2-6cm proximal to the calcaneal insertion) tendon­itis, parate­non­itis, & tendon rupture
Aetiology (risk factors):
- Lifetime incidence of 24% in athletes
- Common in runner
- M>F (3.5:1)
- Intrinsic factors: anatomic factors, age, sex, metabolic dysfun­ction, foot cavity, dysmetria, muscle weakness, imbalance, gastroc dysfun­ction, anatomical variation of the plantaris m., tendon vascul­ari­sation, torsion of the achilles tendons, slippage of the fascicle, & lateral instab­ility of the ankle
- Extrinsic factors: mechanical overload, constant effort, inadequate equipment, obesity, medica­tions (corti­cos­ter­oids, anabolic steroids, etc), improper footwear (arch support), insuff­icient warming or stretc­hing, hard training surfaces, & direct trauma, etc
- Systemic risk factors: diabetes, hypert­ension, inflam­matory arthro­pathy, gout, & cortic­ost­eroids
- Mechanical tension concen­trated at medial­/ce­ntral paratenon & middle segment, common site of injury (sports-related)
- Tendon twists counte­rcl­ockwise on the R & clockwise on the L, rotating 90° during descent
- Soleus fibres insert antero­med­ially, while larger gastroc fibres insert posterolaterally
- Config­uratio may influence biomec­hanics & contribute to achilles tendinopathies
- Insert­ional achilles tendin­opathy charac­terised by degene­ration: loss of parallel collagen I fibres, fatty infilt­ration, & capillary proliferation
- Degene­ration leads to thickening of the tendon in advanced imaging
- No evidence of acute or recent inflam­matory process
Clinical presen­tation:
- Pts may present w/ Ssx from acute strain or gradual onset repetitive irritation
- Complaints inc. px or tenderness in the tendon or heel, intens­ifying w/ activity, esp. walking or running
- Difficulty standing on toes or walking downst­airs, morning px, & stiffness are common
- Warmth & swelling increases throughout the day, related to activity
- Symptoms can be tracked using the VISA-A Questionnaire
- Shoe insole assess­ment: may reveal wear patterns indicating hallux limits (dispr­opo­rti­onate wear under the 2-5th metatarsal heads & the pad of the great toe)
Physical examin­ation:
- Palpation helps localise the injury to the "­wat­er-shed area" or calcaneal insertion
- Mid-tendon px suggests non-in­ser­tional tendon­itis; posterior calcaneal px suggests insert­ional tendinitis
- Chronic tendin­opathy may show fusiform swelling & tendinous or bony enlargement
- ROM reveals passive dorsiFX deficits w/ px on resisted plantarFX
Special tests:
- Silver­skiold test: differ­ent­iates achilles vs gastroc tightness
- Thompson test (calf squeeze test) excludes tendon rupture
- Motion palp of subtler joint assesses mobility & identifies restrictions
Functional deficits throughout kinetic chain:
- Non-in­ser­tional tendin­opathy in runners linked to foot hyperp­ron­ation (subtalar eversion)
- Assess­ments inc.: loss of medial longit­udinal arch, forefoot abduction, calcaneal eversion, & navicular drop
- Check posterior tibialis strength (calcaneal eversion during heel raises), gastro­c/s­oleus flexib­ility, knee flexor­/ha­mstring strength, & hip abductor (glute med) strength
- Glute medius is associated w/ ankle dysfunction
Hallux limitus & foot functional stability:
- Limitation in passive dorsiFX of the 1st MTP joint associated w/ achilles tendon px
- Functional assessment inv. simulating a ground reaction force & checking for fluid dorsiFX & concurrent plantar FX of the 1st metatarsal head
- Radiog­raphs often unnecessary
- Ottawa ankle rules for ankle or mid-foot px post-trauma
- No defined rules for imaging non-tr­aumatic heel px, consid­eration may given in cases of signif­icant trauma w/ altered gait or to rule out other pathology
- Radiog­raphs of achilles tendin­opathy: tendon calcif­ication & spurs/­ent­hes­ophytes on the posterior calcaneus
- US or MRI to help identify & define tendon pathology
Major compli­cat­ions:
- tendon avulsion or rupture, any reoper­ation, DVT, reflex dystrophy, persistent neuralgia, deep infect­ions, deep suture reactions, & major wound problems
- Minor compli­cat­ions: discom­fort, superf­icial infect­ions, minor wound problems, scar sensit­ivity, hypert­rophy, mild parest­hesia, prolonged hospit­ali­sation
- Non-op­erative treatment is the 1° approach
- Best proven care: rest, eccentric rehab, & correcting mechanical faults
- Eccentric exercise programs, e.g. Alfred­son's heel drops, are effective
- Soft tissue therapy, stretc­hing, & myofascial release are necessary for flexibility
- Slowly progre­ssive loading programs are favoured over complete rest
- Return­-to­-play criteria inc. ankle dorsiFX, calf circum­fer­ence, & heel raises
- Referral suggested for pts failing conser­vative care, w/ limited proven alternatives
- Supple­ments like Boswellia serrata & curcum­inoids may improve Ssx
- In children & adoles­cents, the epiphyseal growth plate is weaker, more prone to Sever's disease (calcaneal apophy­sitis) from stressors that would cause achilles tendin­opathy in adults
- Achilles tendon rupture
- Retroc­alc­aneal bursitis
- Plantaris tendinopathy
- Disloc­ation of plantar flexor tendons
- Posterior ankle impingement
- Os trigonum syndrome
- Fascial tears
- Calcaneal fracture
- Irrita­tio­n/n­euroma of sural n.
- Fat pad irritation
- Systemic inflam­matory disease

Achilles Tendon Rupture

Partial or complete rupture
- Most common tendon rupture of the LL
- Common in 30-40 yo, esp. "­weekend warriors"
- Acute ruptures, often w/ sudden onset of px, accomp­anied w/ a "­sna­ppi­ng" sound or audible "­pop­" at the injury site
- Pts may describe the sensation as being kicked
- Injury leads to signif­icant px & disability
- Often associated w/ soccer, racket games, or basketball
- MisDx as ankle sprains in 20-25%
- Risk factors: prior intrat­end­inous degene­ration (tendi­nosis), steroid use, & inflam­matory arthri­tides
Aetiology (risk factors):
- 40/100,000/year
- M>F (75% of recrea­tional sports)
- Runners (7-18%)
- Dancers (9%)
- Gymnasts (5%)
- Tennis players (2%)
- American football players (<1%)
- Causes inc. sudden forced plantarFX, direct trauma, & long-s­tanding tendin­opathy or intrat­end­inous degene­rative conditions
- Systemic factors: chronic renal failure, collagen defici­ency, diabetes, gout, infect­ions, lupus, parath­yroid disorders, RA, thyroid disorders
- Foot problems: cavus foot, insuff­icient gastro­c-s­oleus flexib­ility & strength, limited dorsiFX, tibia vara, varus alignment w/ functional hyperp­ron­ation
- Involves a combin­ation of mechan­ical, struct­ural, & biomec­hanical factors
- Mechanical factors: AT descends from its origin, twists counte­rcl­ockwise on R & clockwise on L, rotating 90°, leading to its strength but can rupture if suddenly exposed to excessive tensile loads
- Structural factors: as people age, parallel collagen fibres become less organised & more prone to degene­ration, additi­onally, certain conditions (e.g. diabetes or chronic kidney disease) can compromise the tendon's structural integrity & increase risk of rupture
- Biomec­han­ical: stiffness is associated w/ potential risk factors, while high foot arches decrease the risk of injury; when the tendon is exposed to chronic stress or repeated microt­rauma, biomec­hanical factors combined w/ a compro­mised blood supply can lead to the degene­ration of tendon fibres & potential rupture
Clinical presen­tation:
- Acute, sharp px in the achilles region, typically following a sport
- Often accomp­anied by audible sound
- Hx of tendin­opathy
Physical examin­ation:
- Inability to stand on toes
- Weakness in ankle plantarFX
- Tendon discon­tinuity or bruising around the posterior ankle may be palpable
- +ve Thompson test (calf squeeze test)
- Imaging tests used to confirm Dx & rule out other injuries
- Plain radiog­raphs for fractures
- MRI or US for confirming achilles tendon rupture
- MRI should be reserved for ambiguous presen­tations or chronic injuries due to cost & time concerns, & to avoid delaying surgical treatment
- Re-rupture
- Wound healing complications
- Surgical nerves injury
- Excellent prognosis, but some pts may have residual deficits (e.g. reduced ROM)
- Good results from both, surgical & conser­vative treatment
- Higher re-rupture rate in non-surgical
- Conser­vative treatment will be prolonged
- RICE, px control, & functional bracing
- Muscle streng­thening & ROM
- Achilles bursitis
- Fractures
- Imping­ement syndrome
- OA
- Sprain
- Calf injuries
- Calcan­eof­ibular ligament injury
- Talofi­bular ligament injury

Ankle disloc­ations

- Common in A&E & come in two forms: tru disloc­ations w/o fracture & fracture - disloc­ation (more common)
- Ankle joint complex: subtalar, taloca­lca­neo­nav­icular, & talocrural joint
- True ankle is the talocrural joint, functi­oning as a hinge joint for PLANTAR & DORSI
- Subtalar joint is for IN & Eversion (frontal plane)
- Taloca­cla­neo­nav­icular joint & subtalar together for IN & Eversion
- Joint stability maintained by 3 ligament groups: tibiof­ibular syndes­mosis (limits motion between tibia & fibula), deltoid lig. (supports the medial ankle & resist Eversion), & lateral collateral ligament (resists INversion)
- Most cases, ligaments are strong enough to cause bones to give way, causing fractu­re-­dis­loc­ation
Aetiology (risk factors):
- Pure ankle disloc­ations w/o fracture is rare (0.065% of all ankle injuries)
- Talocrural disloc­ations accompany 21-36% of ankle fractures
- Most cases occur in M (72%) due to sports (31%) or motor vehicle accidents (30%)
- Common disloc­ation direction: poster­o-m­edial (46%)
- Irredu­cible ankle fractu­re-­dis­loc­ation may occur, e.g "­Bos­worth Fractu­re" where fibula locks behind the tibia
Mechanism varies:
- Pure ligame­ntous disloc­ation can occur in multiple directions & mechanisms
- Common mechanism involves maximal PLANTAR w/ axial load & forced IN of the foot
- This mechanism damages anterior talofi­bular & calcan­eof­ibular ligaments, leading to poster­o-m­edial dislocations
- Superior disloc­ation happen when EVERTED foot is DORSI, leading to rupture of the tibiof­ibular syndesmosis
- Predis­posing factors: peroneal muscle weakness, ligame­ntous laxity, & previous strains
- Common ankle fractu­re-­dis­loc­ations occur via similar mechanics as non-di­slo­cated ankle fractures
- Sometimes disloc­ations sponta­neously reduce, leaving a malleolus fracture
Clinical presen­tation:
- Pts typically present w. dislocated foot relative to the tibia
- Urgent need for approp­riate analgesia & rapid realig­nment of foot & ankle to proper anatomical position
- Delay can lead to skin breakdown & formation of fracture blisters, potent­ially resulting in permanent disability
- Severe pain
Physical examin­ation:
- Note direction of foot relative to the ankle mortise
- Assess presen­ce/­absence of dorsalis pedis & posterior tibial pulses
- Check capillary refill of the distal foot
- Evaluate for associated injuries of the foot
- Identify localising areas of tenderness & swelling
- Sensory exam should inc. dorm of the foot, lateral & medial aspects, & sensation proximal to 1st & 2nd MT (inner­vation od deep peroneal n.)
- Assess ability to FX & EXT toes
- Plain X-rays are crucial as 1st step (AP, lateral, Mortise)
- CT after ortho surgeon recomm­end­ation
- Infection
- Malunion/nonunion
- Skin necrosis
- Post-t­rau­matic arthritis (PTOA)
- Smokers have higher rates of post-s­urgical infections
- Diabetics higher rate of compli­cations e.g. malunion, wound healing issues, & deep infections
Pure ankle disloc­ations:
- Generally favourable
- Majority of pts become asympt­omatic after proper treatmemt
- Sympto­matic cases, mainly F, report stiffness or PTOA
- Closed disloc­ations lead to fewer Ssx compared to open dislocations
- Prognostic factors for worse outcomes: advanced age, vascular injury, delay to reduction, & inferior tibiof­ibular ligament injury
- Late compli­cat­ions: stiffness, degene­rative changes, joint instab­ility, & capsular calcification
Ankle fractu­re-­dis­loc­ation:
- Prognosis varies
- Worse outcomes compared to non-di­slo­cated ankle fractures
- Up to 63% of pts develop PTOA
- Factors contri­buting to PTOA: type of #, pt's sex, & reduction accuracy
- Study: 82% of pts had an "­exc­ell­ent­" to "­goo­d" outcome after 2-6 yrs follow-up
- Immediate referral
- Subtalar disloc­ation may occur alone or w/ ankle disloc­ation / fractu­re-­dis­loc­ation, potent­ially leading to misdia­gnosis during physical exam
- Plain films reveal reduced tibiotalar joint in isolated subtalar disloc­ations, aiding correct Dx
- High-e­nergy mechanisms may cause total talus extrusion, inv. both tibiotalar & subtalar disloc­ations

Recurrent ankle sprain

- Common condition
- About 40% can lead to chronic Ssx lasting at least 12 months post-injury
- Roughly 20% progress to chronic instability
- Both general public & athletes are susceptible
- Impairment of propri­oce­ption may contribute to recurrence
Aetiology (risk factors):
- Often caused by 1st-time ankle sprain
- Most commonly due to INversion + ADduction, 1° affecting ATFL
- Associated factors: diminished postural control, impaired propri­oce­ption, loss of muscle strength, ligame­ntous laxity (e.g. Ehlers­-Danlos s., Marfan s., Turner's s.), decreased ankle joint ROM, cavus foot-type
- 2.15 / 1000 in US
- Peak incidence 10 & 19 yrs (younger pts have higher rates)
- M 15-24yrs>F
- F 30-99yrs>M
- African American & Caucasians
- Nearly 50% of sprains occur during sports (baske­tball 41.1%, football 9.3%, soccer 7.9%)
- Milita­ry>­civ­ilians
- Index ankle sprains result in micros­copic tears & attenu­ation of ligaments
- Attenu­ation can result in functional & mechanical instability
- Most commonly injured: ATFL, CFL, PTFL
- Lateral ankle instab­ility: functional or mechanical
- Proper Dx crucial for treatment
- Functional instab­ility: chronic, described subjec­tively by pts
- No clinical or radiog­raphic findings for functional instability
- Propri­oce­ptive deficits common
- Mechanical instab­ility: excessive motion in ankle joint
- Clinically assessed w/ anterior drawer sign or radiog­rap­hically
Clinical presen­tation:
- Detailed Hx, inc. mechanism of injury
- Consid­eration of previous ligame­ntous attenu­ation from index ankle sprain
Physical presen­tation:
- Observe for disloc­ation or asymmetry
- Palpate for tender­ness, inc. medial ankle & fibula length
- Assessment of edema & ecchymosis
- ROM evaluation comparing contra­lateral side (normal: dorsi 10° w/ knee EXT, 20° knee FX)
- Muscle strength tests: PLANTARfx, DORSIfx, INversion, & Eversion
- DTR & sensation
-Special tests: anterior drawer test (ATFL integr­ity), "­dim­ple­" sign (subtalar instab­ility), Talar tilt test (CFL integrity & subtalar instab­ility), Kleiger EXT rot test (deltoid ligament injury­/ankle syndes­mosis injury)
Ankle sprain classi­fic­ation:
- Grade 1: mild stretching of lateral ligament complex w/ micros­copic tearing, no joint instab­ility, mild edema, no functional loss
- Grade 2: ligament tear or partial rupture (usually ATFL), modera­te-­severe edema & ecchym­osis, moderate functional loss, mild-m­oderate joint instability
- Grade 3: complete disrup­tio­n/r­upture of ligament w/ modera­te-seve ankle joint instab­ility, immediate edema & ecchym­osis, modera­te-­severe joint instability
- Plain films to rule out fractures (present in 15% of ankle sprains)
- MRI for soft tissue assess­ment, reserved for ligame­ntous surgical planning
- Ottawa ankle rules
Dx criteria for acute ligament injury:
- Healthy ligaments: thin, linear, low-signal intensity
- Acute injury: intras­ubs­tance edema seen as increased signal intensity
- Chronic injury: thicke­ning, elonga­tion, irregular contouring w/o signif­icant soft tissue changes
- Prone to reinjuring the same ankle
- 20-50% of cases of recurrent injuries lead to chronic px & instab­ility (CAI)
- CAI stems from propri­oce­ptive deficits & increased ligament laxity due to repeated sprains
- Pts w/ CAI usually have a Hx of multiple ankle sprains & severe INversion injuries
- Up to 85% of injuries is treated conservatively
- Neurom­uscular training therapy (propr­ioc­eption tasks & balance exercises) crucial for reducing recurrence rates
- Immobi­lis­ation recomm­ended for up to 10 days
- After 10 days progress to bracing & taping
- Mobs
- Exercises phase 1: single leg stance, ankle alphabet, standing gastroc stretch, standing soleus stretch
- Exericses phase 2: resisted ankle dorsifx w/ band, resisted ankle EVersion w/ band, wobble board
- Ankle fracture
- Posterior tibial tendonitis
- Neurom­uscular disorder
- Superf­icial peroneal nerve neuralgia
- Peroneal tendon tears
- Anterior process of the calcaneus fracture
- Base of 5th MT fracture

Calcan­eof­ibular ligament (CFL) sprain

Grade 1 to 3:
- Mild stretching of the ligament complex w/o joint instability
- Partial rupture of the ligament complex w/o joint instability
- Complete rupture of the ligament complex w/ instab­ility of the joint
- Common A&E visit (7-10%)
- 40% of sports injuries (usually affect the lateral ankle compartment)
- Lateral ankle inc: ATFL (2/3rds of lateral ankle injuries), CFL, PTFL
- Hard to differ­entiate between ATFL-s­upe­rim­posed CFL injuries & isolated CFL injuries
Aetiology (risk factors):
- Large % of lateral ankle injuries are sports related, esp. indoor & court sports
- Isolated CFL injuries are rare (usually classified under lateral lig. injury)
- 30,000 ankle sprains occur / day
- 25-40% of sports injuries
- Lateral ligament compar­tment is inv. in 85% of ankle injuries (10,000 / day)
- Origin & insertion: anterior lateral malleolus - posterior lateral tubercle of the calcaneus
- Crossed over by fibulas brevis & longus tendons
- Resists INversion during PLANTARfx & DORSIfx, stabilises the subtalar joint during PLANTARfx
- Mechanism of injury: results from combined INversion & supina­tion, but can also occur from INversion in extreme DORSIfx
Clinical presen­tation:
- Pt may report cracking sound
- Swelling, redness & px
- Inability to continue activities
Physical examin­ation:
- Special tests: anterior drawer test +ve; Talar tilt test +ve
Subsequent physical findings:
- Ecchymosis w/ localised px on palpation 4-5 days post-t­rauma, indicates 90% chance of lateral ligament rupture
- TTP over the CFL suggests 72% risk of ligament injury
Ottawa ankle rule:
- Palpation of 4 px locations
- Ability to bear weight
- US offers dynamic imgaging
- MRI useful for cases w/ high suspicion of ligament injury
Lateral ankle injury classi­fic­ation:
- Grade 1: ligament stretchuing
- Grade 2: moderate sprain
- Grade 3: severe sprain w/ full ligament lesions
- Re-injury of the lateral compar­tment is a common occurrence in low-grade ankle sprains
- Potential feeling of instab­ility & px which inhibits functional mobility
- Chronic joint instab­ility can progress to post-t­rau­matic ankle joint OA
- Education: 74% of pts experience chronic Ssx 4 yrs after injury, potential instab­ility or px, 32% pts report Ssx of original injury 7 yrs after
- RICE (4-5 days) & NSAIDs
- Immobi­lising w/ cast or boots ONLY in 1st week
- 3 phases of healing: inflam­matory (1-10 days), prolif­erative (4-8 weeks), & remode­lling (up to one year)
- Bracing or taping aids in return to activity after the initial immobi­lis­ation phase
- Conser­vative & surgical approach has similar outcomes
- Osteoc­hondral injury
- Fibularis tendon injury
- Ankle frcatures
- Achilles rupture
- Tendon dislocation
- Subtalar joint injury


- Also known as "­disease of kings & king of diseases"
- One of the most common causes of chronic inflam­matory arthritis
- Charac­terised by the deposition of monosodium urate (MSU) monohy­drate crystals in tissues
- Well-u­nde­rstood & manageable among rheumatic diseases
Aetiology (risk factors):
- Older age & males (20:1)
- >40 yrs
- Purine diet & alcohol
- Comorb­idites: hypert­ension, diabetes, hyperl­ipi­demia, & metabolic syndrome
- Genetic, metabolic factors can influence hyperu­ricemia (key factor)
- Monosodium urate crystal deposition in periar­ticular soft tissue
- Inflam­matory response: macrop­hages phagoc­ytise monosodium urate crystals → vasodi­lation → inflam­mation
Clinical & physical findings:
- Four distinct stages: asympt­omatic hyperu­ric­emia, acute gout attacks, inter-­cri­tical period, & chronic tophaceous gout
Asympt­omatic hyperu­ricemia
- Many pts w/ this stage don't develop gout
- Risk of gout increases w/ serum urate levels
- This stage ends w/ the first gout attack
Acute gout attack
- Sudden, severe px & swelling
- Common in LL, especially 1st MCP
- Can also affect other joints, tendons, & bursa
- Px is severe & may not respond to home remedies
- Subsequent attacks can be prolonged
- Certain factors like trauma, alcohol, diet, & medica­tions can trigger attacks
- Physical exam shows red, swollen, warm, & tender joints
- Tophi, urate deposits, can occur in chronic cases
Interc­ritical gout
- Follows resolution of acute attack
- Hyperu­ricemia persists, & subcli­nical inflam­mation may be present
Chronic tophaceous gout
- Tophi, granulomas around MSU crystal deposits develop
- Appears as chalk-like nodules under the skin
- Develops years after initial attack
- Can lead to destru­ctive arthritis & deformities
- Top can appear in various sites, including digits, knees, & olecranon bursa
- Deposits also reported in cornea & heart valves
- Synovial fluid analysis
- Labs inc. WBC, ESR CRP, still don't confirm gout
- Imaging (DECT) not commonly used
- Tophi
- Joint defomrity
- OA
- Bone loss
- Urate nephropathy
- Nephrolithiasis
- May also cause ocular compli­cat­ions, eg. conjun­cti­vitis or uveitis
- Prognosis depends on pts comorbidities
- Mortality is higher in pts w/ CV disease
- Medication
- Rest & ice
- Lifestyle modifi­cations
Gout flare
- Septic arthritis
- OA
- Psoriatic arthritis
- Cellulitis
- Trauma
Tophaceous gout
- Dactylitis
- RA
- Osteom­yelitis

Hallux rigidus & limitus

- Also known as "turf toe"
- Sprain of the plantar capsul­e-l­igament of the great toe MTP joint
- Typically results from forceful hyperEXT of the 1st MTP, commonly experi­enced in sports
- Injury to the plantar plate of the great toe causes px during push-off & decreases agility
- Turf toe can severely impact elite athletes & cause inconv­enience in the general pop
Aetiology (risk factors):
- Often caused by forceful hyperEXT of the 1st MTP joint
- Common in sports like basket­ball, soccer, & gymnas­tics, but partic­ularly in football
- Higher prevalence on artificial turf fields, especially older astroturf surfaces
- Modern high-pile turf mimics natural grass better, reducing the risk of turf toe
- Injury occurs due to the rigidity of the playing surface, placing strain on the feet
- The 1st MTP functions as both a hinge & sliding joint
- Has shallow articu­lation between the convex MT head & the concave base of the proximal phalanx, resulting in little bony stability
- Stability 1° relies on the complex attach­ments of the capsule, ligaments, & muscul­ote­ndinous structures surrou­nding the joint
- Strongest stabiliser of the 1st MTP is the plantar plate, which is a thickening of the joint capsule
- Plantar plate attaches to the transverse head of the adductor hallucis, the flexor tendon sheath, & the deep, transverse interm­eta­tarsal lig.
Injuries to the plantar plate classification:
- Grade 1: sprain of the plantar plate
- Grade 2: partial tear of the plantar plate
- Grade 3: complete tear of the plantar plate
Clinical presen­tation:
- Pt will complain of px & swelling of 1st MTP
- May also complain of antalgic gait & px, especially w/ foot flat to toe-off during gait cycle
- May or may not describe an inciting event of acute forceful hyperEXT of the 1st MTP
- Some reports of subacute to the chronic develo­pment of turf toe
Physical examin­ation:
- Swelling & ecchymosis at the 1st MTP
- Note antalgic gait, difficulty in toe raises, & joint deformities
- TPP over plantar aspect of 1st MTP
- Tenderness over medial, lateral, or dorsal joint
- Compare sesamoid bone position to assess proximal migration
ROM: Passive & active ROM
- Px w/ passive EXT & active FX of 1st MTP
Muscle strength:
- FX toes or EXT toe against resistance
- Perform ABD
Special tests:
- Valgus & varus stress test: assesses medial & lateral stability
- Vertical Lachman test: measure vertical transl­ation of proximal phalanx compared to MT; compare B
- Initial X-rays to assess for fracture or dislocation
- MRI w/o contrast to assess for plantar plate or surrou­nding soft tissue injury
Anderson classi­fic­ation:
- Grade 1: acute sprain w/o bony pathology or joint instab­ility, pt will have normal ROM & should be able to WB
- Grade 2: partial tear of the plantar plate or joint capsule, the pt will have painful ROM, ecchym­osis, swelling, & px w/ WB
- Grade 3: complete tear w/ loss of continuity of the plantar plate or capsule, may not sesamoid bone migration, marked TTP, decreased ROM, swelling, ecchym­osis, & difficulty WB
- Loss of push-off strength
- Hallux rigidus
- Cock-up deformity
- Traumatic bunion deformity
- Loose bodies in the joint space
- Joint fibrosis
- Acute compli­cat­ions: infect­ions, scar formation 2° to hypert­rophy, & plantar n. neuroma develo­pment
- Prognosis varies based on grade of the injury
- Initial treatment: RICE, stiff sole/r­ocker bottom sole to limit motion
- For severe injuries: CAM boot/w­alking cast to minimise motion & aid healing
Progre­ssive motion:
- Start once injury stabilises
- Grade 1: return to play in 1-2 weeks
- Grade 2: recovery in 4-6 weeks; may require taping to resist hyperEXT of MTP joint
- Cortic­ost­ero­id/­ane­stehtic injections not advised for grade 2 injuries
- Grade 3: conser­vative treatment w/ immobi­lis­ation (4-6 weeks), then gentle ROM
- Expected healing time for grade 3: 6-12 months
Surgical repair:
- If conser­vative management fails
- Indica­tions: large capsular avulsion, unstable joint, sesamoid issues, instab­ility, hallux valgus deformity, chondral injury, intra-­art­icular loose body, sesamoid fracture, failed conser­vative treatment{{nl}Post-op manage­ment:
- Gentle passive motion at 7-10 days, then be non-WB in removable splint or boot w/ hallux protected for 4 weeks
- At 4 weeks, increase active motion & allow ambulation in the boot
- Pt wear modified shoe at 2 months & return to contact activity w/ protection from excessive DORSI at 3-4 months
- Expect 6-12 months for a full recovery
- Hallux rigidus / limitus / valgus
- Reverse turf toe
- Soccer toe

Hallux Valgus (HV)

- Also known as bunion
- Common forefoot deformity
- Exact cause enot understood
Aetiology (risk factors):
- F>M
- Est. 23% of adults 18-65
- Est. 36% of adults >65
- Multi-factorial
- Associated w/ connective tissue disorders, e.g. Marfan syndrome, Ehlers­-Danlos syndrome, & Downs syndrome
- Muscle imbalance due to conditions like stroke, cerebral palsy, or myelomeningocele
- Slight increased risk in tight shoes & heels
- Interplay of various factors
- Imbalance between extrinsic & intrinsic muscles, along w/ ligament involvement
- 1st metatarsal alignment maintained by tension from peroneus longus laterally & abductor hallucis medially
- Collateral ligaments prevent transverse plane movement at the 1st MTP joint
- Increased pressure at 1st MT head lead to medial­-dorsal movement, increasing hallux angle
- Muscle stabil­isation during walking worsens this condition
- Forces pushing 1st MT medially & hallux laterally strain & eventually rupture medial collateral ligament & medial capsule
- W/o medial stabil­isation struct­ures, lateral structures exacerbate HV deformity, inc. adductor hallucis muscle & lateral joint capsule ligaments
Clinical presen­tation:
- Commonly presents w/ a chronic progre­ssive onset
- Proximal phalanx pronation & lateral deviation, & medial deviation of the 1st MT head, often causing redness & px
- Often sharp or deep px at the MTP joint exacer­bated by walking
- Aching px at the head of the 2nd MT may also be reported
- Px, frequency, duration, & severity increases as the deformity progresses
- Tingling or burning px at the dorsal part of the deformity may indicate medial dorsal cutaneous n. neuritis due to compression
- Ssx are 1° due to pressure on the 1st MT, toes, & other MT bones
- Additional Ssx inc. blisters, ulcera­tions, interdigit keratosis, & irritated skin, which can limit physical activities
Physical examin­ation:
- HV deformity severity more obvious in weight­-be­aring stance
Biomec­hanical exam
- Forefoot / rearfoot varus of valgus
- 1st ray hypermobility
- Subtalar joint stiffness
- Midtarsal joint stiffness
- Resting calcaneal stance position
- Tibial torsion
- Neutral calcaneal stance position
Non-weight bearing:
- Assess hallux position relative to the 2nd digit (under­-ri­ding, overri­ding, or w/o contact)
- Evaluate lateral deviation of the MTP joint & medial prominence
- Assess 1st MTP joint ROM & quality
Weight bearing:
- Evaluate for increased hallux abduction, medial promin­ence, 1st MTP joint dorsif­lexion, hallux purchase, & metatarsus varus
- Labs if there's suspected metabolic or systemic disease (rheum­atoid factor, CRP, ESR, uric acid, CBC)
- MRI & radion­uclide imaging for suspected osteomyelitis
- Plain radiog­raphs help determine the extent of damage to the 1st MTP joint
Lateral callus deviation, w/ normal angles:
- Hallux valgus angle (HVA) less than 15°
- Interm­eta­tarsal angle (IMA) less than 9°
Classi­fic­ation of hallux valgus severity:
- Mild: HVA 15-30° / IMA 13-20°
- Moderate: HVA 30-40° / IMA 13-20°
- Severe: HVA over 40° / IMA over 20°
Imaging views:
- WB A-P
- Lateral oblique
- Lateral
- Sesamoid axial
- Bursitis (most common)
- Second toe hammertoe deformity
- Degene­rative disease of the metatarsal head
- Central metatarsalgia
- Medial dorsal cutaneous n. entrapment
- MTP joint synovitis
- Good prognosis
- First a trial of conser­vative treatments (Ssx manage­ment): shoe modifi­cation, orthoses, analge­sics, icing, bunion pads, & stretching
- Surgery if px & functi­onality isn't improved
- Post-op care varies based on the procedure, commonly involves limited WB, ROM exercises, & long-term monitoring
- OA
- Freiberg disease
- Hallux rigidus
- Morton neuroma
- Turf toe
- Gout
- Septic joint

Meidal Tibial Stress Syndrome (MTSS)

- Also known as shin splints, Jogger's foot, & Medial plantar nerve s.
- Common overuse lower extremity injury in athletes & military
- Exerci­se-­induced px over the anterior tibia
- Early stress injury in the continuum of tibial stress #
Aetiology (risk factors):
- 13.6-20% in runners
- Up to 35% in military
- Overdue condition
- Tibial bony overload injury w/ associated periostitis
Causes & predis­posing factors:
- Signif­icant increasing loads, volume, & high impact exercises
- F gender
- Previous Hx of MTSS
- High BMI
- Navicular drop
- Hip EXT rot ROM
- Vitamin D deficiency
- Results from accumu­lation of unprepared micro damage in the cortical bone of the distal tibia
- Perios­titis, inflam­mation of the perios­teum, is typically present at the site of bony injury
- Affected area correlates w/ tendinous attach­ments of the soleus, flexor digitorum longus, & posterior tibialis muscles
- Sharpey's fibres, connective tissue fibres linking periosteum to bone, play a role
- Repetitive muscle traction is believed to contribute to perios­titis & cortical microtrauma
- Uncertain whether perios­titis or cortical microt­rauma occurs 1st in the develo­pment
Clinical presen­tation:
- Presence of exerci­se-­induced px along the distal 2/3s of the medial tibial border
- Presence of px provoked during or after physical activity, which reduces w/ relative rest
- The absence of cramping, burning px over the posterior compar­tment &/or numbne­ss/­tin­gling int he foot
Physical examin­ation:
- Presence of recogn­isable px reproduced w/ palpation of the poster­o-m­edial tibial border >5cm
- Absence of other findings not typical of MTSS (e.g severe swelling, erythema, loss of distal pulses, etc)
- Dx though clinical & physical findings
- Imaging is often used when uncertain of the cause or to rule out other lower extremity injuries
- Plain radiog­raphs normal for MTSS & early stress fractures, but a "­dreaded black line" indicates #
- MRI is the preferred imaging for MTSS & higher grade bone stress injuries (e.g tibial stress #)
- Evaluation for vitamin D deficiency may be necessary, especially for persistent cases
- Px leading to decreased perfor­mance &/or time away from training/participation
- Presum­ption: MTSS may progress to a tibial stress #
- Cortical microt­rauma may evolve into cortical #
- Not every pt experi­encing MTSS develops a tibial stress #
- Several tibial stress # may necess­itate surgical interv­ention
- Full recovery expected w/ adequate rest & activity modification
- Foot arch support/orthotic
Exercises phase 1: Ant. tib. stretch - sitting, Post. tib. stretch - standing, Dynamic gastroc stretch, standing soleus stretch
- Exercises phase 2: Semi-stiff dead lift, Resisted post. tib. strengthening
- Optimising calcium & vitamin D
- Gait training
- Tibial stress #
- Chronik exertional compar­tment s/ (CECS)
- Vascular ethologies (e.g. functional popliteal artery entrapment s., peripheral arterial disease, etc)
- FPAES & PAD both manifest as claudi­cations


- Px & inflam­mation of the ball of the foot
- Commonly occurs in runners & jumpers
- Other causes inc. foot deform­ities & ill-fi­tting footwear
- Rest & ice can alleviate Ssx
- Proper footwear w/ shock-­abs­orption insoles or arch support
Aetiology (risk factors):
- Partic­ipating in high-i­mpact sports (running & jumping
- Ill-fi­tting shoes (espec­ially heels)
- Obesity
- Other foot problems (hammertoe & calluses on the bottom of the foot)
- Inflam­matory arthritis (RA & gout)
- Intense training or activity
- Certain foot shapes: high arch, 2nd toe that's longer than the big toe
- Foot deform­ities: hammertoe & bunions
- Excess weight
- Poorly fitting shoes
- Stress fractures: can change WB distribution
- Morton's neuroma: noncan­cerous growth usually occurs between 3-4th MT head, causes Ssx similar to metata­rsalgia & can also contribute to metatarsal stress
Clinical & physical findings:
- Sharp, aching or burning px of the ball of the foot
- Px that worsens when standing, running, flexing the foot or walking
- Improves w/ rest
- Sharp or shooting px, numbness, or tingling in toes
- Feeling of having a pebble in the shoe
- Tender on palpation
- Mulder sign (squeeze test) helps Dx conditions like Morton's neuroma, which can present similar to to metata­rsalgia
- X-ray to rule out stress fractures & other conditions
- Rest & ice
- Wear proper shoes
- Use metatarsal pads
- Consider arch supports
- STW (gastroc & soleus)
- Exercises: toe curls & spreads, active arch, single limb heel raise
- Morton's neuroma
- Stress fracture
- Capsulitis
- Freiberg's disease
- Sesamoiditis
- Arthritis
- Bursitis
- Tendonitis

Morton's Neuroma

- Compre­ssive neuropathy of forefoot interd­igital n.
- Compre­ssion, irritation at plantar aspect of transverse inter-MT lig.
- Not a true neuroma: degene­rative, not neolpastic
- Also known as Morton metata­rsalgia / entrapment, Interd­igital neuritis / neuralgia / neuroma / n. compre­ssion s., & InterMT neuroma
- Most common location: between 3 & 4th MT head (termed Morton neuroma)
Aetiology (risk factors):
- Common in middle - aged F (F>M, 5:1)
- Rarely B, & rare to have 2 neuromas on the same foot
Common causes:
- Narrow toe-box footwear
- HyperEXT of toes in high-h­eeled shoes
- Deviation of toes
- Inflam­mation of interMT bursa
- Thickening of transverse MT lig
- Forefoot trauma
- High-i­mpact sporting activities
- MTP joint pathology
- Lipoma
- Compre­ssion & repetitive trauma to the n. results in vascular changes, edoneurial edema, & excessive burial thickening leading to perineural fibrosis
4 main hypoth­eses:
- Chronic trauma theory: walking causes chronic micro-­traumas to interMT plantar digital n., compressed between MT heads & MTP joints
- Entrapment theory: interd­igital neuromas occur due to compre­ssion of interd­igital n. against deep transverse MT lig & plantar soft tissue structures
- InterMT bursa theory: bursitis in interMT region causes compre­ssion, inflam­mation, & subsequent fibrosis of affected common plantar digital n.
- Ischemic theory: based on histop­ath­olo­gical findings of common plantar digital artery exhibiting degene­rative changes before n. thickening
Clinical & physical findings:
- Plantar px located between MT heads
- Aggrav­ation of px by walking & wearing tight-­fit­ting, high-h­eeled shoes
- Relief when resting & removing shoes
- Described as burning, stabbing, or tingling, sometimes w/ electric sensation
- Sensation akin to walking on a stone or marble
- Numbness between the toes is present in <50% of pts
- Prolonged walking may lead to px radiating to the hind foot or leg, possibly causing cramps
- Palpation may reproduce px
- Compre­ssion of the forefoot mediol­ate­rally can cause "­Mul­der's click"
- Dx based mainly on clinical & physical findings
- Plain WB radiograph to tule out various conditions
- US aids in Dx
- MRI, especially to rule out other Dx
- Chronic px (CRPS)
- Recurrence of the deformity due to inadequate excision or converting a Morton neuroma into a true neuroma
- Surgical compli­cations (infec­tion, px, bleeding)
- Cortic­ost­eroid injection compli­cations (skin/fat pad atrophy, skin discol­our­ation)
- Good prognosis if proper protocol followed
- MT pads
- Nerve release
- Exercises: Resisted flexor hallucis longus, Standing gastroc stretch, Plantar fascia - towel & golf ball
- MT stress fracture
- Hammertoe
- RA or OA
- Malignancy
- Ganglion cyst

Plantar Fasciitis

- Results from degene­rative irritation at the origin of the plantar fascia
- Overuse stress is a 1° cause, leading to sharp localised px at the heel
- Heel spurs may occasi­onally accompany plantar fasciitis
- Treatment is challe­nging, w/ pt dissat­isf­action common despite various approaches
- Non-su­rgical management is typical but often results in recurring px
Aetiology (risk factors):
- Lead cause of heel px
- 10% of general population
- 40-60 yrs
- 10% of runner­-re­lated injuries & 11-15% of foot Ssx needing medical care
- Often B in 1/3 of cases
- F>M (espec­ially w/ higher BMI)
- 1° an overuse injury causing micro-­tears in the plantar fascia, but trauma or other causes can contribute
- Predis­posing factors include pes planus, pes cavus, limited ankle dorsif­lexion, prolonged standing or jumping, & excessive pronation or supination
- Tightness in posterior leg muscles can alter ambulation biomechanics
- Risk factors include obesity, aging, occupa­tions w/ prolonged standing, & certain medical conditions
- Linked to some spondy­loa­rth­rop­thies
- Multif­act­orial cause
- Believed to start w/ microtears due to repetitive trauma → stretching of plantar fascia → chronic degene­ration of fascia
Histol­ogical findings:
- Granul­ation tissue
- Micro-tears
- Collagen disarray
- Lack of tradit­ional inflam­mation
Clinical & physical findings:
- Pts typically report progre­ssive px at the inferior & medial heel
- Px can radiate proximally in severe cases
- Sharp, worse in the morning, exacer­bated by prolonged standing or sitting
- Px decreases w/ ambulation but increases throughout the day
- Px reprod­ucible by palpating the plantar medial calcaneal tubercle or passive dorsif­lexion of foot / toes
- +ve windlass or Jack test: px elicited w/ passive dorsif­lexion of 1st MTP joint
- 2° findings: tight Achilles heel cord, pes planus, pes cavus
- Assessment of gait to evaluate biomec­hanical factors or predis­posing factors
- Consider Ddx including fat pad contusion or atrophy, stress fractures, & nerve entrap­ments (e.g tarsal tunnel s.)
- Usually Dx clinically
- X-rays or US used if other injuries suspected or pt doesn't improve conservatively
- MRI considered to check for tears, fractures, or defects
X-ray findings:
- Calcifications
- Heel spurs
- Thickening
- Swelling
MRI findings:
- Thickening
- Increased signal on specific images
- Rupture of the tendon, 1° if cortic­ost­eroid injections are employed
- Fat pad necrosis
- Flattening of the arch
- 75% resolve sponta­neously within. 12 months
- 5% need surgery (not consis­tently +ve)
- Foot arch taping
- Support brace (Stras­sberg sock)
- Exercises Phase 1: Hamstring doorway stretch, golf ball, standing gastroc stretch on step, flexor digitorum brevis streng­the­ning, plantar fascia stretch
- Exercises Phase 2: Resisted post tib streng­the­ning, Vele's, Eccentric achilles streng­thening
- Calcaneus injury
- Infection
- Sickle cell bony px
- Bone contusion
- Neurop­athic px
- Tendinitis
- Osteoporosis
- Malignancy


- Inflam­mation of the sesamoid bones in the ball of the foot & the tendons they are embedded in
Aetiology (risk factors):
- Athletes get it from over-p­rac­ticing movements that transfer weight to the ball of the foot
Population at risk:
- Dancers
- Runners
- Athletes
- High-heel shoes
- High arches
- Flat feet
- Overpr­onated feet
- People w/ gout
- Sesamoid bones are only connected to tendons
- These bones endure stress from movement & interact w/ tendons during motion
- Bear additional stress from shock absorption during walking
- Activities that frequently transfer weight to the ball of the foot can overstress these tendons & bones, causing inflam­mation & px
Clinical & physical findings:
- Px under the big toe
- Struggle to flex big toe
- Struggle to WB or walk
- Swelling
- Redness
- Bruising
- Passive axial compre­ssion test +ve
- X-ray, CT, US, or MRI to rule out conditions
- Stress fracture
- Turf toe
- Hammertoe
- OA
- Gout
- Hallux rigidus (espec­ially if previous big toe injury)

Sinus Tarsi Syndrome (STS)

- Persistent antero­lateral ankle px 2° to traumatic injuries to the ankle
- Recent theories: 1° an instab­ility of the subtalar joint due to ligame­ntous injuries that results in a synovitis & infilt­ration of fibrotic tissue into the sinus tarsi space
Aetiology (risk factors):
- Associated w/ ankle sprains, potent­ially leading to talocrural joint instability
- Est. 10-25% of pts w/ chronic talocrural joint instab­ility also have subtler joint instab­ility
- Arises from a single traumatic event or multiple ankle sprains causing signif­icant damage to ligaments
- Injuries 1° affect the talocrural intero­sseous & Cx ligaments, leading to subtler joint instab­ility & excessive supination / pronation movements
- Excessive movement in the subtalar joint applies increased forces on the synovium & sinus tarsi tissues
- Resultant forces induce subtalar joint synovitis, chronic inflam­mation, & fibrotic tissue infilt­ration in the sinus tarsi, causing antero­lateral ankle px charac­ter­istic of STS
- Traumatic injuries may also harm ligaments in the tibiotalar & taloca­lcaneal joints, increasing rearfoot & mid foot mobility & instability
- Athletes w/ heightened mobility in the talocrural & subtalar joint are at higher risk of instab­ility following an ankle injury
Clinical & physical findings:
- Deep sinus tarsi px
- Swelling, bruising, TTP
- Feeling of instability
- Px at end of PF + SN in sinus tarsi
- Ankle instab­ility + px over sinus tarsi indicates STS
- Tests: foot hyperp­ron­ation cluster, anterior drawer, ROMs, subtler instab­ility test, standing ankle torsion test
- Used to assess soft & bony tissue
- Ice
- Support brace
- Exercises Phase 1: Lower extremity Y-balance, Single leg stance, Active arch, Wobble board
- Exercises Phase 2: Semi-stiff dead lift, Resisted ankle invers­ion­/ev­ersion w/ band, Eccentric post tib
- Instab­ility of talocrural & subtalar joints
- Cuboid subluxation
- Fracture


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