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Introduction
This chapter was compiled to review common orthopedic pathologies. Evaluation including pathology and clinical diagnosis will be reviewed from proximal to distal.
Rearfoot
Rearfoot pathology is based on the subjective patient symptoms in conjunction with a known history of trauma. Patients can be seen primary or as a referral from the emergency room where the ankle is routinely x-rayed AP and Lateral and Mortice view to rule out ankle fracture. Lateral ankle sprains are associated with a varus stress to the ankle with the ankle in either a plantar flexed or dorsiflexed attitude. The location of the anterior talo-fibular and calcaneofibular ligaments must be palpated to locate the PMT (point of maximum tenderness). The best way is to locate this is by placing your thumb in the sinus tarsi (Figure 1) so that your thumbnail is pointing upward.
The distal medial aspect of your thumb should be resting on the anterior talofibular ligament that will be painful upon light pressure if the patient has had an inversion sprain where the ankle was in a plantar flexed attitude. This simple palpation can differentiate lateral ankle sprain from other ankle pathology as well as identifying malingerers. The fibers of the anterior talofibular ligament can sustain a partial tear or a complete one. This should be clinically documented at the initial visit via grading as one or two. Grade one being defined as a partial tear with mild symptoms, which will heal within 6-8 weeks with no adverse sequela. Grade 2 being a total tear of the ligament, which will present with more symptoms and an observed edema and ecchymosis (Figure 2).
Figure 2. Lateral Ankle Sprain With Edema And Ecchymosis Orthopedics | Common Orthopedic Pathologies of the Foot and Ankle
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Treatment would consist of PRICE. Protection Rest Ice Compression Elevation The icing and compression of the ankle should begin right after the trauma to prevent the edema and ecchymosis via constriction of the capillaries and compression of the interstitial fluid. The compression should be 30 mm of mercury at minimum. This can be accomplished with a three-inch or four-inch elastic bandage such as an ACE or using a soft cast Unnas Boot. The ice should be continued 20 minutes on and off for as much as possible for the first 48-72 hours. Anti-inflammatory and/or narcotics can be used in selected cases but will not be sufficient by themselves unless the mechanical therapy is instituted.
Peroneal Tendinitis
The peroneals are the lateral crural muscles and are innervated by the SUPERFICIAL PERONEAL NERVE. These two muscles the peroneus longus and brevis are the pronators of the subtalar joint with the peroneus longus being the strongest pronator of the STJ. The peroneal tendons or lateral crurals are located behind the lateral malleolus within the fibular or lateral retro-malleolar groove. This groove or notch behind the malleolus is lined with fibrocartilage in which the brevis is closest to the bone and the longus overlays the previous. The superior aspect of this anatomical unit is bound down by the superior peroneal retinaculum that are thickenings of the deep fascia running from the posterior superior of the fibular malleolus proximally within the transverse plane and investing into the lateral aspect of the Achilles tendon and paratenon. The peroneal tendons run distally to the lateral wall of the calcaneus covering the calcaneofibular ligament, which is extra capsular, and beneath the peroneals. The trochlear process [peroneal trochlear and or peroneal tubercle] is located more distally on the lateral wall of the calcaneus and forms an anchor for the peroneal tendons with the brevis being above it and the longest being below it. The peroneal tubercle can be variable in size and can be absent in 20-30% of the population. In 2-5% of the population the peroneal tubercle can be grossly enlarged which can irritate the tendons and overlying synovium by repetitive friction on the lateral shoe counter. There might be a clinical correlation between cavo-varus feet and hypertrophic peroneal tubercles as in Haglunds deformity. Peroneal spasm excluding UMN disease is reflexive contraction of the peroneals to prevent the STJ from moving, thus intrinsically splinting the joint. This protective contraction is induced by weight bearing on a foot with an irregularity within the subtalar and or mid tarsal joint. Peroneal spastic flatfoot can be the secondary complications of talocalcaneal or calcaneonavicular coalition/intraarticular STJ fracture/OA or RA of the STJ or midfoot and as the end stage in PTDS. Peroneal subluxation is defined as either traumatic or congenital. The traumatic cases are the sequela of weight bearing with an accentuated hyperextension of the ankle with medial rotation of the leg. This can occur with competitive basketball. The superior peroneal retinaculum is stressed and some fibers tear and the peroneus longus tendon slips out of its groove behind the fibular malleolus. This is followed by pain, swelling, and localized tenderness to the fibular malleolus. Traumatic peroneal subluxation is commonly misdiagnosed as a lateral ankle sprain. There is absence of pain with palpation of the sinus tarsi and anterior talofibular ligament. Pain and swelling is localized in the fibular malleolus. Treatment is predicated on early diagnosis in which non-weight bearing for three to four weeks would be the appropriate treatment. In the absence of weight bearing, the foot assumes its off weight-bearing attitude which would be plantar flexion of the ankle and supination of the STJ, which would reposition the peroneal tendon back into its normal anatomical position while the superior peroneal retinaculum heals. Congenital peroneal subluxation is also referred to as Snapping Peroneals. This is a developmental condition in which the fibular retro-malleolar groove is either shallow or the labrum [fibrocartilaginous] insertion of the superior retinaculum into the fibular malleolus is either weak or dystrophic. This condition is NOT PAINFUL but is evidenced by a loud snapping during normal walking and sporting activities.
Pereneo-Cuboid Syndrome
Pereneo-cuboid syndrome has been referred to in the past as cuboid syndrome or calcaneo-cuboid subluxation. The lateral wall of the cuboid is proximal and medial to the base [styloid process] of the fifth metatarsal. The plantar aspect of the lateral wall of the cuboid has a normal fibrocartilaginous groove which is called the cuboid notch in which the tendon of the peroneus longus courses from lateral plantar proximal to medial dorsal distal inserting into the lateral plantar aspect of the base of the 1st metatarsal and the medial cuneiform; being above the long plantar ligament. The lateral wall of the cuboid has an articulating facet covered with hyaline cartilage, which articulates with the os perineum, which is invested within the tendon that of the peroneus longus. The medial surface of the sesamoid is covered with fibro cartilage; thus forming a joint which has its own capsule and internal synovial membrane the pereneo-cuboid joint. The os perineum is present usually be it either fibrous or cartilaginous in nature with rare cases of complete ossification. Symptoms associated with this specific anatomical location would be consistent with pereneo-cuboid syndrome. The base of the fifth metatarsal encompasses the insertion of the tendon of the peroneus brevis. The base of the fifth metatarsal develops from a separate ossification center, which can be demonstrated radio graphically in children between the ages of 8-12. This traction apophysis fuses at osseous maturity. Symptoms localized to this area in a youth can be clinically diagnosed as apophysitis [Islens disease]. The Os Vesalianum is an accessory bone found within the tendon of the peroneus brevis before it inserts into the base of the fifth metatarsal. It is uncommon (one-ten thousanth) and is not pathological. Fracture of the base of the fifth metatarsal must be considered when there is a history of trauma either direct or indirect with pain and swelling localized to the base of the fifth metatarsal. These fractures can be classified as mild avulsion type/moderate more distal bring comminuted and not through both cortices and/severe located at the proximal diaphysis and through both cortices [Joness fracture] (Figure 3).
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To view the actual breath of the degenerative process the ski jump/tangental view (Figure 6 on page 103) can be performed, where the calcification and spuring can be evaluated accros the posterior aspect of the heel. The treatment for this diagnosis would be PRICE inittially with physical therapy and appropriate shoe modifications which would include heel lifts, wedges, or an opened back shoe (clog). This degenerative process will take anywhere from eight months to one year until it resolves. In thoses instances where pain and functional disability continues, surgical intervention would be warranted to debride the necrotic tendonous tissues while removing the hypertrophic bone and calcifications and reenforcing the Achilles tendon insertion. Clinical treatment regiments can include many modalites except for steroid injection, which would be contraindicated as a treatment for this diagnosis.
Haglunds Deformity
The symptoms associated with Haglunds deformity are similar to the insertional tendinosis except that it is seen more often in the younger adult population and is inflammatory in nature with symptoms being closer to a bursitis or tendinitis. This condition is diagnosed clinically as a red swollen posterior enlargment lateral to the Achilles tendon insertion (Figure 7). There is a point of maximum tenderness at this location which is not involving the tendon in the initial stages. This has been described as winter heel or pump bump due to the fact that it is caused by the heel rubbing against the counter of the boot or shoe.
Lateral x-rays can be ordered to view the posterior superior aspect of the heel. The heel that has an enlarged superior posterior tubercle can be prone to shoe irritation and soft tissue inflammation.
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The angulation of the slope of the back of the heel can be measured [Fowler Phillips angle] (Figure 9) and if increased over 65-70 will document the degree of the bone mass involved.
Treatment would consist of PRICE followed by opened back shoe [clogs] and other shoe and or foot orthotic modification. Injection of steroid would be frowned upon, but in certain cases might be appropriate if care is taken to avoid the Achilles tendon.This condition if left unattended to can develop into a bursitis and tendinitis, which would be more recalitrant to treatment. Acute symptoms must be reduced in order to recommend the appropriate care. A biomechanical theory that has not been substantiated is that a foot with an increased heel varus would be prone to the development of Haglunds due to the relative position of the superior posterior aspect of the tuber of the calcaneus which would rub against the shoe counter.
Achilles Tendinitis
Inflammation of the Achilles tendon can be associated with trauma, infection, or autoimmune conditions such as sero-positive or negative disease. Achilles tendinitis presents with symptoms of pain increased in the morning with stiffness of the ankle joint, which is symptomatic all day, and even in bed. The initial stages can be acute or sub-acute and questioning the patient about a traumatic event is essential. Achilles tendinitis is an inflammatory condition of the tendon itself, which in the younger is seen in the younger individual 20-30 years of age as opposed to the older person 40 years or older, which would be more prone to insert ional tendinosis (Figure 10) and or achillobursitis. With inflammation of the tendon, rest and nonweight bearing must be instituted at the onset to prevent further damage to the tendon. Treatment consisting of nonweight bearing crutch walking for three-four weeks in conjunction with anti-inflammatory medication with cold packs to the tendon. As the acute symptoms subside, a removable walking brace can be used or partial weight bearing with crutches.
Stretching exercises can be instituted as the acute symptoms subside with regular physical therapy sessions scheduled. This condition improves VERY SLOWLY, and it must be explained to the patient that the total resolution can take up to one year. In cases where the individual returns to sporting activities when not healed,one must be cautioned of tearing the tendon.
PLANTAR FASC IA
With an acute total tear of the tendon, the indivdual can relate an incident of occurance with an audible sound similar to a popping noise. Clinical evaluation of weight bearing will demonstrate a positive Thompson/Dougherty/Simmons test, which is performed by putting the patient in a prone position with the involved foot off the end of the table. The calf is compressed with moderate pressure and if the ankle does not plantarflex, this is positive confirmation of total Achilles tendon rupture. A palpable defect in the tendon can be seen and felt. This is then followed by acute pain and falling to the ground. The individual will only be able to bear weight on the HEEL of the involved side. This is due to the fact that 90% of the power of the posterior crurals comes from the gastroc-soleus complex inserting into the Achilles tendon, and with complete rupture, heel lift to toe off can not be overcome by the deep posterior crurals[Flexor Digitorum Longus/Tibialis Posterior/Flexor Hallucis Longus]. This total rupture is quite painful and disabling and it has been demonstrated via clinical studies that primary suture of the tendon will result in almost no reoccurrence or rerupture. Total rupture with surgical repair will give the best long-term results. In cases of partial Achilles tendon rupture, treatment might be more conservative in nature with healing occurring over time, six-eight months, with little residual disability.
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The fibers of the tendon weaken and tear with localized symtoms, which include pain and swelling behind the medial malleolus without a history of acute trauma. As the individual continues to walk on the affected extremity, the symptoms progress and without intervention, the heel slips into a valgus attitude as the peroneus Longus overtakes the degenerating Posteror Tibial Tendon. In time the Deltoid and spring [plantar-calcaneo-navicular Ligament] deform under the excessive stress. The medial longitudinal arch colapses and the forefoot laterally displaces with the valgus heel. The end stage of this condition would be a rigid flatfoot (Figure 14) with reflexive spasm of the peroneals. This condition is unilateral with onset of symptoms in middle age.
MRI can be ordered to rule out tumor and demonstrate location in relationship to the tibial nerve and its distal branches (Figure 16). Varicosities/ganglions and or other lesions can compress the nerve and cause these neuritic symptoms. These symptoms should abate with surgical removal of the lesion. It is important to be familiar with other diagnoses which are present with similar symptoms, especially radiculopathy due to L-4 , L-5 , S-1 spinal nerve roots. The symptoms might be presented as an atypical heel spur syndrome with pain being more intense at the end of the day as apposed to the first step in the morning.
Tibial Nerve
Lateral Calcaneal
Medial Calcaneal
F i r s t B r an c h of L P N B AX T E R S N e r ve
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The fascia covers the tendinous origin of the flexor digitorum brevis that originates from the plantar medial calcaneal tubercle. The plantar medial tubercle overlyes the first branch of the lateral plantar nerve [Baxters nerve], which becomes compressed via fascial strain and inflammation Figure 18.
The symptoms present with the most acute pain at the initiation of heel contact, the first step in the morning. This syndrome is self-limiting and will usually resolve with conservative therapy such as strapping/arch supports/foot orthoses/steroid injection/physical therapy. This condition is seen in the younger 20-30 year old athlete due to repetative stress and in the middle age 40 years or more as a degenerative condition associated with weight gain. The spur is found on x-ray in 50% of cases, while in 30% of the cases no evidence of plantar medial spur is seen.
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Mortons Neuroma
This diagnosis is consistent with symptoms of sharp/shooting/burning type pain between the toes, which is sporatic in nature without a history of trauma. The condition is anatomically situated between toes three and four [third interspace] where the common digital nerve bifurcates into common digital nerves. This is located deep to the transverse metatarsal ligament (Figure 20). The neuritic symptoms are due to compression of the nerve by epineurial fibrosis due to repetitive trauma associated with shoes. The diagnosis is made via nerve block of the associated common digital nerve and the permanent cure would be surgical resection of the nerve.