<div>RC 2016 - When doing a subtalar arthrodesis from the lateral side, what is the structure you see once you have debrided the medial aspect of the joint? </div>
<ol> <li>FDL </li> <li>EDM </li> <li>FHL </li> <li>Tib post</li></ol>
C.<div><ul> <li>Discussed with LaMothe:</li> <ul> <li>If POSTERIOR to middle facet then FHL</li> <li>If ANTERIOR to middle facet the FDL as FHL under sustentaculum</li> </ul></ul></div>
<div>RC 2015 - Contraction of the gastroc results in:</div>
<ul> <li>A. Plantarflexion</li> <li>B. Flexion of the knee and ankle</li> <li>C. Flexion of the knee and ankle and subtalar supination</li> <li>D. Flexion of the knee and ankle and subtalar pronation</li></ul>
C.<div><div>The Achilles tendon is part of a musculotendinous unit that spans three joints, producing knee flexion, tibiotalar flexion, and subtalar inversion</div></div>
RC 2008 - A fisherman sustained an open medial malleolus fracture and sharp laceration to tib post tendon. How should you manage the Tib-post tendon injury? <ul> <li>A. Repair primarily</li> <li>B. UCBL orthosis</li> <li>C. Tenodesis the distal part to FHL</li> <li>D. Reconstruct the deficit with FDL to navicular</li></ul>
A.<div>Acute repair of a tibialis posterior tendon laceration can lead to a good result.</div><div>Small case series of these<br></br></div>
<div>RC 2008 - Question on lesser toes, which is true</div>
<ol> <li>on ground 75% during stance phase</li> <li>max peak pressure of MT head is significantly larger</li> <li>equal distribution across lesser toes</li> <li>don’t provide stability in stance phase</li></ol>
<div>answer: b</div>
<ul> <li>They concluded that the toes are in contact for about 3/4 of the walking cycle and exert pressures similar to those from the metatarsal heads</li> <li>The great toe takes the highest pressures (30% of total toe pressure), with the second taking 25%, the third 20%, the fourth 15% and the fifth 10% = C is false</li> <li>While the extremes of the foot (heel and hallux) are in contact with the ground for only 54% to 64% of stance phase the forefoot, specifically the middle forefoot, contacts the ground for 86% of stance phase.</li></ul>
RC 2014 - List 4 inverters of the subtalar joint
<ul> <li>Tib post</li> <li>Tib Ant</li> <li>FDL</li> <li>FHL</li> <li>Achilles</li></ul>
<div>RC 2015 - In a Chopart amputation, what 2 things can you do to prevent equinus contracture?</div>
<div><div><ul> <li>Soft Tissue</li> <ul> <li>Transfer for MORE DF (to dorsum of talus)</li> <ul> <li>Tibialis anterior</li> <li>Peroneus longus</li> <li>Peroneus brevis</li> <li>EDL</li> </ul> <li>Less PF strength = Recession of gastrocs/Achilles</li> </ul> </ul> <ul> <li>Boney procedures:</li> <ul> <li>TTC fusion</li> </ul></ul></div></div>
RC 2013 - Symes amputation due to diabetic toes. Which is an important part of the operation: <ol> <li>Attach fat pad to posterior tibia</li> <li>Attach fat pad to anterior tibia</li> <li>Resect fat pad</li> <li>Attach Tibialis Posterior to anterior tibia</li></ol>
“B.<ul> <li>"”Several techniques have been used to prevent migration of the heel pad on the end of the stump, such as taping the heel flap, skewering the heel flap to the bone with a kirchner wire, or leaving a small sliver of calcaneus attached the heel flap””</li> <li>Drill several holes through the anterior edge of the tibia and fibula, and suture the deep fascial lining the heel flap to the bones””</li></ul>”
<div>RC 2018, 2014, 2012 - Patient has a Symes. All of the following except</div>
<ol> <li>Rigid socket not needed for success</li> <li>Lift often needed on contralateral side</li> <li>Heel pad migration may preclude weight bearing</li> <li>The long lever arm is an advantage</li></ol>
“B.<ul><li>A: SYMES amp has a bulbous end - so the prosthetics have cutouts that make them ‘nonrigid’</li><li>Carroll K - Prosthetics and Patient Management: A Comprehensive Clinical Approach</li><ul><li>Amputation limb is appreciably shorter than contralateral limb (so no contra-lateral lift needed)</li><li>Connection between socket and foot must be rigid</li></ul></ul><div><ul> <li>A: Rigid SOCKET is necessary to prevent fat pad migration; rigid prosthesis (aka. foot) is NOT necessary (can use carbon fiber energy storing foot)</li> <li>(rigid socket bears weight up the whole lower leg instead of being an end loading stump)</li> <li><br></br></li><ul> </ul></ul></div>”
<div>RC 2018, 2016, 2014 - A 47yo male insulin-dependent diabetic presents with a callus on the plantar aspect of the 5th metatarsal head. This was managed with trimming of the callus and local skin care, but is worsening. On exam he has mild cavus alignment bilaterally. What is the best treatment?</div>
<ol> <li>Gastrocsoleus stretching exercises and referral for specialized diabetic footwear</li> <li>Medial calcaneal slide osteotomy</li> <li>Dorsiflexion osteotomy of the 5th metatarsal</li> <li>Percutaneous lengthening of the Achilles tendon</li></ol>
A.<div><ul> <li>Variations in 2016 question (poorly remembered) included improved glycemic control and ulcer debridement</li> </ul> <div>JAAOS 1995 The Diabetic Foot</div> <ul> <li>This patient is presenting with a Wagner Grade 0 ulcer ie. No open lesions</li> <li>Management should involve shoe modification and molded inserts</li> <li>For grade 1 or 2 (superficial & deep ulcers), total contact casting is the treatment modality of choice (90% healed at 5.5 weeks)</li><li>grade 3 = deep ulcer with exposed tendon + infection = debride, abx</li> <li>Nothing in this reference about perc TAL</li> </ul> <div></div> <div>JBJS 2003 Effect of Achilles lengthening on neuropathic plantar ulcers</div> <ul> <li>RCT of Achilles lengthening + total contact casting in patents w/ grade II ulcers and <5 degrees dorsiflexion (NOT THIS PATIENT)</li> <li>100% HEALING in the TAL group (vs 88% in the cast only)</li> <li>75% less recurrence at 7 months and 50% less recurrence at 2 years in TAL group</li></ul></div>
<div>RC 2013, 2011 - Regarding diabetic healing, what is predictive of good healing?</div>
<ol> <li>Transcutaneous oxygen pressure > 30mmHg</li> <li>ABI of 1.5</li> <li>Toe pressure of 20 mmHg </li> <li>Your patient ate Lisa’s cooking</li></ol>
“A.<div><br></br></div><div><img></img></div><div><br></br></div><div>ie predictors of non healing</div><div><ul> <ul> <li>ABI < 0.45</li> <li>Transcutaneous pressure < 30mmHg</li> <li>Serum albumin < 2.5g/dl</li> <li>Absolute lymphocyte count < 1,500</li> </ul></ul><div><br></br></div></div>”
<div>RC 2012 - What Transcutaneous O2 is needed for wound healing in diabetics?</div>
<ol> <li>15 mm</li> <li>30 mm</li> <li>50 mm</li> <li>70 mm</li></ol>
“2.<div><img></img><br></br></div>”
RC 2015, 2012 - What is the most important predictor of healing in a diabetic ulcer? <ol> <li>severity of DM</li> <li>blood supply</li> <li>peripheral neuropathy</li> <li>chronicity of the ulcer</li></ol>
<div>ANSWER: B ***</div>
<ul> <li>Peripheral neuropathy is NUMBER 1 risk factor for development of ulceration but blood supply is predictive of healing potential</li> <li>Predictors of non-healing:</li> <ul> <li>ABI < 0.45</li> <li>Transcutaneous pressure < 30mmHg</li> <li>Serum albumin < 2.5g/dl</li> <li>Absolute lymphocyte count < 1,500</li> </ul></ul>
<div>RC 2011 - DM is a common cause of Charcot arthropathy of the foot and ankle. List 3 other causes.</div>
<div><ul> <li>JAAOS 2009 Charcot Neuroarthropathy of the Foot and Ankle</li> <ul> <li>CNS: SCI, TBI, syphilis, myelo, syringomyelia, MS</li> <li>PNS: Alcoholism, Leprosy, CMT</li> <li>Congenital: insensitivity to pain</li> </ul></ul></div>
<div>RC 2012 - Diabetic guy, with what sounds like a Charcot foot in the stem with medial arch collapse. What would you find on exam? </div>
<ol> <li>Pain doing a single heel rise</li> <li>Warm dry foot with prominence along medial talar head, increase callosities</li> <li>Decreased eversion and normal inversion</li></ol>
B.<div><br></br></div><div><div>Hard to rule out any option as could be painful for heel raise and could have change in ROM but I think best answer is B as it describes Charcot foot pathology</div></div>
<div>RC 2014, 2009 - What is the cause of osteopenia in a neuropathic (Charcot) joint?</div>
<ol> <li>Increased blood flow</li> <li>Non-weight-bearing due to treatment</li> <li>Neuropathy</li> <li>Cannot remember the last option</li></ol>
A.<div><ul> <li>Autonomic Dysfunction:</li> <ul> <li><b><i><u>AV shunting / increased blood flow--> increased cytokines --> upregulation of osteoclasts --> bony resorption</u></i></b></li> </ul> <li>Neurotraumatic Destruction:</li> <ul> <li>Repetitive microtrauma –> sensory anomaly prevents recognition and activity modification</li> </ul> <li>Motor Neuropathy:</li> <ul> <li>Extrinsics > intrinsics –> equinus –> altered ground reaction forces –> fracture/deformity</li> </ul> <li>Inflammatory:</li> <ul> <li>TNFa, IL1 release –> NTKB –> osteoclast stimulation</li> </ul></ul></div>
“<div>RC 2018, 2013 - Patient arrives in your clinic walking with a red and swollen foot. No fever. History of DM. XR looks like this (Dislocated midfoot). No skin breakdown. No pain. Treatment?</div> <div></div> <div><img></img></div> <ol> <li>Total contact cast</li> <li>ORIF</li> <li>Midfoot fusion</li> <li>Amputation</li> </ol> <div></div>”
<div>A.</div>
<div><br></br></div>
<div><ul> <li>Eichenholtz Classification:</li> <ul> <li>Inflammatory --> treatment total contact casting</li> <li>Fragmentation ---> total contact casting</li> <li>Coalescence --> total contact casting --> crow</li> <li>Reconstruction</li> <ul> <li>Indications for surgery:</li> <ul> <li>Ulceration from exostoses/dislocations</li> <li>Fusions in reconstructive phase</li> <li>Amputation for recurrent ulcerations/OM</li> </ul> </ul> </ul></ul></div>
<div>RC 2018, 2016, 2013 - What is true regarding the sesamoid bones in the foot? </div>
<ol> <li>They are supplied by a single artery</li> <li>Together they receive 50% of weight during normal gait</li> <li>The fibular sesamoid is larger than the tibial</li> <li>Both sesamoids lie within the 2 muscle bellies of the flexor hallucis brevis</li></ol>
b.<div><ul> <li>Sesamoid complex transmits as much as 50% of body weight</li> <li>The larger tibial sesamoid lies within the medial head of the flexor halluces brevis, the smaller fibular sesamoid lies within the lateral head</li> <li>Usually a single artery per sesamoid, but up to 2-3 per sesamoid have been described</li></ul></div>
RC 2017, 2014, 2012 - List 5 causes of adult cavovarus foot
<ul> <li>JAAOS - Adult Cavovarus Foot</li> <ul> <li>Congenital</li> <ul> <li>Myelomeningocele</li> <li>Syrinx</li> <li>Diastematomyelia </li> <li>SMA</li> <li>Hereditary motor and sensory neuropathy (CMT)</li> </ul> <li>Acquired/adult</li> <ul> <li>Neuro</li> <ul> <li>CNS: Stroke, SCI, TBI, tumour, MS</li> <li>PNS: tumor, polio</li> </ul> <li>Trauma</li> <ul> <li>Compartment syndrome</li> <li>Talus malunion</li> </ul> </ul> <ul> <li>Residual congenital cavovarus</li> </ul> </ul></ul>
<div>RC 2016 - List 6 clinical / pathoanatomic findings in the flexible adult flatfoot</div>
“<ul> <li>Alignment</li> <ul> <li>Forefoot: ““too many toes”” sign</li> <li>Midfoot: pes planus, Loss of longitudinal arch</li> <li>Hindfoot: Excessive hindfoot valgus</li> </ul> </ul> <ul> <li>Equinus contracture</li> </ul> <ul> <li>Pain and tenderness along medial border of foot, posteromedial ankle</li> <li>Inability to perform single heel raise</li> <ul> <li>Weak Tib post</li> </ul></ul>”
<div>RC 2013 - Flexible Pes Planovalgus with no abduction. She is unable to do a single stance heel raise. What operation</div>
<ol> <li>TN fusion</li> <li>Triple fusion</li> <li>FDL transfer with medializing calcaneal osteotomy</li> <li>TP advancement</li></ol>
C. NEVER DO TENDON TRANSFER IN ISOLATION - NEEDS MDCO
RC 2012 - Middle age female with severe flat foot deformity acquired over last 2 years. What is the cause? <ol> <li>Tarsal coalition</li> <li>Posterior tibial tendon dysfunction</li> <li>Charcot foot</li> <li>Ryan operated on it 2 years ago</li> </ol> <div></div>
2.<div><div>Charcot foot is possible with the right history, but two years is a long time course for this and PTTD is much more likely</div></div><div><br></br></div><div>PEDS DDX:</div><div><ul> <li>Tarsal coalition</li> <li>Tarsal coalition</li> <li>Tarsal coalition</li> <li>Poorly corrected club foot with midfoot break</li> <li>Congenital vertical talus</li> <li>Congenital oblique talus</li> <li>Spastic diplegia (hemiplegia is spared for some reason)</li></ul></div>
RC 2016, 2014 - A patient with flexible flat feet undergoes lateral column lengthening through the anterior calcaneus. Which of the following is a complication of lateral column lengthening? <ol> <li>Calcaneocuboid arthritis</li> <li>Subtalar instability</li> <li>Increased pressures and stress fracture of the sesamoids</li> <li>Pronation of the forefoot</li></ol>
A.<div><ul> <li>JAAOS - Adult Acquired Flatfoot</li> <ul> <li>Lateral column lengthening provides correction to the abducted talonavicular joint and raises the arch</li> <li>It also decreases eversion and increases the pressure along the plantar lateral border of the foot</li> <li>Lengthening may result in lateral foot overload, fifth metatarsal stress fracture and significant stiffness</li></ul></ul> <ul> <li>Roche and Calder. Foot Ankle Clin N Am. 2012.</li> <ul> <li>Evans suggested preserving the joint through his osteotomy; however, studies have shown that the contact pressure generated across the calcaneocuboid joint after lengthening may actually rise, raising concerns that this may predispose to early degenerative change…They found that joint contact pressures were increased from baseline levels after Evans procedures by 111%. The addition of a medializing calcaneal osteotomy reduced this pressure increase to 93%. </li> <ul> <li>Lots of biomechanical evidence for CC arthritis, little clinical evidence</li> </ul> </ul> <li>Neufeld SK (Foot and Ankle Clin 2001)</li> <ul> <li>Calcaneal lengthening osteotomies can result in over correction and result in excessive and fixed SUPINATION, thought to be a cause of lateral foot pain</li> <li>Overlengthening can cause metatarsocuboid arthritis or instability</li></ul></ul> <ul> <li>Moseir-LaClair S, Pomeroy G, Manoli II A. Intermediate follow-up on the double osteotomy and tendon transfer for stage II posterior tibial tendon insufficiency. Foot Ankle Int 22:283-291, 2001</li> <ul> <li>14% CC arthritis (but 50% of cases had pre-existing arthritis) </li> </ul></ul></div>
<div>RC 2011 - Advantage of lateral column lengthening over medial calc osteotomy for stage 2 PTTD? </div>
<ol> <li>better forefoot abduction</li> <li>improved restoration of hindfoot alignment</li> <li>better fusion</li> <li>Less non-union</li></ol>
A.<div><ul> <li>Jer: I’m guessing ‘A’ should say ‘better forefoot abduction correction’?</li><li>Bolt PM (FAI 2007) A comparison of lateral column lengthening and medial translational osteotomy of the calcaneus for the reconstruction of adult acquired flatfoot</li> <ul> <li>Lateral column lengthening had greater initial and final re-alignment</li> <li>Lateral column lengthening had higher non-union</li> <ul> <li>High radiographic prevalence of OA</li> </ul> <li>Rate of repeat surgery was 2x higher with osteotomy than lengthening</li> </ul><ul> </ul></ul></div>
RC 2015 - 55yo lady presents 6mos following a minor ankle inversion injury with progressive pain and swelling posterior to the medial malleolus. What would you expect to find on exam? <div> a. Positive anterior drawer test</div> <div> b. Rigid subtalar motion</div> <div> c. Positive Coleman block test</div> <div> d. Unable to do single limb heel raise</div>
D.<div><ul> <li>I think they’re getting at PTTD possibly…</li> <li>Anterior drawer should have corresponding pain at anterolateral ankle</li> <li>Rigid subtalar motion indicates subtalar coalition or end stage disease, unlikely with this presentation and age group</li> <li>Possible to do Coleman block</li></ul></div>