Foot and Ankle Injuries.pdf

Foot and Ankle Injuries STRESS FRACTURES Microscopic injury of bone that occurs due to repetitive, submaximal loading of bone Stress fracture occurs when the bone’s ability to rebuild itself is outpaced by continued repetitive forces Intrinsic Risk Factors Anatomical considerations...

Foot and Ankle Injuries STRESS FRACTURES Microscopic injury of bone that occurs due to repetitive, submaximal loading of bone Stress fracture occurs when the bone’s ability to rebuild itself is outpaced by continued repetitive forces Intrinsic Risk Factors Anatomical considerations ○ Cavus foot type ○ Short/Long metatarsals ○ Dorsiflexed/Plantarflexed metatarsals ○ Leg length discrepancies ○ Excessive forefoot varus ○ Tarsal coalitions ○ Prominent posterior calcaneal process ○ Equinus Female gender → Triad ○ Amenorrhea Osteopenia/osteoporosis Poor vascular supply Abnormal hormonal levels ○ Estrogen (low) / testosterone (high) Extrinsic Risk Factors Type of activity ○ Military (marching) ○ Runners → increase mileage quickly w/ou proper training ○ Ballet, jumping sports Excessive/new training regimen ○ Muscle fatigue Muscles help w/ shock absorption → increased fatigue = can't redistribute energy along mm as well → stress goes to bone → stress fx Poor equipment/footwear ○ Won't be absorbing shock its supposed to → shock goes to foot instead Improper technique ○ FF strike vs RF strike Type of training surface ○ Concrete much harder than rubber/grass etc Nutrition Etiology 2 different types ○ Fatigue stress fracture Abnormal stresses on normal physiologic bone  Biomechanical abnormalities, changes in activities etc ○ Insufficiency stress fracture Normal stresses on abnormal physiologic bone Bone cyst → weakens bone; day to day walking could result in fx Need to tx underlying condition History Progressive onset of pain with weight-bearing activity over a period of days to weeks Rapid increase in mileage/intensity/duration of activity Changes in playing surface Changes in sport Inadequate rest period Diet/nutrition Medications Footwear Menstrual cycles in female athletes Physical Exam Point tenderness Edema, Calor, Ecchymosis Palpable bone callus Pain with weightbearing/range of motion Tuning fork (50% false negative) Evaluation of Etiology Biomechanics ○ Limb length discrepancy ○ Limb alignment ○ Foot alignment/deformities Rigid/flexible ○ Range of motion ○ Muscle strength ○ Anatomical considerations ○ *Must address biomechanics.. If you don’t, and you tx the fracture and it heals → it will happen again b/c biomechanics are still a problem Esp important for fatigue type Gait analysis ○ Running form/technique Skin ○ Callosities Imaging Radiographs ○ Often negative for 2 weeks until resorption, sclerosis, or callus formation occurs CT  ○ CAN identify incomplete/complete fractures Gold standard to evaluate navicular stress fracture If pt has pain dorsal/mid navicular → order CT ○ CANNOT aid in identification of stress reactions ○ CT Navicular Stress Fractures (Saxena et al. ) Type 1 involves a dorsal cortical break Type 2 involves fracture propagation into the navicular body Type 3 consists of fracture propagation into another cortex Types 2 and 3 may benefit from early surgical intervention Type I Type II Type III MRI ○ High specificity and resolution of stress fractures/stress reactions ○ Note: stress FX = actual break in the cortex vs stress RXN = increased pressure causing edema ○ Due to delay in radiographic evidence, order an MR if suspecting stress rxn/fx Bone Scintigraphy (Bone Scan) ○ Changes can be seen within 48-72 hours ○ Uptake in all 3 phases is characteristic of stress reaction/fracture ○ Not done very often; time consuming for the pt Treatment considerations Healing potential of bone  ○ High risk fractures → areas with reduced vascular supply Sesamoids Proximal second metatarsal Navicular Esp central ⅓ Intra-articular fracture Very concerning for post traumatic arthrosis Note: with high risk fxs, nonunion and post traumatic arthrosis are far more likely Txs will take longer, longer period of NWB, slower and later return to sport, etc ○ Less critical → areas w/ increased vascular supply Base of fifth metatarsal Medial malleolus Talus ○ Non critical Distal metatarsals Lateral malleolus Calcaneus ○ Systemic factors Osteopenia/porosis DM Neuropathy etc Initial tx for all stress fxs ○ PRICE Protect Rest/reduce activity Cross training (swim, bike, etc → no impact but maintains cardio status) Immobilization Compression Elevation Systemic Considerations ○ Bisphosphonates Decreases bone turnover by inhibiting osteoclast function ○ Calcitonin Inhibits osteoclasts, increasing bone mineral density ○ Calcium/vitamin D Can improve bone mineral density Bone stimulators ○ Consider for fxs that aren’t healing as expected → esp high risk fxs  Insurance covers after ~ 90 days ○ Electromagnetic stimulators Piezoelectric effect: generates electromagnetic fields around fracture so that fluid can flow around and through bones, open calcium channels in cell membranes and increase cell proliferation ○ Ultrasound stimulators Increases growth factors and promotes angiogenesis via micro motion Biomechanical considerations ○ Once healed, orthosis or shoe modifications can be used to prevent recurrence of stress fractures ○ Ex: Long 2nd MT Try to PF 1st Ray to decrease amt of weight 2nd MT bears First ray cut out Reverse morton’s extension Cast w/ 1st ray PF’d ACHILLES TENDINOPATHY Anatomy ○ Watershed area: Area of Achilles 2-6 cm proximal to the insertion site of the calcaneus Has reduced vascularity and is more prone to injury Only received blood from peritenon Types ○ Insertional Within 2 cm of insertion at tendon/bone interface ○ Non-insertional/Mid-substance 2-6 cm proximal to insertion → Watershed area ○ Tendinitis Acute inflammatory state ○ Tendinosis Chronic degenerative process Etiology of Achilles Tendinopathy Mechanical overloading Equinus ○ Esp w/ minimalist shoes that don't have much of a heel to toe drop → increase stress on achilles Overpronation History and Physical History ○ Pain aggravated by activity ○ Stiffness associated with prolonged periods of rest Physical Examination ○ Pain to the distal 2cm of the Achilles tendon vs pain to the midsubstance of the Achilles tendon, 2-6 cm proximal to the insertion ○ Swelling/redness on posterior calcaneus vs along Achilles tendon itself ○ Ankle ROM/Silverskiold test → eval equinus AJ DFion w/ KE vs KF (knee flexion removes gastroc influence) Imaging Radiographs ○ Lateral weightbearing radiographs Enthesophytes, intratendinous calcifications, haglund’s deformity (physically irritates tendon) Kager’s triangle to evaluate for retrocalcaneal bursitis/Achilles tendonitis If blurry → indicates more fluid in the area → tendinitis White arrow in image C marking retrocalcaneal recess → if lost → bursitis Ultrasound/MRI ○ Evaluate for soft tissue changes Tendon degeneration, neovascularization, bursitis, paratendinitis ○ Evaluate for bone changes Enthesophytes, intratendinous, calcifications Treatment  Physical therapy modalities ○ Strengthening Eccentric exercise program helps to strengthen calf, lengthen myotendinous unit, and decrease neovascularization More helpful in non-insertional Achilles tendinopathy ○ Stretching Night splints Really need to address equinus Address biomechanics ○ Orthoses Can help reduce effect of equinus/reduce strain on Achilles ○ Heel lift Can help temporarily reduce strain on the Achilles tendon Immobilization with/without lift Be wary of corticosteroid injections in any tendinopathy ○ May lead to further tendon degeneration/potential tear Treatment for Chronic Tendinosis Chronic → not responding to traditional therapies such as: ○ NSAIDS, immobilization, PT, etc ○ OR, has been present for years and wasn’t treated Treatment methods attempt to take chronic issue and turn it into an acute issue so that it can then be treated with modalities for acute problem ○ Shockwave Essentially a meat tenderizer → promotes GF via microtrauma ○ Platelet-rich plasma injection Surgical Treatment If all else fails → consider these surgical options ○ Open debridement and decompression Removal of pathologic tendon/calcification/enthesophytes Tendon may need to be detached and reattached Requires longer NWB period postoperatively ○ FHL tendon transfer FHL may be used to augment the Achilles tendon if there is severe degeneration of the Achilles ○ Grafts can be used as well to improve strength of tendon ○ Gastrocnemius recession/Achilles tendon lengthening May be useful adjunct procedure if equinus is major contributing factor Achilles rupture Males 30-40 years old, women 60-80 years old  ○ Sports injuries in younger population (“weekend warrior”) ○ Activities of daily living in older population (Achilles degeneration) Often neglected → pt doesn’t know they ruptured it Fluoroquinolone (Cipro, Levaquin) use or steroid injection may increase risk of rupture History and Physical History ○ Sudden onset of pain ○ Non-contact injury ○ Feels as if they had been kicked in the back of the ankle What they are feeling is the tendon snapping against the back of their calf ○ Audible snap/pop ○ Difficulty with plantarflexion/weight bearing/limp Physical Examination (Dx is often clinical) ○ Simmonds-Thompson test ○ Palpation of defect/gap ○ Decreased resting ankle tension ○ Achilles tendon strength (reduced) ○ Ankle dorsiflexion (increased in ruptured side) ○ Apropulsive gait Imaging Achilles tendon rupture is mostly a clinical diagnosis Can evaluate with ultrasound or MRI if exam is inconclusive ○ MR often used for surgical planning Treatment considerations Non-operative vs operative ○ Cast immobilization vs. direct repair with/without graft More research supporting cast immobilization →  don’t have a lot of the complication you may have with direct repair Cast in plantarflexed position → gravity equinus Functional rehabilitation ○ Early motion/weightbearing Controlled weightbearing/range of motion will stimulate healing Complete unloading of midsubstance repairs is generally detrimental (Less healing, increased adhesions, decreases callus size/mechanical strength of healing tendon) Chronic/neglected Achilles rupture ○ FHL transfer Current literature ○ Soroceanu et al 2012 → Non op? DO EARLY FXNL REHAB → Similar outcome to op tx → great for non ideal surgical candidates Surgery reduced risk of rerupture by 8.8% when compared against non-operative treatment without functional rehab If functional rehab protocol with early ROM was implemented as part of conservative treatment, rates of rerupture were equivalent Increased risk of complications in surgical group No difference in functional outcome measures ○ Lantto et al 2016 Performance scores between 2 options were similar Surgery restored calf muscle strength earlier and maintained increased strength at 18 months HAGLUND’S DEFORMITY/ “Pump bump” Haglund’s deformity: ○ Hypertrophy or prominence of the posterosuperior-lateral border of the calcaneus Causes chronic mechanical irritation of posterior heel Superficial Achilles tendon bursitis or retrocalcaneal bursitis Hyperkeratosis/keratoma Etiology Can be structural or positional, or combination Common biomechanical etiologies ○ Heel in varus to begin with: Compensated Rearfoot Varus ○ Supinated to compensate → causes heel to rock back and forth: Compensated Forefoot Valgus Rigid Plantarflexed 1st Ray Cavovarus ○ Forefoot varus History  Pain at the posterior heel with walking/activity May be irritated with certain shoes Can be associated with limping/swelling Physical Exam Prominent bump present posterior heel Inflammation, swelling, erythema, tenderness to posterior heel Tenderness to Achilles tendon/retrocalcaneal bursa Imaging Radiographs ○ Bony prominence at posterosuperior part of the calcaneal tuberosity ○ Kager’s triangle Buritis: Retrocalcaneal bursa causes loss of retrocalcaneal recess Tendinitis: Achilles tendon thickening >9mm Loss of distinction of posterior margin ○ Fowler and Philip angle (FPA) Normally 44-69 >75 normally will present with posterior swelling, cutaneous compromise and prominence superior to Achilles insertion which often leads to retrocalcaneal bursitis FPA Angle > 75 → STRUCTURAL Haglund's = calcaneus at increased pitch to create bump ○ Total Angle of Ruch Takes into account the calcaneal inclination angle and posterior structural prominence >90 correlates highly with retrocalcaneal bursitis and Haglund’s deformity ○ Parallel Pitch Lines Used to assess the prominence of the posterosuperior prominence of the body of the calcaneus MRI ○ Evaluates associated soft tissue pathology Achilles tendonitis/bursitis ○ Marrow edema posterior tuberosity Treatment Conservative ○ Change in shoes Avoid shoes with tight counters/elevated heel height ○ Padding of the shoe Heel counter pad ○ Orthosis to address biomechanical etiology  Deep heel cup to prevent heel rocking ○ Address associated soft tissue pathology ○ Immobilization if severe ○ Anti-inflammatories ○ Physical therapy ○ Stretching ○ Ultrasound ○ Cryotherapy Surgical Treatment ○ Calcaneal ostectomy Lateral incision Remove the bump ○ Calcaneal osteotomy Increased FPA Keck and Kelly ANKLE IMPINGEMENT SYNDROMES General overview Ankle Impingement Syndrome ○ Abnormal entrapment or contact of structures resulting in pain or restricted motion ○ In ankle, generally grouped as anterior or posterior impingement Anterior Ankle Impingement Syndrome Compression of the structures of the anterior margin of the tibiotalar joint during dorsiflexion Presents as anterior ankle pain during dorsiflexion Pain with climbing stairs, running, walking up hills, ascending ladders, deep squatting ○ All activities that prompt dorsiflexion Common in soccer players Etiology ○ Anterior ankle exostosis ○ Anterior intra-articular soft tissue (fibrous bands, thickened ATFL ligament, synovial plica) ○ Chronic lateral instability may lead to increased microtrauma to anterior ankle Posterior Ankle Impingement Syndrome Compression of the structures of the posterior tibia and calcaneus during plantarflexion Presents as less specific deep pain to the Achilles tendon area Worsens with plantarflexion of ankle, and repetitive push-off maneuvers (downhill running, walking, descending stairs, high heels) Common in dancers (en-pointe, demi-pointe positions) Etiology ○ Pathology of lateral process of  the posterior talus ○ Stieda process (elongated tubercle) ○ Os trigonum ○ Osteophytes (ankle, STJ DJD) ○ Posterior intra-articular soft tissue (scarring and thickening of capsule, PTFL, posterior deltoid ligament) ○ FHL tenosynovitis FHL runs just posterior to lateral tubercle of posterior process of the body of talus Examination Inspect ○ Alignment of ankle/foot ○ Joint effusion, soft tissue edema Palpate ○ Anterior impingement: anterior/anterolateral tenderness ○ Posterior impingement: deep ankle pain Posteromedial tenderness with resisted plantarflexion of the hallux indicative of FHL tenosynovitis Posterolateral tenderness with forced ankle plantarflexion indicative of trigonal process pathology ○ Sural/tibial nerve, peroneal, posterior tibial, and Achilles tendon Range of Motion ○ Passive/Active ROM Ankle, STJ, Midfoot ○ Anterior drawer/talar tilt → exclude ankle instability Straight Leg test → excludes L5/S1 radiculopathy Imaging Radiographs ○ Osseous sources of impingement CT ○ Visualization of the morphology of osseous structures that may be causing impingement MRI/Ultrasound ○ Evaluate for soft tissue sources of impingement Treatment Conservative Treatment ○ Rest, ice, immobilization ○ Physical therapy Increase early ROM Improve ankle instability (proprioception) ○ Shoe modifications Heel lift to prevent dorsiflexion ○ Injection therapy Help breakdown some of the scar tissue  Surgical Treatment ○ Anterior and Posterior impingement Remove offending pathological lesion Resect/debride bone and soft tissue lesion Arthroscopic arthrotomy PLANTAR FASCIOPATHY Anatomy Plantar fascia/plantar aponeurosis is a dense connective tissue Helps to support the medial longitudinal arch Extends from the calcaneus to the Distal MPJs ○ Divided into medial, central, and lateral portions Vital part of the windlass mechanism during gait Plantar Fasciitis/Plantar Fasciosis Plantar fasciitis → acute inflammation of the plantar fascia ○ Most common cause of foot pain in adults Can become a chronic condition, characterized by degeneration of the plantar fascia = plantar fasciosis Risk Factors Intrinsic = all things that increase the strain on the PF ○ Anatomic considerations Pes planus (pronation stretches PF → increases strain on achilles) Pes cavus Limb length discrepancy Obesity ○ Functional considerations Equinus (pulls on the achilles → pulls on the PF) Intrinsic foot muscle weakness Overpronation ○ Degenerative considerations Atrophy of plantar fat pad Extrinsic Risk Factors ○ Overuse ○ Incorrect training Increase in distance/intensity/duration/frequency ○ Inadequate footwear Inappropriate replacement of shoes Poorly cushioned shoes History & Physical Exam History/Presentation ○ Characterized by pain with first steps in the morning or after a long period of rest (post-static dyskinesia) You sleep with feet PF’d → achilles and PF contract and stiffen → first steps force  DF which increases strain on stiffened structures ○ Pain will often reduce after it “loosens up” but will often return later on in the day ○ Pain can occur after extensive walking/standing Exam ○ Tenderness to palpation of the insertion of the plantar fascia and/or along the medial band of the plantar fascia ○ Scarring/nodule may be palpable ○ Edema/Calor ○ Foot deformities (Planus/cavus) ○ Ankle ROM to evaluate for Equinus Imaging Radiographs ○ Helps to rule out differentials/evaluate biomechanics ○ Plantar calcaneal bone spur Heel spurs Main point: heel spur IS NOT CAUSING THE PAIN → THE INFLAMED, TIGHT PLANTAR FASCIA IS Kirkpatrick et al. (2017) ○ Reviewed plantar calcaneal spur ○ Plantar heel spurs present in 10-63% of asymptomatic controls in multiple studies ○ Noted study by Lapidus and Guidotti (1965) where 45% of heels analyzed were painful without spur or had spur but were asymptomatic Tountas and Fornasier 1996 ○ Evaluated 21 patients who underwent plantar fascia release and heel spur resection ○ Found that recurrence of spurs did not correlate with recurrence of symptoms, and no active inflammatory process in heel spur histologically ○ Concluded that intrinsic changes within plantar fascia (not heel spur) are responsible for pathogenesis of syndrome Ultrasound ○ Dynamic method to evaluate for plantar fascia tears/thickness of plantar fascia MRI ○ Used to evaluate soft tissue and bone Treatment Acute Plantar Fasciitis (present < 6 mos or so) ○ Reduce acute inflammation (ice, medications, injections)  Consider injections when pt has severe pain → limping, miserable etc Injections can cause atrophy of fat pad so we don’t want to use them all the time ○ Physical therapy Stretching/Strengthening Anti-inflammatory modalities ○ Address biomechanics!!! Foot deformity (Orthosis/Taping) Equinus (stretching is KEY) Chronic Plantar Fasciosis ○ Note: if you did a steroid injection and the pt saw no relief → indicates CHRONIC condition Injection didn’t work b/s there was not a lot of inflammation present ○ All of these treatments aim to turn the chronic issue back into an acute issue, then likely better effect of acute txs Topaz Radiofrequency Ablation PRP Shockwave Amniotic membrane injection Regeneration new fascial tissue Reduce scarring Surgery Plantar Fascia release (usually of the medial band) Last resort POSTERIOR TIBIAL TENDON DYSFUNCTION (PTTD) Anatomy PTT is largest and most anterior of medial ankle tendons Acts as primary dynamic stabilizer of medial longitudinal arch and main inverter of the midfoot History and Physical What is PTTD? ○ Adult acquired flatfoot deformity ○ Progressive loss of strength of the posterior tibial tendon → collapse of the medial longitudinal arch as a result of ○ Leads to abduction of the forefoot, calcaneal valgus, forefoot supinatus, plantarflexion/abduction of the talus Physical Exam ○ Posterior tibial tendon strength  ○ Pain along posterior tibial tendon, navicular tuberosity, posterior aspect of medial malleolus ○ Too many toes sign (Forefoot abduction) ○ Hindfoot everted ○ Collapse of medial longitudinal arch ○ Single limb rise test Assess strength of PTT Stand on 1 foot → go up on toes → if unable to lift heel off ground or have pain = (+) for PTT pathology/reduced strength ○ Double limb rise test Assess strength of PTT and flexibility of deformity Same as SLR test but perform w/ both feet at same time Look at the level of heel rise → is one side lower? Weakness of PTT on lower side Note amount of heel inversion → PTT is still intact and inverting the heel = FLEXIBLE deformity If heel remains everted = RIGID deformity ○ Hubscher maneuver/Jack’s test Determines flexibility of deformity Pt is WB → examiner DFs hallux → this should activate the windlass mechanism and cause resupination of foot Flexible if resupination occurs Rigid if foot remains pronated ○ Supination lag test Pt sits with heels together → supinate both feet at same time 1 side lower? Less supinated? → PTT weaker on that side/attenuated/ruptured or rigid deformity Imaging Radiographs ○ Useful for identifying biomechanical abnormalities Pes planus planal dominance (Transverse/Frontal/Sagittal) Look at Meary’s, Talocalc, Calc inclination, talar declination, FF abduction, etc ○ Can help stage PTTD  Evidence of hindfoot/ankle arthritis ○ Accessory navicular Puts the PTT @ mechanical disadvantage → can’t support the navicular as well MRI ○ Useful for identifying soft tissue abnormalities ○ Posterior tibial tendon tear/degeneration **PTTD Classification** Johnson and Strom Classification (1989) ○ Original ○ Stages I-III Myerson modification (1996) ○ Added stage IV Treatment considerations Stage Rigid/Flexible Conservative Treatment Surgical Treatment I Flexible Physical therapy, orthoses Debridement II Physical therapy Bone osteotomies, soft tissue Custom orthoses and/or bracing techniques III Rigid Custom AFO bracing (hold (significant Hindfoot arthrodesis arthritic deformity in place to limit painful changes) procedures  IV ROM) Hindfoot/ankle arthrodesis procedures TARSAL TUNNEL SYNDROME History and Physical Compressive neuralgia/neuropathy of the posterior tibial nerve in the tarsal tunnel Etiology → Anything that reduces the amt of space the PT nerve has ○ Idiopathic ○ Post traumatic Arthrosis, tenosynovitis ○ Mass lesion Swannoma/ganglion ○ Iatrogenic Post op nerve injury/scarring ○ Anatomic Hypertrophic or accessory muscles/tendons ○ Comorbidities Diabetes mellitus, hypothyroidism, gout History ○ Paresthesia/burning sensation in sole of foot/heel/medial ankle ○ Protracted walking/standing exacerbates symptoms ○ Dysesthesia during night can disturb the patient’s sleep Physical Exam ○ Hoffmann-Tinel sign – electrical paresthesia on percussion of the nerve (+) if percussion causes distal shooting pain/burning/etc ○ Symptoms may be exacerbated by forced eversion and dorsiflexion of the foot ○ Long standing TTS: Sensory loss to distribution of the affected nerve Weakness of toe abductors and short toe flexors Muscle atrophy  Trophic disturbances (diminished sweating) Neurophysiological testing ○ Nerve conduction velocity (NCV) Differences in amplitude between the two limbs Low amplitude, prolonged distal motor latencies ○ Electromyography (EMG) Distal muscle activity supplied by tibial nerves may be reduced ○ Note: have pt walk around before/during if possible b/c nerve recovers quickly w/ rest Treatment Conservative ○ Be sure you know where the issue is before tx ○ Rest ○ Corticosteroid injection ○ Treat underlying condition/etiology ○ Orthosis may help or worsen symptoms Controlling pronation may be helpful Orthoses could also push directly on the lateral plantar n as it dives into the foot exacerbating the symptoms Surgical Treatment ○ Decompression of the tibial nerve and its branches Flexor retinaculum is released along the entire nerve course Release the fascia of the abductor hallucis muscle to decompress medial and lateral plantar nerves Release all the way to abductor canal → many pts return w/ symptoms if they aren’t released this far and there is still compression on these areas PERONEAL TENDON DISORDERS Peroneal tendinosis/Peroneal tendon tear Posterolateral ankle pain that worsens with activity and improves with rest Tenderness over peroneal tendons Palpable mass that moves with tendon → tendinosis Thickening/focal tendon degeneration and swelling Tendon tears can result from chronic microtrauma or from acute injury ○ Increased risk of tendon tear can be due to increasing degeneration/malalignment of tendon  Peroneal subluxation Mechanism of injury: ○ Forceful dorsiflexion of the ankle ○ Hindfoot inversion ○ Contraction of the peroneals ○ Together causing disruption of the SPR Physical Examination Overall alignment of the ankle/leg/hindfoot/first ray ○ Rearfoot varus may increase peroneal forces that predispose it to injury Esp uncompensated RF varus ○ Peroneal weakness may cause rearfoot varus → b/c decreased eversion force on ankle Ankle stability (anterior drawer/talar tilt) Swelling posterior to fibula/lateral wall of calcaneus Tenderness to palpation along the course of the tendons Pain with resistance to eversion/plantarflexion 1st ray (PL pathology) Pain with passive inversion stretch Circumduction of the ankle/peroneal compression test to recreate peroneal subluxation Imaging Radiographs ○ Determines foot morphology ○ Accessory bones (os peroneum) ○ Bone abnormality (fracture/osteophytes/tumors) CT ○ Assess osseous anatomy that can contribute to pathology Retromalleolar groove, hypertrophic peroneal tubercle Ultrasound ○ Dynamic real time imaging ○ May help identify subluxation Can visualize tensonds shifting anteriorly over lateral malleolus MRI ○ Visualize soft tissue and bony abnormalities well Evaluates for concurrent ankle pathology Magic angle effect: tendon fibers 55 to magnetic axis can result in artifactual signal (decreases sensitivity to 80% and specificity to 75%) Can make you think there is a tear when there isn’t Can reduce this effect by placing foot in plantarflexion Pathology most commonly seen on axial views Torn tendon unravels and appears flat Treatment Peroneal tendinosis/tear ○ Conservative Rest, activity modification Orthoses with lateral forefoot posting Immobilization in short leg cast/CAM walker ○ Surgical → 50% of the time Open synovectomy Debridement of tendon Repair of tendon tear Tendon is strongest as a tightrope → when it unravels and flattens, it becomes weak → FIX THAT Tenodesis Removal of associated pathology Peroneus quartus/hypertrophic peroneal tubercle/exostosis calcaneus/os peroneum Peroneal Subluxation ○ Conservative: Below knee cast immobilization → low success rates (26%-57%) ○ Surgical → better outcomes Direct superior peroneal retinaculum repair Cut, clean up, repair/anchor Retromalleolar groove deepening Bone block procedure Prevents recurrence LATERAL ANKLE SPRAINS Etiology & DDX Lateral ankle sprains → from an injury that causes the ankle to invert excessively, stretching or tearing the ATFL, CFL, and/or PTFL ○ ORDER of tearing: ATFL → CFL → PTFL (rare, severe injury) Differential diagnoses for inversion mechanism of injury ○ Anterior process fracture of calcaneus ○ 5th metatarsal base fracture ○ Peroneal injury ○ Osteochondral injury ○ Fibular fracture  ○ EDB muscle strain Associated injuries ○ Peroneal tendon tear ○ Osteochondral lesion Risk Factors Intrinsic Risk Factors ○ Previous sprain Esp w/ inadequate rehab → often heals in lax position ○ Increased height and weight ○ Anatomic foot and leg considerations RF varus, PFFR, Tibial Varum ○ Foot size/width ○ Possibly generalized joint laxity ○ Muscle strength ○ Muscle reaction time ○ Postural sway/center of gravity Extrinsic Risk Factors ○ Bracing and taping ○ Shoe type ○ Type of sport/activity Pivot, jump, cutting, etc ○ Duration and intensity of competition History and PE Signs and Symptoms ○ Pain and swelling along the lateral collateral ankle ○ Occasionally there may be ecchymosis ○ Inability or trouble weight-bearing with increasing severity of sprain ○ Instability may be noted Exam ○ Neurovascular ○ Inspect Edema, ecchymosis ○ Palpation Bone, tendon, ligaments ○ Range of motion Passive/active/resistive ○ Anterior Drawer Test Tests for integrity of ATFL Knee slightly bent with ankle over edge of table Ankle slightly plantarflexed, or close to neutral One hand cups calcaneus and other hand stabilizes lower leg  Calcaneus/talus is drawn anteriorly Test positive with pain, anterior translation, dimple/sulcus Sometimes may hear a suction sound Talar Tilt/Stress Inversion Test ○ Tests for integrity of lateral ankle ligament (Mainly CFL) ○ One hand stabilizes medial lower leg and the other grasps calcaneus Ankle is stressed with inversion ○ Ankle can be neutral/slightly plantarflexed ○ Test positive with pain, talar tilt/gapping Imaging **Ottawa Ankle and Foot Rules** ○ Ankle series indicated if patient has pain in malleolar zone and bone tenderness at A, B, or inability to bear weight ○ Foot series indicated if patient has pain in midfoot zone and bone tenderness at C, D, or inability to bear weight ***Stress Radiographs*** ○ Anterior Drawer Test Tests for integrity of the ATFL ligament Lateral ankle view with stress anterior drawer of the ankle Anterior translation of the talar dome is measured Abnormal if >5-10 mm Can compare to contralateral ankle if unsure (3 mm difference) Suction/dimple sign ○ Talar Tilt/Inversion Stress Test Tests for integrity of the lateral ankle ligaments (mainly CFL) AP ankle with stress inversion of the ankle Angle between tibial plafond and talar dome is measured  Abnormal if tilt > 10 degrees Can compare to contralateral ankle if unsure Ankle Sprain Classifications O'Donoghue ○ 1st degree – ligament stretch with minimal disruption ○ 2nd degree – partial ligament disruption with joint instability ○ 3rd degree – complete ligament disruption/failure Leach ○ Grade I – mild functional loss, mild pain ○ Grade II – moderate functional loss, difficulty walking, toe raising, diffuse tenderness ○ Grade III – severe functional disability, marked tenderness, joint effusion, decreased ROM Rasmussen ○ Stage I – rupture of ATFL ○ Stage II – rupture of superficial fibers of PTFL ○ Stage III – rupture of CFL ○ Stage IV – rupture of deep fibers of PTFL Dias ○ Grade I – partial rupture of CFL ○ Grade II – complete rupture of ATFL ○ Grade III – complete rupture of ATFL, CFL, PTFL ○ Grade IV – complete rupture of all 3 lateral ligaments and partial rupture of deltoid ligament Henry ○ Grade I – Mild injury. Pain on palpation over ATFL. Anterior drawer negative. Talar tilt 15 AMA ○ Grade I – Stretched fibers, mild swelling/pain ○ Grade II – injury to ATFL/CFL, moderate instability/pain ○ Grade III – Rupture ATFL/CFL, unstable joint, severe swelling and function loss AOFAS → Know this one ○ Differences based on how fast they recover after injury Grade Severity Structures Torn Clinical Signs I Mild ATFL Mild swelling (Stretch/no Little/No ecchymosis frank Mild restriction active ROM disruption) Difficulty with weight bearing No laxity noted  II Moderate ATFL ± CFL Localized swelling, ecchymosis, hemorrhage, (Partial/ tenderness to anterolateral aspect of complete tear) ankle Mild or absent laxity III Severe Localized swelling, ecchymosis, hemorrhage, (complete tenderness to anterolateral aspect of disruption) ankle/heel/anterolateral capsule, ATFL, CFL IIIA Same as stage III + decrease in ROM >10, edema ATFL ± CFL ± >2 cm, normal stress radiographs IIIB capsular tear ± PTFL Same as stage IIIA + >3mm difference in distance between posterior articular surface of tibia and talus when comparing injured and uninjured ankles Ankle Sprain Grading/Treatment Grade I Grade II Grade III Stretching/Slight tearing Incomplete tear of ligament Complete tear of ligament of ligament Time to recovery: days TtR: weeks TtR: months RICE (Rest, Ice, RICE Compression, Elevate) RICE Protect ankle, Reduce Immobilization w/ brace/splint Swelling Maintain ROM Immobilization w/ Cast / walking Bracing/taping boot +/- crutches Functional rehabilitation Bracing/taping Functional rehabilitation Surgery Immobilization, Ambulation Aids, Bracing Walking boots and casts → ankle held in closed packed position ○ ATFL and CFL stable and taut Crutches, walkers, knee scooters, wheelchairs Bracing → Control and support ○ Utilize in mild injuries or after periods of boot/cast immobilization for higher grade injuries to aid with transition back to normal activity ○ Gauntlet Controls frontal and sagittal plane motion  ○ Stirrup Controls frontal plane motion ○ Elastic Mainly for swelling control Taping ○ Basket weave (Gibney boot) ○ Figure 8 Simulates gauntlet Pros/Cons to Bracing and Taping Functional Rehabilitation → For ANY GRADE!!! Control acute inflammatory process Range of motion Isometric/isotonic strength training Proprioception ○ Increases functional stability Helps your body track where your ankle is and determine when it is about to sprain so that you can catch yourself ○ Ergen E et al. (2008) Ankle sprains can be prevented with use of external protection and proprioception conditioning and training, especially in athletes with previous ankle sprains ○ Wobble Board ○ BAPS Board ○ BOSU Ball ○ Balance exercises ○ Balance pad Surgical Treatment Anatomic Repair ○ Reapproximate the ligaments ○ Brostrom → Most common ○ Brostrom-Gould Incorporates  extensor retinaculum w/in repair Non-anatomic Repair ○ Single ligament reconstruction Using P.Brevis to reapproximate the ATFL Watson-Jones Evans ○ Double ligament reconstruction Chrisman-Snook Elmslie Split PB lateral ankle stabilization (SPBLAS) Turf Toe **Anatomy** Stability of 1st MTPJ comes from capsule, ligaments, and short flexor complex ○ Collateral ligaments provide varus/valgus stability ○ Plantar plate provides stability plantarly Injured the most ○ Short flexor complex (FHB, hallucal sesamoids, adductor hallucis, abductor hallucis) provides dynamic stabilization of joint Example: ○ (-) Varus/Valgus stress test ○ + Lachman’s test (Dorsal plantar Drawer test) ○ 5/5 strength on flexion  ○ = Plantar plate injury History and Physical Hyperextension injury of the 1st MTPJ causing attenuation or disruption of the capsular ligamentous complex supporting the joint ○ Hyperextension strains plantar plate Classically described to occur on surfaces such as artificial turf ○ Studies have shown similar injury patterns on natural grass Etiology/Mechanism of Injury ○ Turf toe is caused by an axial load delivered to a foot while it is in a fixed equinus position at the ankle with the great toe in extension at the MTPJ → drives the 1st MTPJ into hyperextension Exam ○ Inspect Edema, ecchymosis (esp w/ ligament tear), gross malalignment ○ Palpate Collateral ligaments, dorsal capsule, plantar sesamoid complex Point tenderness distal vs proximal to sesamoids Plantar plate more likely to tear distally Turf toe typically is painful distal to sesamoids where as pain proximal to sesamoids may indicate FHB strain ○ Range of motion Varus/valgus stress Dorsoplantar drawer test (Lachman test) Grab proximal phalanx and 1st MPJ → try to pull up ○ Increase pain or motion = (+) Plantar plate tear Active flexion/extension Weakness to flexion may indicate plantar plate or FHB disruption Note: if acute injury, you may need to anesthetize the toe w/ mayo block prior to doing these tests Chronic → must move toe  side to side Imaging AP, Lateral, Sesamoid Axial ○ Small fleck of bone may indicate capsular disruption or avulsion ○ Proximal migration of sesamoids may indicate plantar plate rupture Forced dorsiflexion lateral ○ Full plantar plate disruption: ○ Sesamoids will not track distally with 1st MTPJ extension (right image on next page) MRI ○ Modality used for visualizing soft tissue injury ○ Increased swelling/edema distal to sesamoid Grading Grade Description/Findings Treatment Return to Play  I Attenuation of plantar structures Return as tolerated Symptomatic Localized Swelling Tape Minimal ecchymosis Orthotic w/ Morton’s extension II Partial tear of plantar structures Up to 2 weeks Walking boot May need taping on Moderate Swelling return to play Crutches as needed Restriction motion due to pain Tape, orthoses III Complete disruption of plantar 10-16 weeks depending Long term on sport/position structures Likely to need taping immobilization in boot on return to play Significant swelling/ecchymosis *Definitely w/ orthoses or cast or shoe modifications Hallux flexion weakness Surgical reconstruction Frank Instability of 1st MTPJ Treatment Conservative ○ Reduce initial pain and swelling Rest, ice, compression, elevation ○ Immobilization: Walking boot, short leg cast, toe spica in hallux plantarflexion ○ Orthotic/shoe modification Stiff FF FF rocker ○ Rehabilitation Range of motion Low impact exercise (cycling, elliptical, pool) Surgical ○ Goal: Restore normal, stable anatomy of 1st MTPJ ○ Indications Large capsular avulsion with unstable MTPJ Diastasis of bipartite sesamoid Retraction of sesamoid  Traumatic hallux valgus deformity Vertical instability Loose body in MTPJ Chondral injury in MTPJ Failed conservative treatment ○ Procedure Reapproximate ligament Place hallux in slight plantarflexion w/ spica splint ~ 1 wk po → start early ROM to prevent scarring/adhesions NWB 4 wks Protective WB and cross training to follow NAIL PATHOLOGIES Nail pathologies with sports → VERY COMMON Most nail pathologies in the athlete are caused by improperly fitting shoes ○ Subungual hematoma ○ Onycholysis ○ Onychocryptosis Subungual Hematoma “Runner’s toe” Dark red/black discoloration of the nail caused by bleeding in the underlying vascular nail bed due to trauma ○ Blister underneath nail → increased pain → avulse the nail Can be caused by chronic microtrauma or acute injury to the nail There can be pain caused by the pressure Prevention: ○ Use of proper fitting shoes with less constrictive toe box Treatment: ○ Will usually resolve over time as nail grows out ○ If painful (or wet blister), can drill holes through the top of the nail (trephining) to relieve pressure ○ Nail avulsion can be done if suspicious of nail bed laceration and underlying fracture is present ○ Biopsy if suspicious of melanoma MUST NOT MISS DIAGNOSIS!!! New problem, no injury, not an athlete/runner etc Onycholysis Separation of the nail plate from the nail bed In athletes, this is most often caused from acute trauma or chronic microtrauma Nutrient deficiencies such as iron and riboflavin deficiency can also lead to onycholysis in athletes Prevention: ○ Well fitting shoes to prevent toenail trauma ○ Nutrient supplementation Treatment:  ○ If the toenail is fairly loose and causing pain, total nail avulsion is indicated Onychocryptosis Ingrown toenail Can be caused by improperly fitting shoes, cutting the toenail too short/improper pedicure, acute trauma to the toe Can present with or without an infection Prevention: ○ Properly fitted shoes ○ Proper nail care Treatment: ○ Partial nail avulsion +/- matrixectomy (no infxn, chronic) SKIN PATHOLOGIES w/ SPORTS Blisters Common in sports that require quick pivoting and direction changes (Shear force) ○ Blisters develop when shear forces cause the epidermis to separate from the dermis, with serous exudate filling the space between the layers Predisposing causes: ○ Shoes that are too tight/narrow ○ Shoes that are too large ○ Synthetic surfaces increase friction at shoe-surface interface, causing foot to slide more ○ Deformities that can rub against shoe Prevention: ○ Properly fitting shoes, thick socks ○ Forgiving surfaces ○ Moleskin → reduce friction Treatment: ○ Drainage/decompression of blister Dr. Yau prefers to leave roof on blister → “biological bandage” ○ Antibiotic ointment/dressing/padding Verruca/Warts Warts are caused from a viral infection (Human Papillomavirus) through damaged skin Often spread via direct contact in communal areas such as locker room floors, shared showers, surfaces surrounding swimming pools Prevention: ○ Protective sandals in communal areas (Avoid walking barefoot in public areas) Treatment: ○ Blistering (vesicants) Cantharidine → blisters 24 hrs after application → see pt back in 1 wk → debride and repeat until you no longer see pin pt signs of wart ○ Acid therapy Keratolytic ○ Immune response modifier (Aldara) Helps body fight virus → increases immune response  ○ DNA synthesis inhibitor (Efudex) Virus replicates via DNA synthesis ○ Cryotherapy Not as good w. Plantar area since warts don’t stick out→ dig into skin and grow deeper ○ Excision Last resort ○ Laser → burn/cauterize it Corns/Callus Hyperkeratotic lesions that develop due to increased pressure ○ Often associated with FF deformity Corns are caused from compressive pressure Calluses caused from shear pressure ○ Similar to blisters Prevention: ○ Properly fitting shoes, orthosis to offload ○ Moisturizing cream to keep skin supple Treatment: ○ Debridement of lesion ○ Strapping/Padding ○ Orthosis to offload pressure areas Ex: 2nd MTH callus Reverse morton's extension/1st ray cut out → allows 1st ray to PF and bear more weight to help 2nd MT out ○ Shoe education ○ Treat deformity that is causing the increased pressure Tinea Pedis “Athlete’s foot” ○ Fungal infection of the skin that manifests as itching and burning **Trichophyton rubrum → MOST COMMON **Trichophyton interdigitale **Trichophyton mentagrophytes ○ Dry cracks/breaks in the skin can be source of entry for bacteria (superinfection) ○ Develops in moist areas of foot (common between toes) ○ Candida can present similarly Prevention ○ Good foot hygiene ○ Cotton socks good for wicking away moisture Hyperhidrosis increases risk of infection ○ Care to clean between toes ○ Antifungal powder prophylactically  ○ Protective sandals in communal areas Treatment ○ Topical antifungal cream/lotion/gel ○ Oral antifungals for recalcitrant cases Foreign body/Puncture wound Foot is common site of puncture wounds either barefoot or through the shoe Treatment ○ ***Tetanus prophylaxis*** ESP w/ PUNCTURES FROM NAILS ○ Remove foreign body ○ Evaluate for deep injuries ○ Evaluate for infection FF @ high risk → osteomyelitis!! ○ Surgical debridement/culture ○ Antibiotics Thermal injury Injury due to exposure to extremes of high or low temperature ○ Heat injuries: Beach sports (ie – beach volleyball) ○ Cold injuries: Winter sports (ie – skiing, skating) Burn injury 1st degree – superficial burn with erythema without blistering (affects epidermis) 2nd degree – superficial burn with erythema/blistering (partial thickness injury to skin affects epidermis and dermis) ○ PAINFUL 3rd degree – deep burn causing full thickness damage to skin (both epidermis and dermis) and may extend to deeper muscle/connective tissue/bone ○ NOT AS PAINFUL Treatment ○ Tetanus prophylaxis ○ Cool area as soon as possible Cool water bath Cool running water Blisters treated with antiseptic ○ Hospitalization usually necessary for 2nd/3rd degree burns IV fluid replacement Antibiotics Debridement/skin grafting Cold injury Systemic vs peripheral cold injuries Systemic Hypothermia ○ Core body temperature has decreased to 35C or less ○ Treatment Prevent further heat loss  Rewarm body core temperature Stabilize patient Peripheral Cold Injuries ○ Frostnip Mild form of cold injury occurring in apical structures ○ Chilblain Chronic, recurrent vasculitis manifested by red-to-violaceous raised lesions; Ulcers, blisters, erosions may be seen ○ Immersion (trench) foot Occurs in patients who have been in wet, but not freezing, environments for long periods of time** Numbness, tingling pain with itching Skin is red, becomes pale, and mottled, gray and blue Soles of feet are wrinkled/macerated ○ Frostbite Superficial 1st degree: hyperemia and edema evident 2nd degree: hyperemia and edema with large, clear blisters that may extend the entire length of the limb, digit, or facial feature Common features: ○ Skin cold, waxy white, non-blanching ○ Anesthetic but painful and flushed with thawing ○ Clear serous bullae appear within 24 hours Deep 3rd degree: hyperemia, edema, and vesicles filled with hemorrhagic fluid 4th degree: complete necrosis with gangrene and loss of affected part Common Features: ○ Involves muscle, tendons, neurovascular structures, bone ○ Frozen part is hard, woodlike, and anesthetic (no pain b/c of nerve damage) ○ Ashen gray, cyanotic, or mottled and may remain unchanged after rewarming ○ Blisters, if present, are hemorrhagic ○ Treatment Remove from cold environment Rewarm to normal body temperature before treating local injury Rewarm the extremity rapidly in water bath (39-42 C) with aseptic technique until extremity has flushed appearance Tetanus prophylaxis