What You Need to Know: Orthopedic Reasoning/Pathology/RehabModule 10: Foot & Ankle Course Description:
This course utilizes the text: Orthopedic Clinical Advisor by Derrick Sueki, PT, DPT, GCPT, OCS and Jacklyn Brechter, PhD, PT. This course will help you access the information you need to confidently handle multiple orthopedic conditions. Essential clinical reference information provides up-to-date diagnostic and therapeutic information on common conditions in a bulleted, quick-reference format ideal for both students and practitioners. Content is written entirely by orthopedic therapists and is logically organized to promote accurate, efficient differential diagnosis and intervention.
Module 10: Foot & Ankle covers: Chapter 13b: Orthopedic Reasoning- Foot and Ankle Chapter 13c: Orthopedic Pathology- Foot Chapter 6d: Rehab & Common Questions- Lower Extremity
Diagnoses covered are: Calcaneal Stress Fracture Cuboid Syndrome Fat Pad Contusion Flexor Hallucis Longus Tendinopathy Osteoarthritis of the Foot Jones Fracture Ligament Injuries of the Phalanges Metatarsal Stress Fractures Metatarsal Joint Synovitis Mid Tarsal Joint Injury Morton's Neuroma Navicular Fracture Phalanges Fractures Plantar Fasciitis Posterior Impingement of the Ankle Retrocalcaneal Bursitis Sesamoid Injury Sinus Tarsi Syndrome
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Talar Dome Damage Turf Toe
Methods of Instruction:
Online course available via internet
Target Audience:
Physical Therapists, Physical Therapist Assistants, Occupational Therapists, Occupational Therapist Assistants and Athletic Trainers
Educational Level: Intermediate
Prerequisites: None
Course Goals and Objectives:
At the completion of this course, participants should be able to: 1. Recognize the prevalence of foot and ankle pain 2. Identify the five most common foot and ankle conditions for the elderly 3. Differentiate between symptom descriptors of foot and ankle pathology 4. Describe special tests of the foot and ankle 5. Identify synonyms for Calcaneal Stress Fracture 6. Recognize the different mechanisms of injury for a Fat Pad Contusion 7. Identify the differential diagnoses for a Jones Fracture 8. Describe the Radiological Grading System for Stress Fractures 9. Recognize the contributing factors for Metatarsal Joint Synovitis 10. Identify the common signs and symptoms for a Morton's Neuroma 11. Recognize the contributing factors for a Navicular Fracture 12. Describe the epidemiology and demographics for Plantar Fasciitis 13. Recognize which patients with lower extremity pain derive the greatest long-term benefits from rehabilitation 14. Differentiate between lower extremity muscle weakness presentations and their compensatory motions 15. Recognize how a clinician should progress an exercise program for the lower extremity
Criteria for Obtaining Continuing Education Credits: A score of 70% or greater on the post-test
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DIRECTIONS FOR COMPLETING THE COURSE: 1. 2. 3. 4.
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This course is offered in conjunction with and with written permission of Elsevier Science Publishing. Review the goals and objectives for the module. Review the course material. We strongly suggest printing out a hard copy of the test. Mark your answers as you go along and then transfer them to the actual test. A printable test can be found when clicking on “View/Take Test” in your “My Account”. After reading the course material, when you are ready to take the test, go back to your “My Account” and click on “View/Take Test”. A grade of 70% or higher on the test is considered passing. If you have not scored 70% or higher, this indicates that the material was not fully comprehended. To obtain your completion certificate, please re-read the material and take the test again. After passing the test, you will be required to fill out a short survey. After the survey, your certificate of completion will immediately appear. We suggest that you save a copy of your certificate to your computer and print a hard copy for your records. You have up to one year to complete this course from the date of purchase. If we can help in any way, please don’t hesitate to contact us utilizing our live chat, via email at
[email protected] or by phone at 405-974-0164.
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Foot and Ankle AUTHORS: ROB ROY MARTIN, CHRISTOPHER R. CARCIA,
RONALD BELCZYK, and DANE K. WUKICH
INTRODUCTORY INFORMATION The foot and the ankle are the body’s first connection to the ground. Therefore, pathology or abnormal mechanics can often lead to compensations in joints and structures up the kinetic chain. Ankle and foot dysfunction can result in problems as far away as the neck and the shoulder. Couple this with the relative complexity of the region and the clinician is faced daunting challenge. The body region demands dynamic stability and mobility. When it is not functioning correctly, pathology often results.
WHAT IS THE PREVALENCE OF FOOT AND ANKLE PAIN? The prevalence of foot and ankle pain will vary greatly depending on age, activity level, and body type. Studies have found that approximately 20% to 25% of individuals have foot and anklerelated complaints,17,18,20 with ankle injuries being the most common of all athletic injuries.6,17 Foot pain was found to be associated with increased age, female sex, obesity, and pain in other body regions.20 Common causes of foot and ankle pain in younger active individuals are ankle sprains, plantar fasciitis, and Achilles tendinopathy. Ankle sprains were found to occur at a rate of one injury per 10,000 people per day. Approximately 10% of all emergency room visits are due to ankle injuries, with 90% being lateral ankle sprains.31 Basketball, football, soccer, and volleyball are the sports in which ankle sprains most commonly occur.49 Plantar fasciitis is another common cause of foot pain affecting approximately 2 million Americans each year and as much as 10% of the population.41 It accounts for 8% to 15% of all adult foot complaints requiring professional care.50 Achilles tendinopathy is most prevalent among runners, with an annual incidence reported between 7% and 9%.22,27
WHAT IS THE PROGNOSIS FOR RECOVERY FROM FOOT AND ANKLE PAIN? The prognosis for recovery from foot and ankle pain will depend on severity of injury, age, general health, comorbidity, previous injury, and biomechanical factors. Additionally, the activity level that individuals need to regain will affect the prognosis. Although recovery from ankle sprains, plantar faciitis, and Achilles tendinopathy is generally good, symptoms can persist. Concurrent injuries such as syndesmotic disruption, articular cartilage lesion, and/or peroneal tendon damage can negatively affect the prognosis after a lateral ankle sprain. It is not uncommon for patients who sustained a sports-related inversion ankle injury to have persistent symptoms for 2 years or more after their injury.4 Full recovery was reported by 36% to 85% of individuals within a 3-year period.53 With respect to plantar fasciitis, 80% of individuals who seek treatment have resolution of symptoms within a 12-month period.29,57 Similar results are observed following intervention for Achilles tendinopathy. Long-term follow-up ranging between 2 and 8 years suggests that between 71% and 100% of patients with Achilles tendinopathy are able to return to their prior level of activity with minimal or no complaints.1,37,38
WHAT IS THE RECURRENCE RATE? After a lateral ankle sprain up to 34% of individuals suffer chronic ankle instability.23,53 These individuals, described as either having mechanical or functional instability, can have permanent limitations. Generally, however, the recurrence rate of foot and ankle injuries has not been established.
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WHAT FACTORS MAKE DIAGNOSIS IN THE FOOT AND ANKLE DIFFICULT? The interrelation and close proximity of potential sources of pathology in the foot and ankle may make diagnosis difficult. Reproduction of a patient’s symptoms is the key to making a correct diagnosis.58 Chronic conditions can be difficult to diagnose as the symptoms in these individuals are often diffuse and not well localized.
CLINICAL PEARL There are usually numerous factors that contribute to chronic pain symptoms and thus tracing the source of pain to one specific structure may not be possible. When the onset of symptoms is insidious inflammatory processes, immune reactions, endocrine factors, and posttraumatic arthrosis should be considered. Patients with inflammatory arthropathy typically have symptoms in adjacent joints, including metatarsal phalangeal joints and the subtalar joint. Also symptoms may not be isolated to the foot and ankle.
HOW SUCCESSFUL IS NONOPERATIVE THERAPY IN TREATING FOOT AND ANKLE PAIN? Nonsurgical treatment of common disorders, such as plantar fasciitis, lateral ankle sprain, and Achilles tendinitis, has been defined. Conservative treatment of plantar fasciitis has a reported success rate of 85% to 95%, but may require 6 to 12 months to resolve.29,57 Recommended interventions included iontophoresis with dexamethasone or acetic acid, calf and plantar fascia stretching, calcaneal or low-dye taping, and orthotics for short-term improvements.33 When comparing custom and prefabricated orthoses, there appears to be no difference in pain reduction or functional improvement. Night splints should be considered as an intervention for patients with symptoms greater than 6 months in duration. The recommended length of time for wearing the night splint is 1 to 3 months.33 Individuals with first-time grade I and II ankle ligament sprains may best return to preinjury status when treated with an AirStirrup brace combined with an elastic wrap.7 Functional intervention is favorable to immobilization when treating acute ankle sprains.25 Also there is evidence to support the benefit of a supervised exercise program over home program for the treatment of acute lateral ankle sprains.52 For Achilles tendinopathy, significant decreases in pain and improvement in function have been reported following 6 to 12 weeks of an intervention program that focused on eccentric exercise.2,42 Recent evidence suggests the addition of low-level laser therapy to an eccentric program further accelerates the recovery process8,47
HOW SUCCESSFUL IS SURGERY IN TREATING FOOT AND ANKLE PAIN? Success rates following surgery vary depending on the treating condition and selected procedure. For instance an arthrodesis of ankle, which is considered the gold standard for posttraumatic arthritis, can achieve 80% to 85% successful outcomes.30 As a guideline, 85% of patients are satisfied, 10% satisfied with reservations, and 5% not improved or dissatisfied with their surgical outcome.
PERSONAL INFORMATION WHAT INFLUENCE DOES AGE HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? Young individuals who are active in sports are more likely to have overuse type injuries including stress fractures and tendinitis.
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Occupations that involve a considerable amount of weight-bearing activity may put patients at risk for overuse injuries. Heavy labor jobs may also put a patient at risk for traumatic injuries such as fractures and sprains. A patient’s job description can be important in guiding treatment to focus on specific job-related activities.
WHAT INFLUENCE DOES GENDER HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? Foot and ankle pathology related to gender may be most closely associated with shoe wear issues. Females have a tendency to wear ill-fitting shoes with a narrow toe-box. A narrow toe-box may lead to Morton’s neuroma, bunion, bunionette, corns, and calluses. Also females have a tendency to choose shoes with a low heel counter. This type of shoe design may rub the posterior aspect of the heel and may lead to posterior heel pathologies. Males have a higher incidence of Achilles ruptures, particularly middle-aged males who engage in jumping activities.
WHAT INFLUENCE DOES ETHNICITY HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? There is little information regarding ethnicity and its relation to foot and ankle pathology. African-Americans may have a higher incident of Achilles ruptures.
TABLE II-13-1 Common Locations of Osteochondrosis
in Children Pathology
Location
Age of Presentation
Gender
Freiberg’s infarction
Metatarsal head 10 to 18 years, but F > M (second metatarsal also can occur as most common) adult Köhler’s disease Navicular 3 to 6 years M>F Sever’s disease Calcaneus 6 to 12 years Both
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The effect of being overweight or obese can increase the likelihood of many foot and ankle conditions, including tendinopathy, plantar fasciitis, and arthritis.14
CLINICAL PEARL If conservative treatment is to be successful weight loss for individuals who are overweight can be an important component of treatment. For each pound of weight loss there is a fourfold reduction in the load exerted per step during daily activities.34 Therefore to decrease stress on the foot and ankle, even the loss of a few pounds could potentially be clinically meaningful.
SYMPTOM HISTORY Symptom location can provide valuable information. However, for individuals with chronic conditions the location of symptoms may provide less information compared to those with more acute or subacute conditions. Generally those with chronic conditions can complain of general pain and have difficulty isolating a specific source of pain.
CLINICAL PEARL Palpation can provide valuable information in identifying the source of symptoms. Metatarsalgia and metatarsal stress fracture can be distinguished by identifying the most painful area as either the metatarsal head or the shaft, respectively. Palpation can also help to identify sinus tarsi syndrome over lateral ankle impingement. Frequently, symptoms of chronic problems present with diffuse pain. Having the patient point to the most painful spot can help identify the origin of symptoms.
MECHANISM OF INJURY WHAT INFLUENCE DOES THE MECHANISM OF INJURY HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? TRAUMATIC INJURIES: The direction of force in a traumatic injury provides useful diagnostic information. Injuries that involve inversion with the foot in a plantar flexed position usually involve the anterior talofibular ligament (ATFL). Injury to the ATFL accounts for 85% of all ankle sprains.13 More severe ankle inversion sprains can involve the calcaneal fibular ligament (CFL) as well as the ATFL. Additionally, inversion injuries with the foot in neutral dorsiflexion can cause isolated injury to the CFL. External rotation or forced dorsiflexion of the ankle can involve syndesmotic or distal tibia-fibula injuries (i.e., high ankle sprains).An Achilles rupture should be suspected when the injuries involve landing from a jump. Traumatic injures that involve the forefoot should suggestz a Lisfranc facture (tarsometatarsal sprain) in the differential diagnosis. Although the ATFL is the most common ligament injured in ankle sprains, the practitioner should maintain a working differential diagnosis and carefully examine the foot and ankle for other less common injuries.The differential diagnosis of an ankle sprain in the acute setting should include a number of potential pathologies as outlined in Box II-13-1. It should be noted that multiple pathologies can occur currently, especially in injuries that involve high force.
ORTHOPEDIC REASONING
WHAT INFLUENCE DOES A PATIENT’S OCCUPATION HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS?
DOES BODY WEIGHT AFFECT YOUR DECISIONMAKING PROCESS?
Section II
Older individuals are more likely to have tendinosis and arthritic conditions. The adolescent patient can have an injury pattern different from those who have achieved skeletal maturity. When growth plates are not yet closed they are susceptible to injury.35 Common foot and ankle pathology to consider in patients who have unfused growth plates includes osteochondrosis, accessory ossicles, tarsal coalition, apophysitis, and epiphyseal fractures.28 Osteochondrosis is epiphyseal ischemic necrosis followed by regeneration or recalcification. This can occur at several locations in the foot and ankle region (Table II-13-1). An accessory ossicle (accessory bone) is an ossification center that has not fused. This occurs in 10% of the population. Common locations include the lateral malleolus, medial malleolus, navicular, and talus.24 A tarsal coalition is a congenital union between two tarsal bones, most commonly at the calcaneonavicular or talocalcaneal joints. Epiphyseal fractures are fractures that involve the growth plate.28 The elderly present with pathologies distinctly different from those previously mentioned. The five most common conditions for the elderly are toenail disorders (74.9%), lesser toe deformities (60%), corns and calluses (58.2%), bunions (37.1%), and signs of fungal infection, cracks and fissures, or macerations between toes (36.3%).11
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BOX II-13-1
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Differential Diagnosis of Traumatic
Injury Syndesmosis disruption Ankle dislocation Malleolar fracture Lateral talar process fracture Talar neck fracture Anterior calcaneal process fracture Osteochondral lesion of the talar dome Lateral collateral ankle ligament injury Medial collateral ankle ligament injury Subtalar joint dislocation/pathology Sinus tarsus injury Peroneal tendon pathology Achilles pathology Extensor digitorum brevis strain Cuboid fracture Lisfranc fracture Fifth metatarsal fracture (Jones fracture)
CLINICAL DECISION MAKING CASE STUDY—PATIENT PROFILE A 21-year-old female injured her foot while playing rugby. She reported twisting her ankle and is having lateral ankle and foot pain. Point tenderness was noted over the sinus tarsi and pain is elicited with passive inversion of the subtalar joint. What do you think is the source of this patient’s pain? Answer Radiographs (Figure II-13-1) and computed tomography (CT) (Figure II-13-2) demonstrated a fracture of the lateral talar process.
FIGURE II-13-2 Lateral view of foot with talar fracture.
BOX II-13-2 Differential Diagnoses Based
on Region Differential Diagnoses for Posterior Heel Pain Haglund’s deformity Retrocalcaneal bursitis Achilles tendinosis or rupture Posterior impingement syndrome Systemic arthritides
SYMPTOM LOCATION
Differential Diagnoses Differential for Plantar Heel Pain Diagnoses for Forefoot Pain Plantar fasciitis Neuroma Calcaneal stress Stress fractures fracture Metatarsalgia Fat pad atrophy Hallux rigidus Tarsal tunnel Hallux valgus syndrome Turf toe Baxter’s neuritis Sesamoiditis Digital deformities Plantar plate rupture Tarsal coalition
WHAT INFLUENCE DOES THE LOCATION OF SYMPTOMS HAVE ON YOUR CLINICAL DECISIONMAKING PROCESS? Differential diagnoses for plantar heel, posterior heel, and forefoot are listed in Box II-13-2. Although plantar fasciitis is the
most common etiology of heel pain, other sources of heel pain should also be considered in the differential diagnosis. Nerve entrapment, specifically the first branch of the lateral plantar nerve, can be a source of plantar heel pain. This is known as Baxter’s neuritis or neuritis of the nerve to the abductor digiti minimi. This nerve can get impinged at the fascia of the abductor hallucis, which is frequently misdiagnosed as plantar fasciitis.
CLINICAL DECISION MAKING CASE STUDY—PATIENT PROFILE An 18-year-old female presents with persistent pain of the left ankle of 11 months duration. She states that the pain developed while she was participating in recreational dance. She denies any history of direct trauma to the area. Pain in the posterior ankle was elicited with both active and passive plantar flexion. Severe pain was present on palpation between the Achilles tendon and the peroneal tendons posterolateral to the subtalar joint. What is the likely diagnosis of this patient’s persistent ankle pain? FIGURE II-13-1
AP view of foot with talar fracture.
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BOX II-13-3 Symptom Descriptors of Foot and Ankle Pathology Patient complaint Sharp stabbing pains associated with weight-bearing activities Instability Dull aching in bone Anterior pinching pain with end range dorsiflexion Posterior pinching associated with end range planter flexion Lateral snapping
FIGURE II-13-3 Lateral view of foot with well-rounded accessory bone on posterolateral talus.
REFERRAL OF SYMPTOMS Symptoms can be referred from the lumbar spine with involvement of L4 to S1 nerve roots. Most commonly, pathology at L5 to S1 can mimic plantar heel pathologies.A peripheral nerve entrapment of the sciatic nerve, or one of its branches, could also cause symptoms to radiate in the foot and ankle.
SYMPTOM DESCRIPTORS QUALITY OF SYMPTOMS Burning pain and numbness are usually from nerve pathology. Common sources of nerve irritation include the tibial nerve being compressed by the flexor retinaculum around the medial malleolus. This is referred to as tarsal tunnel syndrome and can cause pain in the plantar aspect of the heel. A forefoot neuroma is compression neuropathy of the plantar digital nerve and commonly occurs at the third digital nerve. When this nerve is involved patients complain of burning or tingling in the third and fourth webspace. Numbness can also be associated with compartment syndrome. However, this numbness is in the pattern of the involved peripheral nerve and is associated with a sensation of tightness in the posterior, anterior, and/or lateral leg.These symptoms of numbness and tightness are also activity related and typically occur as the individual exercises. Diabetes can cause symptoms of burning pain and numbness associated with neuropathy. The decreased sensation that can result presents in a “stocking” distribution. Symptoms related to neuropathy generally occur in an older population with a history of diabetes and do not change relative to activity. Other symptoms that are useful in the diagnostic process are shown in Box II-13-3.
WHAT INFLUENCE DOES THE DEPTH OF SYMPTOMS HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? Deep ankle symptoms are usually from ankle cartilage injuries, including arthritis. The three major categories of arthritis
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Subluxing peroneal tendons Forefoot neuroma Achilles rupture Posterior tibial tendon dysfunction
are inflammatory, osteo-, and posttraumatic arthritis, with posttraumatic arthritis being most common.30 Although rheumatoid arthritis is the most common form of inflammatory arthritis, it affects the ankle only 10% to 50% of the time.21,30 Posttraumatic arthritis and osteoarthritis accounted for 12% and 70% of ankle arthritis cases, respectively.43 Deep posterior calf pain can be associated with deep vein thrombosis (DVT) and is usually associated with swelling, warmth, and redness in the calf. Another sign of a DVT is increased pain in passive dorsiflexion (Homan’s sign).
WHAT INFLUENCE DOES A PATIENT’S DAILY PAIN PATTERN HAVE ON YOUR DECISION-MAKING PROCESS? When pain is worse at night a nonmusculoskeletal cause, such as neoplasm, should be considered, particularly if symptoms are difficult to reproduce. When symptoms of a red, warm, swollen, and painful joint occur related to eating certain foods, gout should be considered. Although gout can occur in any joint it commonly occurs at the first metatarsal phalangeal joint. Gout is associated with an abnormal metabolism of uric acid and can occur after consuming red meats, yeast, oily fish, and alcoholic beverages.
STABILITY OF SYMPTOMS HOW DOES THE PROGRESSION OF A PATIENT’S SYMPTOMS IMPACT YOUR CLINICAL DECISION-MAKING PROCESS? As conditions become chronic the symptoms progress from being intermittent to constant. When the patient’s history suggests a chronic condition, with associated constant pain, the overall prognosis for full recovery is poorer. Plantar fasciitis is thought to be caused by irritation of the proximal plantar fascia near the insertion of the calcaneal tuberosity. Therefore patients complain of “start-up pain” as pain occurs with the first steps in the morning or after sitting for a lengthy period of time as the healing tissue is stretched. It is thought that with prolonged rest the plantar fascia tightens up. A sudden stretch with standing causes pain and possibly microtears in the plantar fascia. Baxter’s neuritis causes heel pain that is generally present after activity compared to pain after the first steps as with plantar fasciitis.
ORTHOPEDIC REASONING
Answer Radiographs (Figure II-13-3) reveal a well-rounded accessory bone on the posterolateral talus (os trigonum) causing a posterior impingement syndrome.
Posterior impingement
Section II
Complaint of a painful lump in the forefoot A “pop” in the calf when landing from a jump Progressive loss of arch height
Pathology Cartilage lesions (i.e., talar dome lesions) Ligament injury Stress fracture Anterior impingement
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FUNCTIONAL AND ACTIVITY PARTICIPATION LIMITATIONS WHAT INFLUENCE DO AGGRAVATING AND EASING FUNCTIONS HAVE ON YOUR CLINICAL DECISION-MAKING PROCESS? As with all musculoskeletal overuse conditions, the symptoms should be reproducible. Muscle and tendon conditions should be aggravated when stress is applied by activities or movements that cause the muscle–tendon unit to stretch or contract. Peroneal tendinopathy and flexor hallucis longus tendinopathy would be painful with resisted eversion and great toe flexion, respectively. Specific behavior of symptoms can help lead to the diagnosis. Pain in the posterior heel when coming up on the toes with contraction can indicate Achilles tendon pathology (tendinitis/ tendinosis). When active movements do not aggravate the symptoms, retrocalcaneal bursitis should be considered. An inability to rise up on the toes suggests Achilles rupture, posterior tendon dysfunction, or degenerative tear. Stress fractures and tendon conditions commonly occur in athletes participating in sports that require jumping, long distance marching, and running. Patients with stress fractures complain of pain that is better at rest and worse with prolonged weight bearing.This pain can at first be intermittent but can progress to being constant as the condition becomes chronic.
TABLE II-13-2
Neuroma pain is worse at the end of the day and is aggravated by poorly fitting shoe wear such as pointed shoes or high heeled shoes or by activities that hyperextend the metatarsal phalangeal joints such as walking, running, or squatting. Turf toe and hallux rigidus cause pain and stiffness of the first metatarsal phalangeal joint and are also aggravated by activities that hyperextend the metatarsal phalangeal joint. Turf toe generally occurs after a traumatic hyperextension injury in a young active population. Hallux rigidus is more insidious and occurs in an older population (Table II-13-2).
CLINICAL DECISION MAKING CASE STUDY—PATIENT PROFILE A 20-year-old male presents with pain in the shin area related to overtraining for a marathon. How do you differentially diagnose the potential sources of pain? Answer Posterior tibialis periostitis (posterior shin splints) should be associated with tenderness at the origin of the posterior tibialis. Tenderness at the origin of the anterior tibialis would most likely be anterior tibialis periostitis (anterior shin splints). Tenderness directly on the tibia would likely be a tibial stress fracture. If tightness and numbness were associated with activity, compartment syndrome should be suspected.
Functional or Activity Participation Limitations
Motion
Functional Activities
Dorsiflexion
Walking—mid to terminal stance Squatting Descending stairs
Plantar flexion
Walking—terminal stance Driving car Coming up onto toes
Inversion and supination
Walking—initial contact Twisting ipsilaterally
Eversion and pronation
Walking—mid-stance Twisting contralateral
Static positions
Sleep Sitting
Other
Running
Pathology if Symptoms Are Aggravated by Activity
Pathology If Symptoms Are Eased by Activity
Posterior tendon pathology—if passive stretch Posterior muscle pathology—if passive Posterior tibialis pathology Tibial and peroneal nerve Anterior talocrural joint pathology Turf toe Sesamoid bone injury Tibiofibular syndesmosis pathology Deep vein thrombosis Malleolar fracture Anterior lateral impingement ATF ligament pathology Cuboid dysfunction Posterior tendon or muscle pathology—if active Posterior impingement Retrocalcaneal bursitis Deep vein thrombosis—if active Malleolar fracture Peroneal pathology Cuboid dysfunction Fracture of the fifth metatarsal Forefoot fracture Plantar fascia Mid-foot laxity Tarsal tunnel nerve entrapment Nerve entrapment at foot Sinus tarsi syndrome Plantar fascia Inflammatory disorders
Anterior talofibular (ATF) ligament pathology Cuboid dysfunction Posterior impingement Retrocalcaneal bursitis Peroneal pathology
Fracture Compartment syndrome Most pathologies
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Posterior tibialis pathology Tibial and peroneal nerve Anterior talocrural joint pathology Turf toe Sesamoid bone injury Tibiofibular syndesmosis pathology Anterior lateral impingement Tarsal tunnel syndrome Syndesmosis injury Plantar fasciitis Peroneal tendon pathology
Fractures Tendon pathology Muscle pathology None
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FIGURE II-13-5 AP weight-bearing view of foot and ankle with Charcot neuroarthropathy.
Section II
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MEDICAL HISTORY WHAT ROLE DOES A PATIENT’S PAST MEDICAL HISTORY PLAY IN THE DIFFERENTIAL DIAGNOSIS OF FOOT AND ANKLE PATHOLOGY? When an individual has a history of diabetes, Charcot neuroarthropathy should be considered, particularly if trauma is involved. Charcot arthropathy is a chronic and progressive disease of bone and joints commonly found in the feet and ankles of neuropathic patients. The acute Charcot foot manifests as a relatively painless, warm, erythematous, and edematous foot.15,59 The patient will usually have a good pulse and sensory neuropathy on examination. Patients usually do not have significant pain despite the presence of intense synovitis, fracture, and instability of single or multiple joints.19,44 Stress fractures can occur and are infrequently diagnosed in patients with peripheral neuropathy as pain is absent and there is no apparent loss of function.9 The most important factor in potentially altering the outcome of patients with Charcot neuroarthropathy is to have a high clinical suspicion in patients who are “at risk.”
ORTHOPEDIC REASONING
CLINICAL DECISION MAKING CASE STUDY—PATIENT PROFILE A 50-year-old female with a history of insulin-dependent diabetes and peripheral neuropathy presented to the emergency room with an acute ankle sprain. At that time, non-weight-bearing x-ray films were taken and were negative for fracture dislocation (Figure II-13-4). The patient was diagnosed as having a sprain of the right ankle. She continued to ambulate without any protective bracing. Despite any significant pain she presented 3 months later to a foot and ankle specialist with complaints of swelling and an inability to wear shoes. She states that she twisted her ankle earlier that day and felt something shift. Protective sensation was absent when tested with a monofilament and tuning fork. An obvious valgus deformity of the ankle was present. What disease state needs to be ruled out? Answer Charcot neuroarthropathy needs to be ruled out. Figures II-13-5 and II-13-6 show the radiograph taken 3 months after
FIGURE II-13-6 Lateral weight-bearing view of foot and ankle with Charcot neuroarthropathy.
injury and reveal extensive collapse of the ankle, hindfoot, and midfoot. Systemic disorders that can cause foot and ankle pain include osteomylitis, gout, pseudogout, sickle cell disease, complex region pain syndrome, and peripheral vascular disease. Systemic arthritic conditions generally have pain in multiple joints outside of the foot and ankle region. A medical history of generalized ligamentous laxity, malalignment issues, recent illness, or other musculoskeletal injuries may also help give a prognosis of injury.5
MEDICAL AND ORTHOPEDIC TESTING WHAT MEDICAL AND ORTHOPEDIC TESTS INFLUENCE YOUR DIFFERENTIAL DIAGNOSIS PROCESS IN THE FOOT AND ANKLE?
FIGURE II-13-4 and ankle.
Lateral non-weight-bearing view of foot
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There are a large number of tests clinicians can use to assess the foot and ankle region; however, the tests we have outlined are the ones we use most frequently. When the origin of symptoms is traumatic in nature, a series of tests is performed to assist in the differential diagnosis process as shown in Table II-13-3.
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TABLE II-13-3
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Special Tests of the Foot and Ankle
Test
Structures Assessed
Test Reproducibility
Anterior drawer
Anterior talofibular ligament Calcaneal fibular ligament Deltoid ligament
Poor interrater reliability16
Talar tilt into inversion Talar tilt into eversion Dorsiflexion external Rotation test Squeeze test Thompson test
Distal tibia-fibula syndesmosis and deltoid ligament Distal tibia-fibula syndesmosis Achilles tendon
Poor interrater reliability in the absence of pain16 N/A Substantial interrater reliability3 Moderate interrater reliability3 N/A
Our assessment includes evaluating individuals standing, walking, and, when necessary, running with a focus on calcaneal position, arch height, and great toe extension. A more thorough biomechanical examination, looking at rearfoot and forefoot abnormalities, can be performed. However, the reliability of this “biomechanical examination” is poor and does not predict dynamic foot function.12,39,40,51 Navicular drop can be measured to assess the change in arch height from subtalar neutral to the normal comfortable standing position. This measurement has been found to have good reliability.36,45 In addition to a biomechanical assessment a trial of arch support taping (treatment-directed test54,55) can be used to help determine if orthotic intervention should be considered.46
WHAT BIOMECHANICAL ABNORMALITIES IN OTHER REGIONS AFFECT FOOT AND ANKLE PATHOLOGY?
Tinel’s and Morton’s tests are commonly done to assess for tarsal tunnel and Morton’s neuroma, respectively. The Windlass test can also be performed and is used to assess for plantar fasciitis. This test is performed by extending the first metatarsophalangeal (MTP) joint, in both weight bearing and non-weight bearing, in an attempt to reproduce the patient’s heel pain. Although the Windlass test had a high specificity (100%), its sensitivity was poor (F Ethnicity Not applicable History/ Typically associated with mechanism overuse; repetitive of injury microscopic tensile overload Symptoms Stiffness/pain
M>F Higher incidence in African-Americans Chronic tendinosis with or without symptoms; tendency to occur during vigorous eccentric contraction
All ages are suscepitble Most common in athletes: soccer, basketball, football, volleyball, and cross-country runners M=F Not applicable Trauma; 80% to 85% result from a combination of inversion and plantar flexion
M=F Not applicable Trauma; results from external rotation of the talus or forced dorsiflexion
M=F Not applicable History of lateral ankle sprains
Clinical findings
Past medical history Diagnostic tests Red flags
Diagnosis
Pain/stiffness often present Unable to perform normal activities upon awakening; decreases with activity; increases after activity Decreased active passive Thompson test (+); palpable gap; dorsiflexion with knee inability to perform unilateral heel extended; pain with rise unilateral heel rise; tender to palpation 2 to 6 cm proximal to insertion; pes planus Previous overuse injuries Fluoroquinolone antibitic use, prior intratendinous injection, retrocalcaneal spurs or chronic tendinosis X-rays can detect MRI and US may be ordered retrocalcaneal spur; MRI and US may be ordered Inability to perform plantar If rupture is suspected patient should be flexion versus gravity; soft referred to a physician tissue deficit may indicate rupture
Instability and pain confined to the Pain just above the ankle Pain, stiffness, and swelling in the anterolateral anterolateral ankle region Symptoms are often increased with Symptoms are often increased with Symptoms are often increased cutting, pivoting, and twisting cutting, pivoting, and twisting with cutting, pivoting and twisting Anterior drawer (+): ATFL Talar tilt (+): CFL Tender lateral ankle joint Ecchymosis and swelling
Recent lateral ankle sprain
X-rays to rule out fracture
X-rays to rule out fracture
MRI or US is beneficial to visualize soft tissues
Skeletally immature: avulsion fractures Ottawa Ankle Rules (+): fracture
Ottawa Ankle Rules (+): fracture
Unremarkable
Tendon
Tendon
Malleolar fractures
Peroneal tendinopathy
Posterior impingement syndrome
Tendon
Posterior tibial tendinopathy/ dysfunction 18 to 40 50 to 80 Sports—ballet dancing, Repetitive/prolonged gymnastics, or downhill weight bearing running
Bone
Bone
Nerve
Anterior/posterior periostitis
Stress fracturee
Tarsal tunnel
18 to 40 18 to 40 Common with Repetitive weight repetitive weight bearing bearing (i.e., running)
25 to 50 Repetitive/prolonged weight bearing
Continued on following page.
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Foot and Ankle
18 to 40 Sports—basketball, football, gymnastics, ice skating
Pain,“pinching” with dorsiflexion; end range inversion is often painful as well
Up to 40% experience recurrence
Bone
Age (years) All ages are susceptible Activity/ Can occur across all occupation activity levels
Squeeze test (+) Dorsiflexion External rotation test(+) Tender distal tibiafibular articulation
ORTHOPEDIC REASONING
Aggravating/ relieving factors
Acute pain, significant calf weakness
Section II
Pathology
260
Gender Ethnicity History/ mechanism of injury Symptoms
Nociceptive and Peripheral Neurogenic Pain (Continued)
Bone
Tendon
Tendon
Tendon
Bone
Bone
Nerve
Age M Not applicable Gradual, related to over training or improper training Vague poorly localized pain
M=F Not applicable Gradual
Inability to bear weight, pain, instability
M=F Not applicable Repetitive trauma Complication following an ankle sprian Posterior ankle pain, local swelling, and at times reports of “catching”
Excessive weight bearing
Worse with prolonged standing or walking
Tenderness over the involved bony region
Tenderness just posterior to the medial malleolus Positive Tinel sign over the tarsal tunnel
Previous stress fractures CT or bone scan
Carpel tunnel
Aggravating/ relieving factors
Weight bearing increases Activities that cause strong Movement into plantar symptoms contraction of evertors; i. e., flexion (active or “cutting and pivoting” passive)
Clinical findings
Tenderness over the involved bony region Pain with movement, swelling, and ecchymosis
Tenderness over the peroneal tendons Pain with resisted eversion in plantar flexion
Local tenderness Reproduction of symptoms with passive or resisted plantar flexion
Past medical history Diagnostic tests Red flags
Osteoporosis
Ankle sprain
Ankle sprain
X-rays—routine
MRI
MRI
Neurovascular complications and acute compartment syndrome
Persistent symptoms may Unremarkable require surgical intervention
Medial ankle pain Progressive loss of arch height General foot pain from stress on supportive ligaments Prolonged weight bearing Worse with Pain with resisted repetitive weighinversion and plantar bearing activities flexion Tender posterior tibialis Pain with tendon palpation; pain Unable to perform singlewith stretching leg heel raise or contraction of muscle–tendon that attaches to the affected area of the bone Unremarkable Previous overuse injuries MRI Not applicable Unremarkable
Bone scan to r/o stress fracture for persistent symptoms
Check dietary history
Pain, burning, and numbness in medial arch and/or the plantar surface of the foot and toes
NCV and EMG r/o lumbar radiculopathy
Tissue
Ligaments
Bursa
Bone
Bone/Cartilage
Cartilage
Bone
Bone
Diagnosis Age (years) Activity/ occupation
Turf toe 18 to 30 Sports with explosive movements
Retrocalcaneal bursitis 20 to 60 Repetitive/prolonged weight bearing
Sesamoid injuries 20 to 50 Repetitive weigh bearing
Sinus tarsi syndrome 20 to 50 Sports with explosive movements
Talar dome damage 18 to 30 Sports with explosive movements
Forefoot fracture 15 to 60 Can occur across all activity levels
Gender Ethnicity History/ mechanism of injury
M>F Not applicable Traumatic first MTP overload (Hyperextension occurring with explosive push-off or change in direction is most common)
M=F Not applicable Repetitive (cumulative) trauma Recent change in footwear (e.g., tight athletic shoes or transition from flats to high heels)
F>M Not applicable Overuse or direct trauma
M>F Not applicable Traumatic inversion injury of the foot
M>F Not applicable Occurs with traumatic ankle injuries
Cuboid dysfunction 18 to 30 Given the stability of the joint, the condition is rare Most commonly reported in ballet dancers F>M Not applicable Acute or repetitive microtraumatic injury
M=F Not applicable Blunt trauma CHAPTER 13
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Foot and Ankle
TABLE II-13-4
Ligaments
Bursa
Bone
Bone/Cartilage
Symptoms
Stiffness and pain at the first MTP
Posterior heel pain aggravated by pressure
Local pain with weight bearing
Aggravating/ relieving factors
Pushing-off
Worse when beginning an activity or after resting
Pain when force is transmitted through the great toe (i.e., push-off)
Recurrent instability/ Ankle pain along with giving way, pain intermittent swelling, inferior/anterior to the weakness, stiffness, ankle, swelling, and catching or locking, stiffness and/or instability/ giving way Weight-bearing activity Weight-bearing activities, that inverts the foot particularly pivoting, (e.g.,walking on uneven increase symptoms ground)
Clinical findings Tenderness around the Tenderness superficial Tenderness over the first MTP joint to the Achilles tendon sesmoids Instability, mechanical (subcutaneous bursa) block, or hypermobility or deep to the Achilles of the first MTP with tendon (subtendinous ROM bursa) Swelling:“pump bump”
Cartilage
Tenderness over the Palpation: tenderness sinus tarsi behind the medical Deep pain in the subtalar malleolus when the area with forced ankle is dorsiflexed inversion of the foot and/or anterolateral ankle joint tenderness in maximal plantar flexion Unremarkable Unremarkable
Past medical history Diagnostic tests
Unremarkable
Unremarkable
Unremarkable
X-rays positive: compare the sesamoid-to-joint distance
X-ray may reveal a Haglund deformity
X-ray may be positive but MRI is typically used
Diagnostic injection of lidocain
Red flags
r/o fracture
Unremarkable
r/o fracture
Unremarkable
X-ray may be positive bur MRI is typically used Diagnostic injection of lidocaine Unremarkable
Bone
Bone
Lateral mid-foot pain
Localized pain and swelling
Sport activities Pain increasing with Landing from a jump weight bearing may increase pain Axial loading of the lateral column of the foot Pressure over the plantar Palpation: localized surface of the cuboid tenderness at the in a dorsal direction involved bones(s) reproduces symptoms
Prior history of ankle sprain Stress and/or weightbearing radiographs may assist with diagnosis
Unremarkable
Injury to peroneal nerve
Unremarkable
X-ray is positive
Fascia
Cartilage
Ligament
Fascia
Visceral
Nerve
Diagnosis
Plantar fasciitis
Post traumatic arthrosis
Lisfranc ligament tear
Deep vein thrombosis
Morton’s neuroma
Age (years)
20 to 60
40 to 70
Chronic compartment syndrome 20 to 40
40 to 60
Activity/ occupation
Prolonged weight bearing
Greater incidence with increasing age Sedentary, obese individuals are at greater risk
Gender
F>M
F>M
Ethnicity History/ mechanism of injury
Not applicable Graudual
Increased risk for females during and following pregnancy Not applicable Recent surgery with general anesthesia, immobility, recent airline travel
All ages, but most common in 20s Repetitive/prolonged weight Specific athletes at elevated bearing risk include gymnasts, ballet, football, and track/ field athletes M>F M>F
Not applicable Athletics/MVA Axial loading with plantar flexed mid-foot
M=F
Not applicable Overuse or trauma
Repetitive/prolonged weight bearing
Not applicable Gradual; related to illfitting/narrow shoes
Continued on following page.
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ORTHOPEDIC REASONING 13 of 77
Foot and Ankle
Not applicable Generally gradual onset, although trauma may precipitate symptoms
Long distance runners, skiers, soccer and basketball players
CHAPTER 13
Tissue
262
Nociceptive and Peripheral Neurogenic Pain (Continued) Fascia
Visceral
Pain, stiffness, catching, Pain, mid-foot instability locking, clicking or painful giving way episodes
Local pain in affected compartment is primary complaint Decreased ability to control the foot during exercise
Pain, swelling, and redness in calf
Aggravating/ Pain with the first few steps relieving factors in the morning or after sitting for long periods: “start-up pain” Clinical findings Tenderness in the medial calcaneal tubercle Positive Windlass test
Prolonged weight bearing
Pain with weight bearing
Exercise/activity-induced symptoms
Tender ankle joint Limited and painful ankle motion
Webspace tenderness Positive Morton’s sign
Past medical history Diagnostic tests
None needed
Red flags
Unremarkable
Previous ankle trauma (i.e., fracture) X-rays are positive for asymmetric joint space narrowing with signs of arthritis (sclerosis and osteophytes) Unremarkable
Ecchymosis in the plantar Physical examination findings Calf is often tender to aspect of the mid-foot are typically normal palpation; a “cord” may be Tenderness over TMT joints, noted with palpation particularly over the base of Homan’s sign may or may not the second metatarsal be positive Unremarkable Recent increase in activity Previous venous thromboembolism X-ray and MRI Measurement of Ultrasound, MRI, and/or compartmental pressure at venography rest and during exercise
Displaced/unstable injuries require surgery
Unremarkable
Symptoms
Fascia
Cartilage
Plantar heel pain
Unremarkable
Ligament
Nerve
Forefoot pain, numbness, and/or paresthesias in the digital nerve distribution commonly between the third and fourth toes Symptomas may be increased Excessive pressure from with dorsiflexion of the poorly fitting shoes ankle
Acute compartment Symptoms that migrate syndrome: pain out of proximally proportion, absence of Shortness of breath may pulse, pain with stretching indicate a pulmonary or weakness of the affected embolism compartment
Foot and Ankle
TABLE II-13-4
Unremarkable MRI or US can help visualize an enlarged nerve
ATFL, anterior talofibular ligament; CFL, calcaneal fibular ligament; MRI, magnetic resonance imaging; US, ultrasound; CT, computed tomography; NCV, nerve conduction velocity; EMG, electromyogram; MTP, metatarsophalangeal; r/o, rule out; ROM, range of motion; MVA, motor vehicle accident;TMT, tarsometatarsal.
CHAPTER 13
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Foot and Ankle
CHAPTER 13
ment outcome. The dates of surgery, hospital location, treating diagnosis, and perioperative complications should be recorded. FAMILY HISTORY: Family history may establish whether there is a history of bleeding, blood clots, rheumatoid arthritis, vascular disease, cancer, or problems with anesthesia such as malignant hyperthermia. Inflammatory arthropathies such as rheumatoid arthritis, seronegative spondyloarthropathies, systemic lupus erythematosus, crystalline arthropathies, and psoriatic arthropathy have been implicated in foot and ankle pain.
RED FLAGS THAT REQUIRE REFERRAL TO A MEDICAL PHYSICIAN
SUMMARY STATEMENT The foot and ankle region has the potential to be a complicated and frustrating region to assess and treat (Table II-13-4). The difficulty results from the fact that the foot and ankle have many articulation, ligament, and muscular attachments. The region has a complex biomechanical arrangement that relies on the proper functioning of multiple joints and structures. It is a weight-bearing region and must support large forces. It is also the most distal part of the body from the heart.Therefore, it is prone to poor circulation. All of these factors make the foot and ankle a challenge for the clinician to rehabilitate and equally challenging for the patient to heal. Table II-13-4 summarizes the factors that help a clinician differentiate among different sources of symptoms in the foot and ankle regions.
REFERENCES 1. Alfredson H, Lorentzon R. Chronic Achilles tendinosis: recommendations for treatment and prevention. Sports Med. 2000;29:135. 2. Alfredson H, Pietila T, Jonsson P, et al. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360.
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ORTHOPEDIC REASONING
For individuals who present with inversion ankle injuries the Ottawa Ankle Rules can be used to help in the decision-making process. Referral to a medical doctor for radiographs is indicated if the individual has pain in the malleolar zone and one or more of the following: (1) is unable to bear weight (walk four steps), (2) has tenderness at the posterior tip of the medial malleolus, and (3) has tenderness at the posterior tip of the lateral malleolus or tenderness in the malleolar zone.48 Radiographs are also indicated if the individual has pain in the mid-foot zone and one or more of the following: (1) is unable to bear weight (walk four steps), (2) has tenderness at the base of the fifth metatarsal, and (3) has navicular tenderness.48 Generally, the inability to bear weight, nocturnal pain, calf pain, and/or tenderness, swelling with pitting edema, increased skin temperature, superficial venous dilation, thrombosis, and an abnormally cold foot should raise the suspicion for potential systemic conditions. Diabetic patients should be under the care of a physician because of the potential for Charcot neuropathy and other diabetic-related problems. A patient should be referred to a medical physician when DVT, compartment syndrome, or stress fractures are suspected. Patients with swelling and inflammation in the joints of the foot, especially the big toe, who also have a history of kidney disease, should be referred to their physician to rule out gout as a potential source of their symptoms.Additionally, if conditions have not improved after 4 weeks of physical therapy the patient should be referred to a physician.
Section II
WHAT SYMPTOMS ALERT YOU TO PATHOLOGIES THAT MAY REQUIRE A REFERRAL TO A MEDICAL DOCTOR?
3. Alonso A, Khoury L, Adams R. Clinical tests for ankle syndesmosis injury: reliability and prediction of return to function. J Orthop Sports Phys Ther. 1998;27:276. 4. Anandacoomarasamy A, Barnsley L. Long term outcomes of inversion ankle injuries. Br J Sports Med. 2005;39:e14 [discussion e14]. 5. Baumhauer J, Nawoczenski D, DiGiovanni B, et al. Ankle pain and peroneal tendon pathology. Clin Sports Med. 2004;23:21. 6. Beynnon BD, Murphy DF,Alosa DM. Predictive factors for lateral ankle sprains: a literature review. J Athl Train. 2002;37:376. 7. Beynnon BD, Renstrom PA, Haugh L, et al. A prospective, randomized clinical investigation of the treatment of first-time ankle sprains. Am J Sports Med. 2006;34:1401. 8. Bjordal JM, Lopes-Martins RA, Iversen VV. A randomised, placebo controlled trial of low level laser therapy for activated Achilles tendinitis with microdialysis measurement of peritendinous prostaglandin E2 concentrations. Br J Sports Med. 2006;40:76. 9. Chantelau E, Richter A, Ghassem-Zadeh P. “Silent” bone stress injuries in the feet of diabetic patients with polyneuropathy: a report on 12 cases. Arch Orthop Trauma Surg. 2007;127:171. 10. De Garceau D, Dean D, Requejo SM, et al. The association between diagnosis of plantar fasciitis and Windlass test results. Foot Ankle Int. 2003;24:251. 11. Dunn J, Link C, Felson D, et al. Prevalence of foot and ankle conditions in multiethnic community sample of older adults. Am J Epidemiol. 2004;159:491. 12. Elveru RA, Rothstein JM, Lamb RL. Goniometric reliability in a clinical setting. Subtalar and ankle joint measurements. Phys Ther. 1988;68:672. 13. Ferran NA, Maffulli N. Epidemiology of sprains of the lateral ankle ligament complex. Foot Ankle Clin. 2006;11:659. 14. Frey C, Zamora J.The effects of obesity on orthopaedic foot and ankle pathology. Foot Ankle Int. 2007;28:996. 15. Frykberg RG, Armstrong DG, Giurini J, et al. Diabetic foot disorders: a clinical practice guideline. American College of Foot and Ankle Surgeons. J Foot Ankle Surg. 2000;39:S1. 16. Fujii T, Luo ZP, Kitaoka HB, et al.The manual stress test may not be sufficient to differentiate ankle ligament injuries. Clin Biomech (Bristol, Avon). 2000;15:619. 17. Garrick JG, Requa RK. The epidemiology of foot and ankle injuries in sports. Clin Sports Med. 1988;7:29. 18. Greenberg L, Davis H. Foot problems in the US. The 1990 National Health Interview Survey. J Am Podiatr Med Assoc. 1993;83:475. 19. Hedlund LMD, Griffiths H. Calcaneal Fractures in Diabetic Patients. J Diab Comp. 1998;12:81. 20. Hill CL, Gill TK, Menz HB, et al. Prevalence and correlates of foot pain in a population-based study: the North West Adelaide health study. J Foot Ankle Res. 2008;1:2. 21. Jaakkola JI, Mann RA. A review of rheumatoid arthritis affecting the foot and ankle. Foot Ankle Int. 2004;25:866. 22. Johansson C. Injuries in elite orienteers. Am J Sports Med. 1986;14:410. 23. Karlsson J, Lansinger O. Chronic lateral instability of the ankle in athletes. Sports Med. 1993;16:355. 24. Kay RM, Tang CW. Pediatric foot fractures: evaluation and treatment. J Am Acad Orthop Surg. 2001;9:308. 25. Kerkhoffs GM, Rowe BH,Assendelft WJ, et al. Immobilisation and functional treatment for acute lateral ankle ligament injuries in adults. Cochrane Database Syst Rev. 2002;CD003762. 26. Kvist M. Achilles tendon injuries in athletes. Ann Chir Gynaecol. 1991;80:188. 27. Lysholm J, Wiklander J. Injuries in runners. Am J Sports Med. 1987;15:168. 28. Martin R. Considerations for differential diagnosis of an ankle sprain in the adolescent. Orthopaedic Practice. 2004;16:21. 29. Martin RL, Irrgang JJ, Conti SF. Outcome study of subjects with insertional plantar fasciitis. Foot Ankle Int. 1998;19:803. 30. Martin RL, Stewart GW, Conti SF. Posttraumatic ankle arthritis: an update on conservative and surgical management. J Orthop Sports Phys Ther. 2007;37:253. 31. Mayeda D. Ankle and foot. 3rd ed. St. Louis: Mosby; 1992. 32. McCrory JL, Martin DF, Lowery RB, et al. Etiologic factors associated with Achilles tendinitis in runners. Med Sci Sports Exerc. 1999;31:1374. 33. McPoil TG, Martin RL, Cornwall MW, et al. Heel pain––plantar fasciitis: clinical practice guildelines linked to the international classification
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34. 35. 36. 37. 38. 39. 40. 41. 42.
43. 44. 45.
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of function, disability, and health from the orthopaedic section of the American Physical Therapy Association. J Orthop Sports Phys Ther. 2008;38:A1. Messier SP, Gutekunst DJ, Davis C, et al.Weight loss reduces knee-joint loads in overweight and obese older adults with knee osteoarthritis. Arthritis Rheum. 2005;52:2026. Micheli L. Overuse injuries in children’s sports. Orthop Clin North Am. 1983;14:339. Mueller MJ, Host JV, Norton BJ. Navicular drop as a composite measure of excessive pronation. J Am Podiatr Med Assoc. 1993;83:198. Ohberg L, Lorentzon R, Alfredson H. Eccentric training in patients with chronic Achilles tendinosis: normalised tendon structure and decreased thickness at follow up. Br J Sports Med. 2004;38:8. Paavola M, Kannus P, Paakkala T, et al. Long-term prognosis of patients with Achilles tendinopathy. An observational 8-year follow-up study. Am J Sports Med. 2000;28:634. Pierrynowski MR, Smith SB. Rear foot inversion/eversion during gait relative to the subtalar joint neutral position. Foot Ankle Int. 1996;17:406. Pierrynowski MR, Smith SB, Mlynarczyk JH. Proficiency of foot care specialists to place the rearfoot at subtalar neutral. J Am Podiatr Med Assoc. 1996;86:217. Riddle DL, Pulisic M, Pidcoe P, et al. Risk factors for plantar fasciitis: a matched case-control study. J Bone Joint Surg Am. 2003;85-A:872. Roos EM, Engstrom M, Lagerquist A, et al. Clinical improvement after 6 weeks of eccentric exercise in patients with mid-portion Achilles tendinopathy—a randomized trial with 1-year follow-up. Scand J Med Sci Sports. 2004;14:286. Saltzman CL, Salamon ML, Blanchard GM, et al. Epidemiology of ankle arthritis: report of a consecutive series of 639 patients from a tertiary orthopaedic center. Iowa Orthop J. 2005;25:44. Schon LC, Marks RM. The management of neuroarthropathic fracture-dislocations in the diabetic patient. Orthop Clin North Am. 1995;26:375. Shrader JA, Popovich JM, Gracey GC, et al. Navicular drop measurement in people with rheumatoid arthritis: interrater and intrarater reliability. Phys Ther. 2005;85:656.
46. Smith M, Brooker S, Vicenzino B, et al. Use of anti-pronation taping to assess suitability of orthotic prescription: case report. Aust J Physiother. 2004;50:111. 47. Stergioulas A, Stergioula M, Aarskog R, et al. Effects of low-level laser therapy and eccentric exercises in the treatment of recreational athletes with chronic achilles tendinopathy. Am J Sports Med. 2008;36:881. 48. Stiell IG, Greenberg GH, McKnight RD, et al. Ottawa Ankle Rules for radiography of acute injuries. N Z Med J. 1995;108:111. 49. Struijs P, Kerkhoffs G. Ankle Sprain, in BMJ. Clin Evid. 2008;1. 50. Taunton JE, Ryan MB, Clement DB, et al. A retrospective case-control analysis of 2002 running injuries. Br J Sports Med. 2002;36:95. 51. Van Gheluwe B, Kirby KA, Roosen P, et al. Reliability and accuracy of biomechanical measurements of the lower extremities. J Am Podiatr Med Assoc. 2002;92:317. 52. van Os AG, Bierma-Zeinstra SM, Verhagen AP, et al. Comparison of conventional treatment and supervised rehabilitation for treatment of acute lateral ankle sprains: a systematic review of the literature. J Orthop Sports Phys Ther. 2005;35:95. 53. van Rijn RM, van Os AG, Bernsen RM, et al. What is the clinical course of acute ankle sprains? A systematic literature review. Am J Med. 2008;121:324. 54. Vicenzino B. Foot orthotics in the treatment of lower limb conditions: a musculoskeletal physiotherapy perspective. Man Ther. 2004;9:185. 55. Vicenzino B, Griffiths SR, Griffiths LA, et al. Effect of antipronation tape and temporary orthotic on vertical navicular height before and after exercise. J Orthop Sports Phys Ther. 2000;30:333. 56. Wen DY. Risk factors for overuse injuries in runners. Curr Sports Med Rep. 2007;6:307. 57. Wolgin M, Cook C, Graham C, et al. Conservative treatment of plantar heel pain: long-term follow-up. Foot Ankle Int. 1994;15:97. 58. Young CC, Niedfeldt MW, Morris GA, et al. Clinical examination of the foot and ankle. Prim Care. 2005;32:105. 59. Yu G, Hudson J. Evaluation and Treatment of Stage 0 Charcot’s Neuroarthropathy. J Am Podiatr Med Assoc. 2002;94:210.
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CHAPTER 13
Calcaneal Stress Fracture
Foot BASIC INFORMATION DEFINITION Stress fractures are generally closed incomplete fractures through the cortex and into the trabecular bone matrix of the calcaneus. Stress fractures and stress reactions, both repetitive stress injuries (RSIs) of bone, are a reaction of bone to repetitive and abnormal forces.
SYNONYMS • • • •
Fatigue fracture Insufficiency fractures Chronic repetitive stress injury of bone Stress reaction
ICD-9CM CODES 825.0 Fracture of calcaneus closed 733.95 Stress fracture of other bone
OPTIMAL NUMBER OF VISITS
MAXIMAL NUMBER OF VISITS 12 • The initial injury involves the bone matrix, which may be the result of a biological or biochemical abnormality or failure at the cellular or bone multicellular unit (BMU) level. • An excessive amount of stress or repetitive stress occurs, causing microdamage; the bone had inadequate rest to allow for adaptation to the stress. The stress that creates these injuries is too much, too soon for the bone. • Over time with repeated stressors and overload to the bone, bone resorption takes place without significant bone production. The forces contributing to the injury include both direct impact to the bone and forces generated by the pull of ligaments and tendons on the bone. • Normal stress to abnormally weakened bone (e.g., osteoporosis) can lead to insufficiency fractures.
RISK FACTORS • Repetitive activity such as sports (e.g., distance running) or in military recruits • Increases in intensity, frequency, and loading of training or activity
General Prevalence • Generally, stress fractures constitute 10% of all athletic injuries. Tibia: ≈50%; tarsals: 25%; and metatarsals: 9% of all lower extremity stress fractures Bilateral in16% • Calcaneal stress fractures occur far less often ( males (relative risk = 3.5) White males > black males (relative risk = 4.7) White females > black females (relative risk = 8.5) • Females with low body mass index (BMI) and fractal analysis of calcaneal radiographic images are more prone to stress fracture. • Track and field athletes and runners sustain this fracture most often.
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MECHANISM OF INJURY • Repetitive weight-bearing activities without sufficient recovery time • Excessive muscle forces • Muscle fatigue • Biomechanical forces: Hyperpronators or supinators, hallux valgus, genu varum or genu valgum, leg length discrepancy, hip retroversion, or changes in footwear or training surface. • Most calcaneal fractures are the result of a traumatic event—most commonly, falling from a height. A smaller number of calcaneal fractures are stress fractures, caused by overuse or repetitive stress on the heel bone. Bone is noted to fail more readily in tension than in compression. An intact plantar aponeurosis is necessary to affect the calcaneus in fracture loads. • Repetitive downward force by the talus compressing vertically can affect beneath the outer two thirds of the posterior facet and create a superior portion stress fracture of the calcaneus. • The trabecular system of the calcaneus is designed to resist all forces relative to a standing position so that the anteroposterior and anterior oblique trabeculae resist tension, while the dorsal-plantar oriented trabeculae resist compressive loads. The subsequent location and orientation of the stress fracture may provide a clue to the source of the dysfunction. • Calcaneal stress reactions occurred in a group of military recruits; the majority (56%) of reactions were in the posterior third of the bone, and 79% occurred in the upper half of the calcaneus. The majority of stress injuries of the calcaneus occur in the posterior part of the bone, but a considerable proportion can generally be found in the middle and anterior part. • Insufficiency fractures are typically present in patients with RA or neurological disorders.
ORTHOPEDIC PATHOLOGY
ETIOLOGY
EPIDEMIOLOGY AND DEMOGRAPHICS
• Females who overtrain and develop the athlete’s triad have menstrual irregularities 50% of the time and thus have reduced bone density. • Males can lower testosterone after 2 days of hard training by up to 25%, which increases osteoclast development and bone resorption. Age Prevalence • Calcaneal stress fractures can occur in any age group, especially active and athletic individuals. • The prevalence is higher in adolescent girls and inactive elderly women, who show signs of osteopenia or osteoporosis. Children younger than 5 years who have gait abnormalities are also more susceptible.
Section III
Physical therapy for this condition depends on the intervention chosen by the physician. Generally, a boot is used for a period of time and a home exercise program can be initiated. Return to function may require 4 to 8 visits over a number of weeks.
• Hyperthyroidism, hyperparathyroidism, and use of fluoride treatment for osteoporosis • White women who smoke and are sedentary • Systemic diseases that weaken bone such as (RA), lupus, osteoarthrosis, pyrophosphate arthropathy, renal disease, osteoporosis, joint replacement, or nutritional deficiency • Low bone mineral density (BMD), especially after prolonged immobilization and not bearing weight. • Prior history of nontraumatic fracture • Low calcium and magnesium intake (20 miles per week. especially on hard surfaces • Overtraining without adequate rest periods • Delayed menarche • Poor nutrition • Amenorrhea
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Calcaneal Stress Fracture
CHAPTER 13 • FOOT
CONTRIBUTING FACTORS
AGGRAVATING ACTIVITIES
• Dramatic changes in training such as increased mileage, twice daily runs, speed work, a new pair of running shoes, poor shoe quality, or aging running shoes. • Menstrual irregularity, oligomenorrhea (six times greater chance of problem in track athletes), osteoporosis, menopause, diabetic or idiopathic neuropathy, smoking and alcohol intake, hypothyroidism, lower contraceptive use, anorexia nervosa, Paget’s disease, neurological disorders, and RA. • Menopause and age-related decreases occur in the H-mean parameter of fractal analysis of calcaneal trabecular bone. This may demonstrate a greater chance of incurring a stress fracture in postmenopausal women. • Heel pad atrophy increases stress to the calcaneus in loading.
• Gradual onset of pain related to activity, relieved with rest but may linger, pain may become constant if activities are not modified. • Walking in hard-soled shoes • Standing and walking on hard surfaces such as tile or concrete • Running or walking downhill • Jumping on hard surfaces • Progressing return to activity and intensity too quickly
COMMON SIGNS AND SYMPTOMS • A good patient history that exposes a relatively sudden or subacute onset of injury, a changing pattern of exercise, and particularly one that notes the onset and character of the pain is very important when differentiating between plantar fasciitis and calcaneal stress fractures. • Often, calcaneal stress fractures are misdiagnosed and continue unrecognized because of improvement through treatments that are aimed at plantar fasciitis. • Tenderness and diffuse pain over the medial and lateral calcaneus • Rule out systemic problems, such as RA, by determining if the patient has morning pain, swelling, forefoot problems, stiffness longer than 2 hours, involvement of the hands, skin lesions, hair loss, fatigue, back or hip pain, recent sexually transmitted diseases, penile discharge, or vision changes • Diffuse heel pain • Deep ache after rapid training change • Pain progression: Pain after activity followed by pain with activity and finally pain at rest • Pain with walking • Night pain rarely occurs (consider another diagnosis) • Fracture site: Intense localized pain • Tenderness to palpation over the medial and lateral aspects of the calcaneus • Tenderness on lateral compression of the body, rather than at the medial calcaneal tuberosity or tenderness that is only plantar to the calcaneus • Positive percussion of bone distant from symptomatic site • Vibrating tuning fork (128 Hz) at suspected site • Local swelling over site
EASING ACTIVITIES • • • • •
Rest Immobilization Ice Certain modalities Rocker heel shoe use
24-HOUR SYMPTOM PATTERN • Depending on the severity of the stress reaction, more chronically there is pain at rest after activity that eases in the morning. • Night pain can occur if the fracture is more severe and chronic.
PAST HISTORY FOR THE REGION • • • •
Osteopenia Osteoporosis Prolonged heel pain Specific high-intensity vertical-loading activities.
PHYSICAL EXAMINATION • Tenderness to palpation, lateral compression of the body, rather than at the medial calcaneal tuberosity, or tenderness that is only plantar to the calcaneus • Percussion of bone distant from symptomatic site elicits pain at the suspected site. • Weaker dorsiflexors in muscle testing • Calcaneal compression test may be positive. • Vibrating tuning fork (128 Hz) at suspected site • Lower limb tension tests • Palpation over painful site • Reduced talocrural joint dorsiflexion range of motion (ROM) • Positive side-to-side glide of calcaneus (pain) • Foot postural malalignment with forefoot pronation (in one third of patients with Sever’s disease) • Gait may be changing: Involved foot position with excessive varum or valgum during weight acceptance or omit direct heel contact altogether in stance.
IMPORTANT OBJECTIVE TESTS • Cup heel and move side to side to elicit pain.
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• Hop test (not validated for this condition) • Percussion over the site of pain versus remotely • Therapeutic ultrasound is unreliable over the actual site of fracture. • Assess the lower extremities for muscle imbalances, including weakness, length, static strength, dynamic strength, function, and other painful areas. • Radiographic findings are rarely abnormal in the early phases of the disorder and only 50% display significant changes in follow-up. There is no actual fracture line in most grades of this injury, especially early after onset. The lack of evidence is most pronounced when radiographs are obtained soon after the onset of symptoms, before the appearance of a fracture line or new bone formation, and when the patient has osteopenia. Detecting stress fracture radiographically offers a 26% sensitivity and 10% specificity. • To obtain a diagnosis, magnetic resonance imaging (MRI) is warranted if plain radiography does not show abnormalities in a physically active patient with exercise-induced pain in the ankle or heel. • MRI demonstrates characteristic findings that include the following: Bandlike areas of very low signal intensity in the medullary space, which usually extend to the cortex Surrounding alteration in signal intensity in the marrow space Low signal intensity on T1-weighted images High signal intensity in fat-suppressed T2-weighted images and increased short TI inversion recovery (STIR), which represents medullary edema and hemorrhage As the injury progresses to a stage of increasing severity, a low signal fracture line and bone callus may be visible. This process of calcification typically takes about 4 to 6 weeks to see on plain x-ray; therefore, periodic follow-up x-rays may aid in diagnosing a stress fracture of the heel. • Tests, such as bone scans, computed tomography (CT), or MRI, usually demonstrate the fracture. A three-phase technetium bone scan can help differentiate the location and degree of inflammation in the calcaneus (specificity: 100%; sensitivity: 76%). Bone scintigraphy is considered sensitive, and MRI is considered to be both sensitive and specific. • CT scans are less sensitive.
Calcaneal Stress Fracture
CHAPTER 13 • FOOT
TREATMENT
Radiological Grading System for Stress Fractures Grade
Radiograph
Bone Scan
MRI
Treatment
SURGICAL OPTIONS
1
Normal Normal
Positive STIR image Positive STIR and T2-weighted images
Rest for 3 weeks
2
3
Discrete line (±), periosteal reaction (±)
Mild uptake confined to one cortex Moderate activity; larger lesion confined to unicortical area Increased activity (>50% width of bone)
Rest for 12-16 weeks
4
Fracture or periosteal reaction
No definite cortical break; positive T1- and T2-weighted images Fracture line; positive T1- and T2-weighted images
• Surgical indicators High-risk fractures for nonunion Nonhealing fractures that last longer than 4 to 6 months • Surgical options Surgery is rarely required for a calcaneal stress fracture. Placement of a calcaneal intermedullary screw or nail has been used successfully in severe cases. Focal drilling or bone grafting has been used successfully. • Surgical outcomes Recurrence and concomitant problems often arise over time. Calcaneal stress fracture has been reported after surgery for Achilles tendinosis.
More intense bicortical uptake
657
Rest for 3-6 weeks
Rest for 16+ weeks
Adapted with permission from Arendt EA, Griffiths HJ:The use of MR imaging in the assessment and clinical management of stress reactions of bone in high-performance athletes, Clin Sports Med 16:291-306, 1997. MRI, Magnetic resonance imaging; STIR, short TI inversion recovery.
REHABILITATION
DIFFERENTIAL DIAGNOSIS
RELATED DIAGNOSES
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ORTHOPEDIC PATHOLOGY
• A stress fracture of the calcaneus is a condition that is often overlooked in the differential diagnosis of heel pain. Plantar fasciitis (also called heel spur syndrome) is so common that most health care providers default to plantar fasciitis as a primary diagnosis when evaluating heel pain. • Radicular pain from lumbosacral origin (EMG, MRI, clinical) • Lumbar stenosis (MRI) • Tarsal tunnel syndrome and compartment syndromes (EMG, sensation, Tinel’s sign, weakness, palpation, pressure measures) • Achilles or retro calcaneal bursitis (resisted manual muscle testing [MMT], palpation, MRI) • Local tendinopathy or ligament sprain (resisted MMT, palpation, MRI) • Haglund’s deformity (radiograph, MRI) • Osteoid osteoma (pain at night relieved with analgesics, CT scan) • Osteomyelitis (radiograph, laboratory tests) • Osteosarcoma (radiograph) • Ewing tumor (radiograph) • Bone metastases (radiograph) • Osteochondral fracture (bone scintigraphy, radiograph) • Accessory navicular (painful) • Inflammatory disorders (psoriatic arthritis) • Medial tibial stress syndrome (radiograph)
• Initial exercises and procedures: Experimental and anecdotal Electromagnetic field devices (expensive, lacks evidence). Electrical stimulation may be used for patients who have delayed healing. • Initial management Rest for 4 to 7 weeks (may require up to 3 months) or until local tenderness subsides, which must be monitored weekly. Non–weight-bearing to slowly progressive weight-bearing with assistive devices until assessed pain-free walking. The degree of pain should guide the progression. Severe pain involves non–weight-bearing or partial weightbearing with assistive devices until the pain subsides (usually 7 to 10 days). Immobilization: A cam walker, pneumatic walker, or low pneumatic walker for 4 to 6 weeks may alleviate pain faster and be clinically superior to a postoperative shoe for stress reactions of the metatarsal area and for other foot stress reactions. An added benefit of the pneumatic walker is that it can be removed for hygiene purposes and to allow limited exercise of the limb. This walker makes showers easier and allows the patient to do ROM exercises of the leg. • Short leg casting indications include noncompliance and high risk for nonunion such as the following: Navicular stress fracture Metatarsal stress fracture Reduce compression in weight bearing • Prevention and education for the patients and coaches as follows: Do not increase exercise intensity >10% per week. Stretch and warm-up before exercise.
Section III
• A number of conditions may confound diagnosis and appear similar to stress fracture on certain imaging studies. In other cases, asymptomatic bone marrow edema may be visible on MRI. • Primary benign bone neoplasm • Rheumatological diseases (RA, seronegative spondyloarthropathies) • Osteoid osteoma • Osteoblastoma • Eosinophilic granuloma • Infections: Chronic or subacute osteomyelitis • Crohn’s disease or ulcerative colitis, sarcoidosis, Behçet’s syndrome (1% to 5% incidence). • Chronic musculoskeletal soft tissue injury Tendinopathy Muscle strain Chronic compartment syndrome • Metastatic neoplasm Prostate cancer Breast cancer Myeloma • Primary malignant bone neoplasms Osteosarcoma • Nerve compression syndromes Tarsal tunnel syndrome (Tinel’s sign, electromyogram [EMG], weakness) Carpal tunnel syndrome Ulnar tunnel syndrome Herniated intervertebral disc • Osteoarthritis • Ankylosing spondylitis (in 15- to 35–yearolds with heel pain) • Gout
• Hypertrophic pulmonary osteoarthropathy • Reiter’s syndrome (laboratory tests, pedal involvement, periostitis at posterior calcaneus, keratoderma blennorrhagicum)
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Choose level running surfaces. Shoes should be lightweight and in good condition. Consider orthoses to correct biomechanical factors. Avoid barefoot walking. Shock-absorbing insoles may be beneficial. A slow and easy approach to increasing exercise is helpful. Dietary calcium should reach recommended levels. Supplements may assist in this. Calcium has been found at lower levels in athletes who incur a stress reaction. Make certain to also meet daily requirements of vitamin D, which aids in both absorption of calcium and in the development of bone.
TREATMENT • Conservative treatment works well for most stress fractures and stress reactions of bone. • Assess and retrain adjacent and distal muscles. • Restore joint ROM and muscle and connective tissue flexibility and extensibility. Notably restoring ankle dorsiflexion is vital from a non–weight-bearing to weight-bearing progression as tolerated. • Progressive pain-free weight bearing • Active rest (cross-training) goals Cardiovascular conditioning Flexibility Proprioception Strength • Asymptomatic weight-bearing progression activities Maintenance of upper body strength Swimming Pool running with float vest Biking Elliptical trainer Progressive walking Stair climbing machines (later stages) to use the gastrocnemius/soleus group concentrically Running at 17 to 26 weeks after injury • Return to function Eliminate the pain of weight bearing where forces should be sufficiently low for healing and remodeling to take place. Use a training log. Progressive pain-free strengthening and cardiovascular-based exercise Sport-specific training Previous radiographic changes are absent.
PROGNOSIS • Long-term prognosis: Most lower extremity stress reactions take between 8 and 26 weeks for full recovery, although
CHAPTER 13 • FOOT
symptoms generally resolve in 6 to 8 weeks with proper rest and rehabilitation. The calcaneus has a rich blood supply, so it generally heals more readily than the adjacent tarsal bones. • Slow progression of forces act on the stress fracture. Superior and posterior locations of a stress fracture would limit the action of the ankle plantar flexors. • Regression of stress fractures: Stage I: Crack initiation: Areas of stress concentration Stage II: Crack propagation: No repair or more damage than repair Stage III: Final fracture: Cracks coalesce, enlarge, ultimate failure • Symptoms and disability may continue for months along with adaptive movement patterns in compensation if progressed too rapidly. • Lower than normal BMD has been seen 1 to 2 years after lower extremity surgery
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Subjective history consistent with mechanism of injury • >3 weeks with acute localized pain • Lack of progression • Other possible diagnoses, especially systemic red flags • The necessity for imaging or other diagnostic tests
SUGGESTED READINGS Akkus O, Rimnac CM. Cortical bone tissue resists fatigue fracture by deceleration and arrest of microcrack growth. J Biomech. 2001;34:757–764. Aldridge T. Diagnosing heel pain in adults. Am Fam Physician. 2004;70(2):332–338. Bennell KL, Malcolm SA,Thomas SA, Ebeling PR, McCrory PR, Wark JD, Brukner PD. Risk factors for stress fractures in female track-andfield athletes: a retrospective analysis. Clin J Sport Med. 1995;5(4):229–235. Bradley WB, Slomiany WP. Shin pain treatments get active patiens back on track. Biomechanics. 2008;31–38. Breithaupt J. Zur pathologie des menschlichen fussess. Medizin Zeitung. 1855;24:169–177. Fredericson M, Bergman AG, et al. Tibial stress reaction in runners. Correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med. 1995;23(4):472–481. Geffen A, Seliktar R. Comparison of trabecular architecture and the isostatic stress flow in the human calcaneus. Med Eng Phys. 2004;26(2):119–129. Hastings MK, et al. Bone mineral density of the tarsals and metatarsals with reloading: case report. Phys Ther. 2008;88(6):766–779. Jansen M. March foot. J Bone Joint Surg. 1926;8:262–272. Jones BH, Thacker SB, Gilchrist J, Kimsey CD Jr, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers:
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a systematic review. Epidemiol Rev. 2002; 24(2):228–247. Kaczander BI, Shapiro J. Consider systemic causes of heel pain. Biomechanics. 2005:59–61. Lebrun M. The female athlete triad: What’s a doctor to do? Curr Sports Med Rep. 2007;6:397–404. Leroux JL, et al. Fractures of the calcaneus during fluoride treatment for osteoporosis. Sem Hop. 1983;8,59(45):3140–3142. Lespessailles E, Poupon S, Niamane R, LoiseauPeres S, Derommelaere G, Harba R, Courteix D, Benhamou CL. Fractal analysis of trabecular bone texture on calcaneal radiographs. Osteoporosis Int. 2002;13(5):366–372. Matheson GO, Clement DB, McKenzie DC, Taunton JE, Lloyd-Smith DR, MacIntyre JG. Stress fractures in athletes. A study of 320 cases. Am J Sports Med. 1987;15(1):46–58. Meyer J, Kulig K, Landel R. Differential diagnosis and treatment of subcalcaneal heel pain: a case report. JOSPT. 2002;32(3):114–125. Niva MH, Sormaala MJ, Kiuru MJ, Haataja R, Ahovuo JA, Pihlajamaki HK. Bone stress injuries of the ankle and foot: an 86-month magnetic resonance imaging-based study of physically active young adults. Am J Sports Med. 2007;35(4):643–649. Prouteau S, Ducher G, Nanyan P, Lemineur G, Benhamou L, Courteix D. Fractal analysis of bone texture:a screening tool for stress fracture risk? Eur J Clin Invest. 2004;34(2):137–142. Sormaala MJ, Niva MH, Kiuru MJ, Mattila VM, Pihlajamäki HK. Stress injuries of the calcaneus detected with magnetic resonance imaging in military recruits. J Bone Joint Surg Am. 2006;88:2237–2242. Stafford SA, Rosenthal DI, Gebhardt MC, Brady TJ, Scott JA. MRI in stress fracture. AJR Am J Roentgenol. 1986;147:553–556. Stechow. Fussödem und Röntgenstrahlen. Deutsche Militärärztliche Zeitschrift. 1897;26:465. Swenson EJ Jr, DeHaven KE, Sebastianelli WJ, Hanks G, Kalenak A, Lynch JM.The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med. 1997;25(June):322–328. Verma RB, Sherman O. Athletic Stress fractures: Part1–3. Am J Orthop. 2001;30(11):798–806. Weber JM, Vidt LG, Gehl RS, Montgomery T. Calcaneal stress fractures. Clin Podiatr Med Surg. 2005;22(1):45–54. Zager E, et al. Conservative approach benefits Calcaneal fracture treatment. Biomechanics. 2005;35–47. AUTHOR: STEPHEN PAULSETH
Cuboid Syndrome
CHAPTER 13 • FOOT
BASIC INFORMATION DEFINITION A disruption or subluxation of the cuboid affects the structural congruity of the calcaneocuboid portion of the midtarsal joint.
SYNONYMS • • • • •
Subluxed cuboid Locked cuboid Dropped cuboid Cuboid fault syndrome Peroneal cuboid syndrome
ICD-9CM CODES 726.70 Enthesopathy of ankle and tarsus unspecified
OPTIMAL NUMBER OF VISITS 6 or fewer
MAXIMAL NUMBER OF VISITS 16
ETIOLOGY
EPIDEMIOLOGY AND DEMOGRAPHICS
MECHANISM OF INJURY • Plantar flexion and inversion (low ankle) sprain • Repetitive use on an unstable foot. If the patient lacks foot stability, the fibularis longus muscle is required to work harder to stabilize the foot. If joint laxity is present, the cuboid is pulled out of alignment by the continuous force of the fibularis longus. • Ballet, due to the stress of jumping and landing with poor foot support
COMMON SIGNS AND SYMPTOMS • Symptoms can begin rapidly as a result of injury or more gradually as a result of overuse. • Tenderness is present locally at the plantar surface of the cuboid bone. • Pain is also commonly experienced in the medial arch or along the fourth metatarsal bone. • Pain is most often present with weightbearing activities such as walking and standing. • Symptoms are most commonly experienced at the terminal stance phase of gait.
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AGGRAVATING ACTIVITIES • • • • • •
Walking Walking barefoot Standing Jumping Coming up onto toes Ballet dancing
EASING ACTIVITIES • Non–weight-bearing activities • Rest • Cold pack or compress
24-HOUR SYMPTOM PATTERN • Symptoms may be better during the morning, especially after sleeping with the foot elevated. • Symptoms may worsen during the day with increased weight-bearing activities.
PAST HISTORY FOR THE REGION • Previous history of ankle injury • History of trauma to the foot • History of repetitive use coupled with poor foot stability
PHYSICAL EXAMINATION • Pain at the terminal stance phase of gait. Decreased stride length noted as a compensatory mechanism. • Weakness when testing the patient’s ability to rise up onto the toes • MMT of the fibularis longus muscle is weaker than the contralateral side because of the altered cuboid position. • Inversion ROM testing may be limited or painful. • Point tenderness at the plantar surface of the cuboid • If the cuboid is severely displaced, there may be a sulcus present over the dorsal aspect of the cuboid. • Altered midfoot mobility is noted (abnormal pronation or supination when compared with the contralateral side). • Neural dynamic testing should be normal. Abnormal findings may indicate that the pain is not from the cuboid but from lateral plantar nerve. • Poor ankle proprioception is often present.
IMPORTANT OBJECTIVE TESTS • MRI, x-ray, and ultrasound have not been found to be beneficial in diagnosing cuboid syndrome. The alterations in structural alignment are too small to be picked up on imaging studies. Imaging may be appropriate to rule out other potential pathology and in identifying joint destruction or inflammatory processes. • No one specific clinical test has been shown to definitively identify the
ORTHOPEDIC PATHOLOGY
• It has been hypothesized that 4% of athletic foot injuries involve the cuboid. • 6.7% of patients with low ankle sprains have a displaced cuboid. • In ballet dancers, 17% of foot injuries involve the cuboid. In male dancers, the mechanism appears to related to trauma, whereas in female dancers it appears to involve repetitive use.
• Patients also experience weakness when rising up onto their toes or with jumping.
Section III
• The cuboid and the calcaneus articulate to form the calcaneocuboid joint. Structural integrity of this joint is important for the maintenance of lateral foot stability. The cuboid plays a unique role in that it is the only bone that articulates with the midtarsal and tarsometatarsal joints. It also is the only bone to link the lateral column to the transverse plantar arch. Proper alignment and mechanics of this bone are critical for the stability and mobility of the foot. • A subluxation or misalignment of the cuboid can potentially irritate the surrounding joint capsule, ligaments, and fibularis longus tendon. • The dorsal and plantar calcaneocuboid, dorsal and plantar cuboideonavicular, dorsal and plantar cuboideometatarsal, and the long plantar ligament all act to passively stabilize the cuboid in the lateral column of the foot.These ligaments are more taut dorsal medially than plantar laterally. Therefore the calcaneocuboid joint rotates around a medially positioned axis. • The function and the stability of the cuboid is affected by the fibularis longus muscle. The muscle’s tendon travels anteromedially through the cuboid’s peroneal groove and inserts on the lateral base of first metatarsal and first cuneiform. The fibularis longus muscle’s strength and function depends on proper position and stability of the cuboid as it uses the bone as a lever to generate force and stabilize the foot. • Fibularis longus is most active during the stance phase of gait. It contracts midway
through the midstance phase and continues to contract through the terminal stance phase. As the foot supinates during the terminal phase of gait, the fibularis longus muscle acts as a dynamic stabilizer of the forefoot as it assists in plantar flexion of the first ray while using the cuboid as a pulley, increasing the mechanical advantage of the muscle. • Cuboid syndrome involves the subluxation or displacement of the cuboid bone. The subluxation is often caused by plantar flexion inversion ankle sprains.As the foot and ankle are placed into plantar flexion and inversion, the fibularis longus tendon places a dorsal and lateral force on the forefoot, creating a close packed position and forcing the cuboid in an inferomedial direction and tearing the interosseous ligaments. The force on the cuboid is further increased by the stretch reflex. When the foot is rapidly plantar flexed and inverted, the fibularis longus muscle is quickly stretched and responds with a more forceful contraction.
659
660
Cuboid Syndrome presence of cuboid syndrome, but the following three findings are often positive: Decreased fibularis longus strength Decreased ability to come up onto the toes Pain on the plantar aspect of the cuboid
DIFFERENTIAL DIAGNOSIS • • • • • • • • • • • • • •
Jones fracture Tumor Fracture of the anterior calcaneal process Tarsal coalition Peroneal and extensor digitorum brevis tendinitis Subluxing peroneal tendons Arthritis Gout Sinus tarsi syndrome Lateral plantar nerve entrapment Lisfranc injuries Stress fractures of the cuboid Lyme disease Metatarsal stress fractures
CONTRIBUTING FACTORS • • • • • • • • •
Overpronation Poorly constructed orthoses Running on uneven surfaces Poor shoe construction Inversion ankle injuries Chronic ankle sprain Balance disorder History of ankle instability Participation in high-level athletic sports or dance
TREATMENT MEDICAL • Surgery is not typically performed on patients with cuboid syndrome. • Medically, the physician may prescribe antiinflammatory medications to reduce the irritation and swelling in the region. • In severe cases, a walking boot or cast may be used to reduce the loading on the foot.
REHABILITATION • Cuboid syndrome responds favorably and quickly to manipulative therapy.
CHAPTER 13 • FOOT
The effectiveness of treatment has been attributed to the fact that most patients with cuboid syndrome have pain and dysfunction caused by a malalignment of the cuboid bone. When the cuboid is returned to its normal position, symptoms resolve and function improves. • Two common techniques used in the clinic and described in research are the cuboid whip and the cuboid squeeze techniques. Cuboid whip: Jennings and Davies found that 7 of 104 patients with lateral ankle sprains had subluxed cuboids. A cuboid whip manipulation was performed on all seven subjects.Symptoms were assessed immediately after the manipulation. All of the patients reported substantial reductions in pain and symptoms. Two of the seven required one additional manipulation, and the authors attributed the need to be a result of the longer duration that the symptoms had been present. A 2- to 8-month follow-up with the patients revealed no return of symptoms in any of the 7, and all had returned to prior levels of function. Cuboid squeeze: Marshall and Hamilton described a cuboid squeeze technique performed on three subjects, all of whom had complete resolution of symptoms after one or two treatments. In a 5-year follow up, none of the three subjects had a return of symptoms. • Low dye taping with or without cuboid pads is commonly used in clinic to support and stabilize the subluxed cuboid. Clinicians also use the taping to support a cuboid immediately after a manipulative technique. • Once the patient’s cuboid has been reduced, it is wise to have the patient refrain from sports for several days after the manipulation to ensure that the cuboid remains in its normal position. If the patient remains symptom-free, they can begin to return to sport. • The patient can return to sport, but care must be taken to slowly progress the loading through the cuboid. Full return to sport can occur when all biomechanical contributing factors have been addressed, balance and proprioception are normal, and strength is at least 90% that of the contralateral side.
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PROGNOSIS • The prognosis for patients with cuboid syndrome is generally good. • If the factors resulting in abnormal forces being placed on the cuboid can be eliminated, then the patient should heal. • Symptoms usually abate rapidly once the cuboid is aligned correctly.The challenge for the clinician is preventing future subluxations.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Red flag signs in the foot are usually few. If the patient is not improving over the course of a month, the patient should be referred to a physician. • If there is suspicion of tumors (unremitting or nonmechanical pain), referral to a physician is warranted. • Suspicions of gout should also be referred back to the referring physician for medical workup. Unresolving inflammation may be an indication of gout or other systemic inflammatory disorders.
SUGGESTED READINGS Caselli MA, Pantelaras N. How to treat cuboid syndrome in the athlete. Podiatry Today. 2004;117(10):76–80. Jennings J, Davies GJ. Treatment of cuboid syndrome secondary to lateral ankle sprains: a case series. J Orthop Sports Phys Ther. 2005;335(7):409–415. Leerar PJ. Differential diagnosis of tarsal coalition versus cuboid syndrome in and adolescent athlete. J Orthop Sports Phys Ther. 2001;331(12):702–707. Marshall P, Hamilton WG. Cuboid subluxation in ballet dancers. Am J Sports Med. 1992;220(2):169–175. Mooney M, Maffey-Ward L. Cuboid plantar and dorsal subluxations: assessment and treatment. J Orthop Sports Phys Ther. 1994;220(4):220–226. Newell SG, Woodle A. Cuboid syndrome. Physician Sports Med. 1981;9:71–76. Patterson S. Cuboid syndrome: a review of literature. J Orthop Sports Phys Ther. 2006;5:597–606. Subotnick SI. Peroneal cuboid syndrome. J Am Podiatr Med Assoc. 1989;779(8):413–414. AUTHOR: DERRICK SUEKI
Fat Pad Contusion
CHAPTER 13 • FOOT
BASIC INFORMATION
COMMON SIGNS AND SYMPTOMS
DEFINITION
• Pain is worse with weight bearing. • Swelling and tenderness on the plantar surface of the heel. Usually, the pain is more posterior on the heel as opposed to heel spurs or plantar fasciitis, which is more anterior • Pain increases with walking.
Fat pad contusion is a condition in which force or trauma is applied to the fat pad of the heel; this force results in damage to the fat pad and the subsequent inflammatory response results in irritation of the fat pad. Contusion occurs when the force is great enough to bruise the underlying bone as well.
SYNONYMS • • • •
Bruised heel Fat pad irritation Policeman’s heel Fat pad syndrome
ICD-9CM CODES 924.2 Contusion of ankle and foot, excluding toe(s)
AGGRAVATING ACTIVITIES • • • • •
Walking Walking in hard-soled shoes Walking barefoot Standing Landing during jumping
EASING ACTIVITIES • • • •
Non–weight-bearing activities Rest Cold pack or compress Wearing cushioned insoles in the shoes
24-HOUR SYMPTOM PATTERN OPTIMAL NUMBER OF VISITS
the tibial nerve in the tarsal tunnel may manifest as heel pain. • Muscle weakness (e.g., in the posterior tibialis muscle) may affect the biomechanics of the foot and result in abnormal loading on the calcaneus.
IMPORTANT OBJECTIVE TESTS • Radiographic imaging A painful heel fat pad can be confused with nerve irritation or plantar fasciitis. MRI can also help distinguish between these conditions. Heel fat pad pathology can demonstrate changes in signal intensity; low-signal-intensity bands represent fibrosis and decreased height of the fat pad. Fat pad inflammation demonstrates edematous changes in the fat pad, with ill-defined areas of decreased signal intensity on T1-weighted images that increase in signal intensity on T2-weighted images. MRI is also useful in identifying spaceoccupying lesions within the fat pad from peripheral nerve sheath tumors or rheumatoid nodules.
PAST HISTORY FOR THE REGION
• Anatomically, the fat pad is a protective layer on the plantar surface of the calcaneus. Normally, it is about 1 inch thick and composed of fibrous tissue septa, which separates the closely packed fat cells. This structure allows the heel fat pad to act as a shock absorber. • Contusion or bruising of the heel can occur when the septa holding the fat pad together are damaged. This allows the fat pad to move laterally along the surface of the calcaneus when force is placed on the heel.The slippage of the fat pad leaves the calcaneus with less cushion and as a result, more force is delivered to the heel itself. Ultimately, the increased force on the calcaneus bone results in damage and irritation of the bone.
• Previous history of chronic ankle sprain • History of ankle instability may place abnormal forces onto the calcaneus. • History of falls onto the foot • History of repetitive use coupled with poor or no footwear
• • • • • • •
PHYSICAL EXAMINATION
CONTRIBUTING FACTORS
• Local tenderness at the posterior aspect of the calcaneus • Pain during heel strike or initial contact phase of gait • Increased foot pronation or increased calcaneal eversion may be present, which would place more pressure onto the medial aspect of the calcaneus during gait. This could result in breakdown of the fat pad in the posteromedial aspect of the heel and damage to the underlying bone. • Increased foot supination or increased calcaneal inversion results in a decreased ability of the foot to absorb shock and therefore greater force placed on the posterolateral aspect of the calcaneus. • ROM testing may reveal decreased dorsiflexion of the ankle, which could contribute to the heel pain. • Neural dynamic testing should be normal. Abnormal findings may indicate that the pain is not from the fat pad but from nerve entrapment. Entrapment of
• • • • • • • •
EPIDEMIOLOGY AND DEMOGRAPHICS The prevalence of fat pad contusion is unknown. Calcaneal fractures account for approximately 2% of all body fractures.
MECHANISM OF INJURY • Repetitive use such as walking or running • Poor footwear such as marching in hard boots • Falls on the heel • Walking barefoot on hard surfaces
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Plantar fasciitis Tibial nerve entrapment Retrocalcaneal bursitis Heel bone spurs Tarsal tunnel syndrome Talus fracture Calcaneus fracture Osteoporosis or osteopenia Balance disorder Chronic ankle sprain History of ankle instability Participation in high-level athletic sports Footwear Overpronation or over supination Repetitive walking on hard surfaces
TREATMENT MEDICAL • Surgery is generally not warranted in patients with fat pad contusions. The physician may prescribe antiinflammatory medications to reduce the irritation and swelling in the region. • In severe cases, a walking boot or cast may be used to reduce the loading on the heel. • If conservative care fails, the physician may inject corticosteroids into the fat pad to reduce the inflammation and pain.
ORTHOPEDIC PATHOLOGY
ETIOLOGY
DIFFERENTIAL DIAGNOSIS
MAXIMAL NUMBER OF VISITS
Section III
16
• Symptoms may be better during the morning, especially after sleeping with the foot elevated. • Symptoms may worsen during the day with increased weight-bearing activities.
6 or fewer
661
662
Fat Pad Contusion REHABILITATION • The bone under the fat pad has the potential to heal, but the load on the bone must be reduced and then gradually reintroduced so that inflammation can be eliminated and then proper bone healing can occur. • Rehabilitation involves decreasing the inflammatory response and addressing the factors that contribute to increased loading on the heel. • To reduce inflammation, the clinician can use cryotherapy, ultrasound, or electrical stimulation. Ice massage is an effective way to deliver localized treatment to the calcaneus. • Reducing the loading on the calcaneus is also an important aspect of rehabilitation. Cushioned heel pads can cushion the shoe during gait. Advising the patient to wear low heels may also reduce some of the load on the heel during gait. • Improving the mechanics of the foot can also place the heel in a better position during gait. Orthotics may help improve foot position during gait, although it is questionable whether the
CHAPTER 13 • FOOT
orthotics benefit the patient during the heel-strike portion of gait. • Improving the mobility of the subtalar joint and the calf can improve ankle dorsiflexion. This is often needed to help improve the biomechanics of the foot, but it is questionable what effect the increased dorsiflexion will have on foot mechanics during initial contact of gait. • Taping of the heel, clinically, has proved effective at stabilizing the fat pad and not allowing it to slip or migrate. Patients often experience significant pain abatement with heel taping.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • The red flag signs in the heel are usually few. If the patient is not improving over the course of a month, they should be referred back to their physician • If there is suspicion of tumors (unremitting or nonmechanical pain), a referral to the physician is warranted. • Infections from cuts or insect bites can also result in swelling and inflammation of the heel. If this is suspected, a referral to the physician should be made.
SUGGESTED READINGS
PROGNOSIS • The prognosis for patients with fat pad contusions or irritation is generally good. • If the factors resulting in abnormal calcaneal forces can be eliminated, then the patient should heal. • Normal healing generally takes 6 to 8 weeks. Reducing the loading in a commonly used area in the body, such as the foot, is difficult. Healing may take a little longer as a result.
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DiMarcangelo MT,Yu TC. Diagnostic imaging of heel pain and plantar fasciitis. Clin Podiatr Med Surg. 1997;14:281–301. Karr SD. Subcalcaneal heel pain. Orthop Clin North Am. 1994;25:161–173. Narvaez JA, Narvaez J, Ortega R, Aguilera C, Sanchez A, Andia E. Painful heel: MR imaging findings. Radiographics. 2000;20:333–352. AUTHOR: DERRICK SUEKI
Flexor Hallucis Longus Tendinopathy
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BASIC INFORMATION DEFINITION Injury to the tendon of the flexor hallucis longus (FHL) muscle can include an acute inflammatory response, in which case the tendon injury is labeled tenosynovitis. If the tendon injury is more chronic, the injury is considered a tenosynovitis. Complete disruption of the tendon is considered a tendon rupture.
SYNONYMS • • • • •
Dancer’s tendinitis FHL tendinitis FHL tendinosis FHL rupture FHL tenosynovitis
ICD-9CM CODES 727.06 Tenosynovitis of foot and ankle
OPTIMAL NUMBER OF VISITS 6 or fewer 16 or more
ETIOLOGY
EPIDEMIOLOGY AND DEMOGRAPHICS The prevalence of FHL tendon pathology is not documented in the literature. FHL injuries as a whole are more prominent in ballet dancers and in sports requiring repetitive plantar flexion of the foot.
MECHANISM OF INJURY • FHL injuries generally result from repetitive plantar flexion combined with vertical loading. Common mechanisms include ballet, because dancers are required to repetitively come up onto their toes. It can also occur in runners who run long distances downhill. Running downhill requires more plantar flexion than running uphill. • Synovitis and tenosynovitis may also occur as a result of inflammatory diseases such as RA. Synovitis and interosseous muscle atrophy of the interosseous muscles commonly seen in RA can result in misalignments of the foot and ankle joints. • Other mechanisms of injury include the following: Repetitive use during walking or standing Poor footwear such as wearing shoes that are too tight Walking in high heels Repetitive jumping sports
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• Insidious onset of posteromedial ankle pain. • Localized swelling in the region of entrapment that is generally at the tarsal tunnel • If scar tissue or fibrosis has occurred, clicking or catching may be noted at the site of entrapment. • Pain is noted with repetitive plantar flexion of the foot and ankle.
AGGRAVATING ACTIVITIES • • • • •
Walking or running down hill Rising up onto toes Walking in high heels Standing Jumping
EASING ACTIVITIES • Non–weight-bearing activities • Rest • Cold pack or compress
24-HOUR SYMPTOM PATTERN • Symptoms may be better during the morning, especially after sleeping with the foot elevated. • Symptoms may worsen during the day with increased weight-bearing activities.
PAST HISTORY FOR THE REGION • Previous history of ankle or foot injury • History of trauma to the foot • History of repetitive use coupled with poor or no footwear
PHYSICAL EXAMINATION • Point tenderness at the site of entrapment is generally posterior to the medial malleolus but can also occur under the base of the first metatarsal where the FDL tendon crosses the FHL tendon or where the FHL tendon passes between the great toe sesamoids beneath the metatarsal head. • Crepitus or catching of the tendon may be palpable at the site of entrapment. • Increased foot pronation or increased calcaneal eversion may be present, which would place more pressure onto the medial aspect of the foot and during gait. • ROM testing may reveal decreased dorsiflexion of the ankle, which could contribute to the foot dysfunction. • Resisted muscle testing of the FHL may produce pain. • Pain is also present when patients are asked to rise up onto their toes. • Neural dynamic testing should be normal. Abnormal findings may indicate that the pain is from the tibial nerve. • Balance and proprioception are often poor in these patients. • Muscle weakness (e.g., in the posterior tibialis muscle) may affect the biomechanics
ORTHOPEDIC PATHOLOGY
• The FHL muscle attaches proximally at the posterior superior third of the fibula and distally attaches at the base of the distal phalanx of the hallux. It functions to flex all the joints of the big toe and also acts to plantar flex the ankle joint. • Together with the flexor digitorum longus (FDL) tendon and the posterior tibialis tendon, the FHL tendon passes behind the medial malleolus and through the tarsal tunnel. Grooves on the talus and calcaneus contain the tendon of the muscle and are lined by a mucous sheath. • A continuum of injuries can involve the FHL tendon and its associated sheath. In the past, the term tendinitis was used to explain all pathology that occurred within a tendon. As the knowledge base has expanded, the definitions of tendon pathology have also changed. Tendinitis usually refers to an acute injury in which there is damage and inflammatory response to the tendon. Tendinosis usually refers to a chronic condition in which there still may be an inflammatory response, but degeneration of the tendon and alteration in tissue has begun to occur. Inflammation is minimal. Paratenonitis occurs when there is irritation of the outer layers of the paratenon and epitenon. Acute edema and hyperemia of the paratenon result.
COMMON SIGNS AND SYMPTOMS
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The paratenon is the tissue between a tendon sheath and its tendon. The paratenon surrounds and nourishes the tendon. Tenosynovitis is inflammation of the fluid-filled synovial sheath (called the synovium) that surrounds a tendon. Tenosynovitis refers to the chronic degenerative state of the tenosynovium. Partial or complete tendon tears can occur centrally, in the intrasubstance, or at the external margins of the tendon. Tendon retraction may or may not occur in the case of complete tendon tears. Complete ruptures of the FHL are rare. Tendon entrapment or checkrein deformity is tethering or entrapment of the FHL tendon that can occur under or just proximal to the flexor retinaculum. Tendon subluxation or dislocation can occur as the tendon travels posterior to the medical malleolus. • Injury to the FHL tendon can occur in the following regions: 1. Within the tarsal tunnel 2. At the knot of Henry, under the base of the first metatarsal. where the FDL tendon crosses the FHL tendon 3. Where the FHL tendon passes between the great toe sesamoids beneath the metatarsal head
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Flexor Hallucis Longus Tendinopathy of the foot and result in abnormal loading on the metatarsal heads.
IMPORTANT OBJECTIVE TESTS • MRI, x-ray, and ultrasound have been found to be beneficial in ruling out other potential pathology and in identifying joint destruction or other inflammatory processes. • Fluid in the synovial sheath is common in 20% of patients because the FHL tendon sheath communicates with the ankle joint. • No one specific clinical test has been shown to definitively identify the presence of flexor hallucis longus tendinopathy.
DIFFERENTIAL DIAGNOSIS • • • • • • • • • • • •
Posterior impingement syndrome Achilles tendinopathy Tibial nerve irritations Lumbar spine nerve entrapment Os trigonum syndrome Tarsal tunnel syndrome Osteoarthritis RA Tibialis posterior tendinopathy Subtalar coalition Fractured Stieda process Calcaneal fractures with impingement
CONTRIBUTING FACTORS • Entrapment of the FHL tendon may be due to an enlarged os trigonum, an associated calcaneal fracture, or fracture dislocation • Overpronation • Hallux limitus • Balance disorders • Chronic ankle sprain • History of ankle instability • Participation in high-level athletic sports that require repetitive plantar flexion • Footwear • Ballet and dance
TREATMENT MEDICAL • Surgery is generally only considered if all conservative options have been exhausted. The physician may prescribe antiinflammatory medications to reduce the irritation and swelling in the region. Steroid injections may be used to reduce inflammation locally around the region of irritation. • In severe cases, a walking boot or cast may be used to reduce the loading on the forefoot.
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• In cases where conservative treatment has failed to relieve symptoms, surgical intervention may be required. If a patient has a complete tear with marked tendon retraction, some surgeons administer a trial of conservative treatment. However, surgical repair with reapposition of the torn ends of the tendon is eventually performed. • In patients with chronic dislocation or subluxation, surgery is performed. The surgery may involve resection of abnormal ossific structures, repositioning of hardware, or fixation of fractures in patients with previous ankle and foot fracture, depending on the structures that are causing tendon irritation.
SURGICAL OUTCOMES Success and complications rates vary, depending on the nature and magnitude of the surgery, but general postsurgical outcomes are good.
REHABILITATION • The body has a remarkable ability to heal. The synovium of the metatarsal joint is no different. The key to healing FHL tendinopathy is identification of the structural and biomechanical abnormalities that are leading to the stress placed on the tendon. • Rehabilitation initially involves decreasing the inflammatory response. Medications, ice, and elevation are appropriate measures to address the inflammation that is present. To reduce the stress placed on the tendon, devices such as foot orthotics have proved effective in reducing the loading on the tendon and improving the mechanics of the foot so that the loads are subsequently reduced. Therapy must allow the inflammation to subside or resolve by relieving the repeated excessive stress and irritation. • Improving the mobility of the talocrural joint and the calf can improve ankle dorsiflexion. This is often needed to help improve the biomechanics of the foot during the mid-to-late stance phases of gait. • The patient can return to sport, but care must be taken to slowly progress the loading through the tendon so that appropriate tissue remodeling can occur. Full return to sport can occur when all biomechanical contributing factors have been addressed, balance and proprioception are normal, and strength is at least 90% that of the contralateral side. • Eccentric training programs have shown good results in patients with chronic tendon pathology.
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• Strengthening must increase gradually and should be relatively pain free. • Programs focusing on training and strengthening of the posterior tibialis muscle are currently being studied and show good potential for improving the mechanics of the foot and ankle, therefore reducing the stress placed on the tendon.
PROGNOSIS • The prognosis for patients with FHL tendinopathy is generally good. • If the factors resulting in abnormal forces being placed on the metatarsal joint can be eliminated, then the patient should heal. • Normal healing would generally take 6 to 8 weeks. Reducing the loading in a commonly used area in the body, such as the foot, is difficult. Healing may take a little longer as a result. • The prognosis for patients with complete ruptures or dislocation or subluxation of the tendon is not as good as for tenosynovitis.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Red flag signs in the ankle and foot are less common. If the patient is not improving over the course of a month, they should be referred back to their physician. • If there is suspicion of tumors (unremitting or nonmechanical pain), a referral to the physician is warranted. • Suspicion of gout should also be referred back to the referring physician for medical workup. Nonresolving inflammation may be an indication of gout or other systemic inflammatory disorders.
SUGGESTED READINGS Boruta PM, Beauperthuy GD. Partial tear of the flexor hallucis longus at the knot of Henry: presentation of three cases. Foot Ankle Int. 1997;18(4):243–246. Bureau NJ, Cardinal E, Hobden R, Aubin B. Posterior ankle impingement syndrome: MR imaging findings in seven patients. Radiology. 2000;215(2):497–503. Sammarco GJ, Cooper PS. Flexor hallucis longus tendon injury in dancers and nondancers. Foot Ankle Int. 1998;19(6):356–362. Trevino S, Baumhauer JF. Tendon injuries of the foot and ankle. Clin Sports Med. 1992;11(4):727–739. AUTHOR: DERRICK SUEKI
Osteoarthritis of the Foot
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BASIC INFORMATION DEFINITION • Osteoarthritis is a pathology associated with inflammation in the joints of the body. In the case of foot osteoarthritis, the arthritis and inflammation most commonly affects the midfoot, hindfoot, or forefoot. • Osteoarthritis is a term derived from the Greek word osteo, meaning “of the bone,” arthro, meaning “joint,” and itis, meaning inflammation, even though the amount of inflammation present in the joint can range from excessive to little or no inflammation.
SYNONYMS • Foot arthritis • Foot degenerative joint disease ICD-9 CODES 715.17 Primary localized osteoarthritis, ankle and foot 715.27 Secondary localized osteoarthritis, ankle and foot
3 to 6
MAXIMAL NUMBER OF VISITS 20 to 36
ETIOLOGY
• About 50% of people in their sixties and seventies have ankle or foot osteoarthritis as seen on x-ray. • Symptomatic foot osteoarthritis is not very common in the general population; there is an increased prevalence in persons with a history of significant foot trauma or extreme sports or activities (e.g., dance) • Seniors, especially those with a history of long-term abnormal use (poor footwear, excessive injuries, career or recreational overuse, or obesity) • Females have more ankle and foot osteoarthritis than males.
MECHANISM OF INJURY • Osteoarthritis is a pathology of overuse. The mechanism of injury is therefore the result of repetitive motions that stress the foot. The more cycles of an activity that the foot sees, the more likely the result will be anatomical damage. • Daily use or misuse of the foot (3-inch heels increase foot and ankle stress 7 times compared to 1-inch heels) • Misalignment of the foot and/or toes • Excessive use or strain of the foot • Injuries, such as fracture and strains or sprains, that cause inflammation and scar tissue in the foot or toes
COMMON SIGNS AND SYMPTOMS • Pain in the foot or toes • Stiffness in the foot or toes • Cracking or deep crunching in the foot or toe joints • Inflammation and thickening of the foot or toe joints • Misalignment of foot and toe bones • Gait abnormalities (increased foot pronation, out-toeing, or limp)
AGGRAVATING ACTIVITIES • Inactivity leads to stiffness • Weight-bearing activities (like walking, running, dancing, jumping, etc)
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EASING ACTIVITIES • Gentle stretching and exercise, use of heat/ice, massage, taking antiinflammatory medication, non–weight-bearing activities, and elevating the feet • Generally speaking, these activities lead to decreased wear and tear and loss of the stiffness and inflammation associated with this condition.
24-HOUR SYMPTOM PATTERN • Stiffness in the morning • Better after a warm shower and taking medication • Can worsen with excessive movement • Stiffens again in the evening
PAST HISTORY FOR THE REGION • Jobs or recreational activities that require excessive use or strain of the foot (dancing, walking, running, jumping, etc) • Abnormal amount of damage from injuries • Past history of poor footwear
PHYSICAL EXAMINATION • Joint thickening (bony changes and inflammation) • Loss of foot or toe ROM • Localized pain and loss of joint mobility • Crepitus with movement
IMPORTANT OBJECTIVE TESTS • No specific clinical testing regimen has been developed to positively confirm the presence of foot osteoarthritis. • Diagnosis is made by a combination of radiographic evidence coupled with clinical and subjective examination.
DIFFERENTIAL DIAGNOSIS • • • • • • • • • •
Foot or toe sprain Tendinitis RA Sesamoiditis Bunions Fallen arches Plantar fasciitis Gout Referral from the lower lumbar region Pitting edema secondary to cardiac dysfunction
ORTHOPEDIC PATHOLOGY
• The wearing down of the hyaline cartilage leads to an inflammatory response. There is thickening and sclerosis of the subchondral bone and development of osteophytes or bone spurs.This leads to a narrowing of the joint space, loss of shock absorption, and ultimately pain. • Daily wear and tear in combination with various injuries sustained throughout life is the most common cause of the breakdown of healthy tissue. • Degeneration of the cartilage and resultant arthritis can also be the result of other factors such as trauma or joint injury. • At a cellular level, as a person ages, the number of proteoglycans in the articular cartilage decreases. Proteoglycans are hydrophilic and work within cartilage to bind water. With the reduction of proteoglycans comes a decrease in water content within the cartilage and a corresponding loss of cartilage resilience. With the decreases in cartilage resilience, collagen fibers of the cartilage become susceptible to degradation and injury. The breakdown of collagen and other cartilage tissue is released into the surround joint space. Inflammation results as the body attempts to respond to the influx of byproducts from cartilage injury.
EPIDEMIOLOGY AND DEMOGRAPHICS
• Long-term standing, especially on harder surfaces like concrete, and wearing tight and/or poorly supportive shoes • Inactivity allows the inflammation to pool and increase pressure, leading to discomfort and loss of available movement. • Joint movement and weight bearing increases wear and tear and inflammation/irritation to the articular surfaces. • Poor footwear (i.e., high heels)
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• As the cartilage degrades, the joint space narrows and ligaments become more lax. In response to the laxity, new bone outgrowths, called spurs or osteophytes, can form on the margins of the joints in an attempt to improve the congruence and passive stability of the articular cartilage surfaces. • Primary osteoarthritis refers to joint degradation resulting from aging and tissue degeneration. • Secondary osteoarthritis refers to joint degradation and tissue degeneration that result from factors besides aging such as obesity, trauma, and congenital disorders.
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Osteoarthritis of the Foot CONTRIBUTING FACTORS • Uncontrollable risk factors that contribute or predispose an individual to ankle osteoarthritis pathology are as follows: Gender (females > males) Age (increase 2% per year after age 40 years) Genetics Prior history of injury to either lower extremity • Modifiable risk factors that contribute or predispose an individual to continue or progress ankle osteoarthritis are as follows: Weight Work or recreational activities Repetitive or significant traumatic injuries to the hip Poor health (smoking, long-term use of steroids) Poor footwear
TREATMENT SURGICAL OPTIONS • Fusion (arthrodesis) • Bunionectomy
REHABILITATION • Pathological changes to cartilage cannot be repaired by the body at this time. Even surgical advances have yet to solve the problems associated with cartilage damage. With this in mind, rehabilitation should focus on decreasing the stress placed on the damaged cartilage and correcting biomechanical and anatomical abnormalities that may predispose an individual to increased stress at the talocrural joint. • Decreased ankle dorsiflexion is a common restriction in patients with foot osteoarthritis. Improving ankle dorsiflexion is an important component of the ankle’s ability to absorb shock. Anterior-to-posterior talocrural joint mobilization, ankle traction mobilization, and soft tissue mobilization (STM) to the calf can help to increase ankle dorsiflexion. • Midfoot dysfunction can also affect hindfoot and forefoot function. Increased pronation is often associated
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with decreased ankle dorsiflexion and a plantar flexed first ray. This motion should be controlled, but making the midfoot too rigid prevents it from dissipating shock. Instead, this shock is transferred to the talocrural joint and to the forefoot. Orthotics or foot and ankle exercises can be used to control foot pronation. • Hip external rotation weakness or femoral torsions can also affect ankle and foot function and should be assessed and corrected. • The clinician should also evaluate the patient for leg length discrepancies that cause abnormal stresses to be placed onto the ankle joint. • Rehabilitation should focus on the following: Education in correct use of ice and heat at home Providing a home exercise program Teaching proper footwear with or without orthotics Manual therapy (STM, joint mobilization); may be able to teach patients self-mobilization techniques. Modalities: Ice or heat, ultrasound, electrical stimulation, tape or braces • Initial exercises to promote healing and pain abatement include the following: Stretches: Calf (gastrocnemius and soleus), toe flexors, plantar fascia Theraband exercises Arch forming exercises Toe strengthening exercises Proprioceptive exercises Pain-free foot motions such as foot alphabets Joint mobilization and manipulation can be used to improve arthrokinematics, decrease pain, and increase ROM Massage can decrease pain by relaxing muscular tension and increasing endorphin release. • Exercise should be used to do the following: Decrease muscular and joint stiffness. Improve joint alignment by increasing muscular support. Improve functional mobility: gait and recreational needs. Improve proprioception and balance.
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Create a sense of control over the symptoms and the condition.
PROGNOSIS • Long-term prognosis for a patient with foot osteoarthritis depends on the extent of wear and tear and ability to reduce the joint strain (posture, activity, etc). • For the most part, ankle osteoarthritis is a degenerative condition. At earlier stages of the pathology, rehabilitation aimed at reducing the load placed on the joint can potentially slow or halt the progression of degeneration. • For patients who are farther along in the degenerative process, outcomes will be less favorable because cartilage has only a limited ability to repair itself.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Unrelenting pain • Unusual responses to therapy • Red flag symptoms, such as excessive redness and swelling and generalized malaise and fatigue may be s igns of infection. • Neurological symptoms
SUGGESTED READINGS Dugan SA. Exercise for health and wellness at midlife and beyond: balancing benefits and risks. Phys Med Rehabil Clin N Am. 2007;18(3):555–575. Frey C, Zamora J. The effects of obesity on orthopaedic foot and ankle pathology. Foot Ankle Int. 2007;28(9):996–999. Glass GG. Osteoarthritis. Dis Mon. 2006;52(9). Jung HG, Myerson MS, Schon LC. Spectrum of operative treatments and clinical outcomes for atraumatic osteoarthritis of the tarsometatarsal joints. Foot Ankle Int. 2007;28(4):482–489. Mahiquez MY. Positive hindfoot valgus and osteoarthritis of the first metatarsophalangeal joint. Foot Ankle Int. 2006;27(12): 1055–1059. Valderrabano V, Nigg BM, von Tscharner V, Stefanyshyn DJ, Goepfert B, Hintermann B. Gait analysis in ankle osteoarthritis and total ankle replacement. Clin Biomech (Bristol, Avon). 2007;22(8):894–904. AUTHOR: SARA GRANNIS
Jones Fracture
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BASIC INFORMATION DEFINITION • The term Jones fracture is controversial because it has been used indiscriminately to describe any fracture of the proximal portion of the fifth metatarsal. • Jones fracture was described by Rosenberg as a fracture of the fifth metatarsal between the diaphysis and metaphysis. It is an intraarticular fracture involving the articulation between the fourth and fifth proximal metatarsals. It is an acute injury without precursory symptoms and is often confused with a tuberosity avulsion fracture. • The location of the fracture is associated with a watershed area of the bone; thus the Jones fracture is notorious for poor healing and nonunion.
SYNONYMS Fracture of the base of the fifth metatarsal ICD-9CM CODES 825.25 Fracture of metatarsal bone(s) closed
• As a result of the rich innervation of the bone, periosteum and surrounding soft tissue pain is usually associated with the fracture.
MECHANISM OF INJURY • Jones fracture commonly occurs with a large external load into adduction and with the foot plantar flexed during activities such as the following: Misstep off a step or curb onto the lateral forefoot Cutting or pivoting off the lateral forefoot with most of body weight on the foot Sudden deceleration with the foot in plantar flexion and forefoot inversion. Crossover maneuvers in sports such as soccer, basketball, and football
COMMON SIGNS AND SYMPTOMS • Pain at the lateral aspect of the foot over the base of the fifth metatarsal • Swelling and bruising at the base of the fifth metatarsal • Difficulty walking or weight-bearing on the affected foot.
AGGRAVATING ACTIVITIES 6 or fewer
MAXIMAL NUMBER OF VISITS 18 • Jones fracture occurs when an acute external force is applied to the lateral foot while it is in plantar flexion, such as with a misstep to the lateral border of the foot, with cutting or pivoting with the foot planted and body weight on the metatarsal heads, in crossover maneuvers (soccer), or with repeated deceleration. • The Jones fracture does not occur as a result of peroneus brevis or plantar aponeurosis avulsion of the tubercle. This is classified as an avulsion fracture. • The pathology involves a fracture of the fifth metatarsal between the diaphysis and metaphysis that does not extend beyond the articulation of the fourth and fifth proximal metatarsals. • Physiologically, a large external load into adduction is applied at the head of the fifth metatarsal, causing a bending moment that surpasses the bone’s tensile strength laterally. This results in a fracture between the diaphysis and metaphysis at the proximal metatarsal.
EPIDEMIOLOGY AND DEMOGRAPHICS • Jones fractures can occur at any age because they are the result of trauma.
Walking Running Ascending and descending stairs Position of injury (plantar flexion and forefoot adduction)
EASING ACTIVITIES • Elevation • Ice • Often, pain medication is prescribed; the use of antiinflammatories is controversial in patients with fracture because they have been associated with delayed bone healing. • Non–weight-bearing activities • Bracing to prevent position of injury
24-HOUR SYMPTOM PATTERN • The patient with a Jones fracture may experience stiffness in the foot on waking. • Symptoms increase during the day if the foot is in a gravity-dependent position for the majority of the day. • Sleeping may or may not be problematic, depending on the foot’s position.
PAST HISTORY FOR THE REGION Because of the acute nature of this fracture, no previous history is required.
PHYSICAL EXAMINATION • The patient may avoid symmetrical weight-bearing positions on the involved foot, especially along the lateral surface of the foot. • Body weight may be biased on the heel of the involved foot to avoid pressure
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IMPORTANT OBJECTIVE TESTS • Ottawa Rules: Set of two findings for the foot and ankle may implicate fracture. • A foot radiographic series is recommended if the patient presents with pain in the midfoot and any one of the following findings: Tenderness with palpation over the navicular or over the base of the fifth metatarsal Inability to bear weight on the affected foot immediately after injury and in the office for four steps. • An ankle radiographic series is recommended if the patient presents with pain in the malleolar region and any one of the following findings: Bone tenderness with palpation in the distal 6 cm of the tibia to the medial malleolus or distal 6 cm of the fibula to the lateral malleolus Inability to bear weight on the affected foot immediately after injury and for four steps in the office. 100% sensitive
DIFFERENTIAL DIAGNOSIS • • • • • •
Dancer’s fracture March fracture Avulsion fracture Lisfranc dislocation S1 radiculopathy Sural nerve pathology
TREATMENT SURGICAL OPTIONS • Fixation with intermedullary screw • Bone graft • Indications for surgery Nonunion of fracture after 6 to 8 weeks in non–weight-bearing cast immobilization
REHABILITATION • After immobilization, the following should be done: Control any residual inflammation Restore normal weight bearing and gait Perform active ROM (AROM) and passive ROM (PROM), especially at the talocrural, subtalar, and midfoot joints. Also, assessment and treatment of knee and hip mobility must also be considered as the patient has been on non–weight-bearing status for 6 to 8 weeks.
ORTHOPEDIC PATHOLOGY
ETIOLOGY
• • • •
on the distal aspect of the fifth metatarsal (long lever arm). • Tenderness from guarding the affected foot may be observed in the peroneals, long toe flexors, and gastrocnemius/ soleus complex.
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Jones Fracture Address strengthening. Since the patient has been immobilized for 6 to 8 weeks, consider a certain amount of atrophy and weakness, not only in the involved calf but also of the proximal musculature of the involved side. Perform balance and proprioceptive training, especially with progression into previous level of function, activity, and/or sport. • Postsurgical: Manage edema and the wound and scar. Watch for signs of infection. • Nuneley gives the following recommendation after surgery: Usually, the patient is toe-touch weight bearing for 2 weeks postsurgery After 2 weeks, the patient uses a walking boot to bear weight as tolerated. AROM is also encouraged. After the fourth week, the walking boot is discontinued and the patient is instructed to wear a tennis shoe with orthotic or insert to ensure stiffness of the sole to prevent stress at the fracture site. • Before clearing the patient to bear weight as tolerated, rehabilitation can focus on proximal strengthening, edema management, early AROM in a pain-free ROM, and scar management. Weight-bearing, gait training, strengthening, and AROM and PROM as per nonsurgical rehabilitation once cleared. Once cleared, weight bearing should be encouraged. A study by Vorlat et al reported that the greatest predictor for poor functional outcome is the amount of time spent in non–weightbearing. In this study, 38 subjects with either Jones or tuberosity avulsion fractures were followed for 490 days, with function measured using the Olerud ankle score and pain and comfort measured using analog scales. Frangolias et al presented a case study in which an elite runner sustained a Jones fracture, opted for nonsurgical casting, and used deep water running to maintain aerobic capacity. He participated in deep water training from 4 weeks after fracture to week 15, combination water running and land run-walk from weeks 16 to 21, and land runs from weeks 25 to 31. X-rays at weeks 4, 8, and 11 showed normal healing and, at week 16, union of fracture. Maximal oxygen uptake (VO2 max) testing at weeks 29 and 30 was 83% of his preinjury VO2 max testing.
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• To reduce inflammation, the clinician may consider the following: Lymphatic massage Joint mobilization: Not at involved site Elevated AROM within a pain-free ROM Exercises that promote movement of the region in a pain-free range Cold or hot pack Ultrasound: Only if there is union of the fracture and no surgical fixation.
CONTRIBUTING FACTORS • No contributing factors are necessary. • A study by Yu et al reported possible increased risk in fracture or injury to the fifth metatarsal with basketball players wearing over-the-counter medial arch supports. In this study of 14 males, plantar forces and pressures beneath the fifth ray were assesses during two basketball tasks: One foot landing after lay-up and shuttle run. They found that with use of the orthoses, there was an increase in the angle of maximal ankle inversion and increased pressure over the fifth metatarsal head and base with both landing on one foot and with the shuttle run.
PROGNOSIS • Reported rates of nonunion in nonsurgical cases of non–weight-bearing in a cast for 6 to 8 weeks to be between 7% and 28%. • Successful union of fracture in nonsurgical cases has been reported to take up to 21.2 weeks. • After failure of conservative care, with surgical intervention of intermedullary screw or bone graft, time to union was reported as approximately 21 weeks. • Vorlat et al reported the greatest predictor for poor functional outcome is the amount of time spent in non– weight-bearing activity. In this study, 38 subjects with either Jones or tuberosity avulsion fractures were followed for 490, days with function measured using the Olerud ankle score and pain and comfort measured using analog scales. However, limitations in his study include a small number of subjects with Jones fracture (6), and his population was generally a sedentary group. • Nuneley reported that if union is confirmed, return to running after surgical fixation can occur approximately 5 to 6 weeks after surgery and return to sport by 8 weeks.
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SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • No change or worsening of symptoms: Nonunion of fracture • Major trauma (if patient comes in without diagnosis): Fracture • Purulent exudate from surgical site: Infection • Significant edema, erythema, and tracking: Infection • Fevers and chills: Infection or tumor • Association with myotomal weakness, dermatomal pattern, and possible (not required lumbosacral symptoms) L5/S1 radiculopathy • Hyperalgesia, allodynia, temperature changes, edema: Complex regional pain syndrome
SUGGESTED READINGS Fetzer GB.Wright RW. Metatarsal shaft fractures and fractures of the proximal fifth metatarsal. Clin Sports Med. 2006;25:139–150. Frangolias DD, Taunton JE, Rhodes EC, McConkey JP, Moon M. Maintenance of aerobic capacity during recovery from right foot Jones fracture: a case report. Clin J Sports Med. 1997;7:54–58. Hawkins BJ. Fractures of the metatarsals and phalanges of the foot. In: Calhoun JH, Laughlin RT, eds. Fractures of the Foot and Ankle: Diagnosis and Treatment of Injury and Disease. Boca Raton, FL: Taylor and Francis Group; 2005. Nuneley JA. Fractures of the base of the fifth metatarsal: the Jones fracture. Orthop Clin North Am. 2001;32(1). Rosenberg GA, Sferra JJ.Treatment strategies for acute fractures and nonunions of the proximal fifth metatarsal. J Am Acad Orthop Surg. 2000;8:332–338. Stiell IG, Greenberg GH, McKnight RD, et al. Decision rules for the use of radiography in acute ankle injuries: refinement and prospective validation. JAMA. 1993;269(1):127–132. Stroud CC. Fractures of the midtarsals, metatarsals, and phalanges. In: Richardson EG, ed. Orthopedic Knowledge Update: Foot and Ankle. Rosemont, IL: American Academy of Orthopedic Surgeons; 2004. Vorlat P, Achtergael W, Haentjens P. Predictors of outcome of non-displaced fractures of the base of the fifth metatarsal. Int Orthop. 2007;31:5–10. Yu B, Preston JJ, Queen RM, et al. Effects of wearing foot orthosis with medial arch support on the fifth metatarsal loading and ankle inversion angle in selected basketball tasks. J Orthop Sports Phys Ther. 2007;37(4):186–191. AUTHOR: MILDRED V. LIMCAY
Ligament Injuries of the Phalanges
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BASIC INFORMATION DEFINITION • Ligament injuries of the phalanges include attenuation or rupture of the medial collateral ligament (MCL), lateral collateral ligament (LCL), dorsal ligament, and/or volar (plantar) plate of toes 2 to 5. • Grading of ligament sprains is as follows: Grade I: Partial tear of a ligament without mechanical instability Grade II: Incomplete tear of a ligament with mild-to-moderate instability Grade III: Complete tear and loss of integrity of a ligament; mechanical instability
SYNONYMS Toe sprain ICD-9CM CODES 845.13 Interphalangeal (joint) toe sprain 845.12 Metatarsophalangeal (joint) sprain
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ETIOLOGY
EPIDEMIOLOGY AND DEMOGRAPHICS • The pathology is not specific to any age group.
COMMON SIGNS AND SYMPTOMS • Pain, discoloration, and edema over the affected toe • Depending on severity of injury, patients may avoid normal weight-bearing positions through the forefoot during gait.
AGGRAVATING ACTIVITIES • Depending on grade of injury: Weight-bearing Extension of the affected toe, passively or actively Flexion of the affected toe, passively or actively Compression of the forefoot, type of shoe worn (tight toebox) Walking, especially barefoot or in flexible-soled shoes Running Rising up onto toes (heel raise) • Activities and positions that require MTP dorsiflexion and/or toe extension places stress on the attenuated or torn plantar support structures. MTP plantar flexion and/or phalangeal flexion places stress on the attenuated or torn dorsal support structures. In the presence of interarticular edema, symptoms can be aggravated with either position. • With walking, symptoms are exacerbated with weight bearing and progression of the body over the forefoot with the transition from midstance to terminal stance.
EASING ACTIVITIES • Non–weight bearing or partial weightbearing activities
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24-HOUR SYMPTOM PATTERN • If swelling is present, the patient can have feelings of stiffness in the affected joint in the morning. • The patient is usually more symptomatic by the end of the day with time spent on the feet and time spent with the foot in a gravity-dependent position.
PAST HISTORY FOR THE REGION • With cases of traumatic onset, there does not have to be a history of injury to the foot and ankle predisposing to injury. • Chronic cases do involve a previous history of one or a repeated injury to the affected joint’s support structures, which has caused complete disruption of the capsuloligamentous structures. • Chronic cases caused by systemic inflammatory disorders can involve other joints of the foot.
PHYSICAL EXAMINATION • The patient may avoid weight-bearing positions on the affected side. • With a chronic injury that has resulted in disruption of second MTP stabilizers, the second toe may be deviated or deformed. The most common presentation is attenuation or disruption of the LCL of the second MTP, causing angulation toward the great toe.
IMPORTANT OBJECTIVE TESTS • AROM and PROM testing In acute injury, both flexion and extension of the involved toe are limited, more so toward the direction of the mechanism of injury due to pain. In subacute and especially chronic phases, hypermobility may be noted toward the direction of the injury caused by attenuation of the capsule and ligaments. If the end-feel is hard or blocked, one should suspect a foreign body within the joint. • Varus and valgus testing to assess for compromise of MCL and LCL of the involved joint. • Accessory mobility (drawer testing) Depending on severity of injury and capsuloligamentous damage, laxity or instability with arthrokinematic motion assessment is associated with direction of injury.
ORTHOPEDIC PATHOLOGY
• The second toe is usually the most affected because is normally longer than toes 3 to 5. • Usually the ligaments at the metatarsophalangeal (MTP) joints are most affected, possibly as result of the greater amount of motion at this joint versus the proximal and distal interphalangeal joints. • Ligament injuries can result from a sudden trauma that exceeds the tensile strength of the ligament, causing attenuation and partial or complete rupture. • Thornton and associates found ligaments to be more susceptible to injury with repeated loading versus static loading in less time when using the same load. • In acute injuries, nociceptors within ligaments and joint capsules are stimulated with attenuation or tear. Inflammation resulting from ligamentous injury bathes the area in chemical mediators (substance P, bradykinin, etc) that can sensitize neurons, thus perpetuating pain. • Edema within the joint can produce feelings of pressure and ache.
MECHANISM OF INJURY • Hyperextension: Plantar plate disruption Fall with landing axially on the lesser toes with toes dorsiflexed Long-term wearing of high-heel shoes Sudden planting and stopping with toes impacting shoe toebox • Hyperflexion: Dorsal plate disruption Fall with landing axially on the lesser toes with toes dorsiflexed Sudden planting and stopping with toes impacting shoe toebox • Varus stress loading: LCL disruption • Valgus stress loading: MCL disruption • Dislocation: Multiple ligaments High-energy trauma, causing hyperflexion or extension of the toes such as a fall, motor vehicle accident (MVA), or toe(s) getting caught in moving bicycle spoke. Preexisting condition causing ligamentous laxity such as RA
• Wearing firm-soled or rocker-bottom shoes that prevent extension at the MTP during walking, thus not allowing attenuation of plantar support structures. • Medication (antiinflammatories, pain relievers) • Ice • In presence of acute injury, ice and medication can address inflammation.
Section III
OPTIMAL NUMBER OF VISITS
• Early stage symptoms are inflammation and acute ligament damage. Once inflammation has cleared, instability can remain, which predisposes the joint to abnormal shear forces that may produce symptoms.
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For example, with the hyperextension mechanism at the second MTP, there may be laxity in end-feel and hypermobility in dorsal glide of the proximal phalanx relative to the metatarsal.
DIFFERENTIAL DIAGNOSIS • • • • • • • • •
Freiberg’s infraction Interdigital neuroma Phalanx fracture Dislocation at the interphalangeal or MTP joint Metatarsal fracture Osteoarthritis Rupture of flexor or extensor tendons of the lesser toes Gout Systemic inflammatory disorders (systemic lupus erythematosus [SLE], psoriatic arthritis, or Reiter’s syndrome)
TREATMENT SURGICAL OPTIONS • Surgery is considered if instability is present and conservative treatment has failed. • Type of intervention depends on severity of deformity and instability. • Surgery for MTP disorders can be the following: Plantar plate repair Capsular reefing Capsular reefing with tendon transfer Weil osteotomy • Surgery for disorders within the digit can be as follows: Proximal interphalangeal (PIP) resection arthroplasty PIP fusion Tendon transfer Amputation
SURGICAL OUTCOMES • Coughlin reported good to excellent results in 93% of cases of surgical reduction and reconstruction for second MTP joint instability. • Bouche and Heit evaluated outcomes 1 year after plantar plate repair with tendon transfer in 15 subjects: All patients reported pain relief after surgery: 60% had full pain relief, 33% had occasional pain, and 7% had moderate pain. Function: 67% reported no limitation, 26% reported mild limitation with some weight-bearing exercise, and 7% reported mild limitation with all weight-bearing exercises • Surgical complications include the following: Metatarsalgia Loss of ROM Recurrence of deformity
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REHABILITATION Nonoperative • Acute stages: Address inflammation and pain • Use taping and external support (orthoses) to decrease load and protect the injured digit • Modify activity (use rigid-soled shoes) • As pain reduces, restore of normal foot mechanics and weight bearing with walking, functional tasks, and sport • Address limitation in mobility of the foot and ankle. Postsurgical • Acute stages: Rest, ice, compression, and elevation (RICE). Use of modalities such as ultrasound and electrical stimulation are contraindicated with metal implantation. • Later stages Gait training, with or without assistive device Restore ROM at the affected digit, foot, and ankle Proprioceptive and balance training Strength training Progressive return to previous level of activity Consider possibility of orthoses to protect area • To decrease inflammation, the clinician should consider the following: Lymphatic massage ROM in a pain arc Cold pack Joint mobilization: Time frame and surgery specific Ultrasound: Contraindicated in patients with metal fixation Electrical stimulation: Contraindicated in patients with metal fixation • Once the inflammation process has decreased, the focus of rehabilitation should be on the following: Identify the factors that would further aggravate the injured digit Gait training: Emphasis on normal weight bearing and progression over forefoot Restore ROM at the affected digit, foot, and ankle, especially if the patient had a period of immobilization. Proprioceptive and balance training Strength training of the affected lower extremity to address weakness resulting from disuse due to surgery or immobilization. Progressive return to previous level of activity • Initial exercises that can be used to promoted healing include: If nonoperative: AROM in a pain-free range to stimulate circulation and reduce edema • Postoperative: Highly dependent on type of surgery and postsurgical precautions
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Tendon transfers: Early active ROM is contraindicated. Joint mobilization or manipulation: Appropriate at nonaffected joints (such as talocrural) that may contribute to excessive loading at the toes. At the affected joint, mobilization may be indicated postsurgically if immobilization rendered the joint hypomobile. Caution should be used in mobilization toward in the direction that would stress the injured ligament. Postsurgically, mobilization is a possibility after healing is confirmed, but caution should be used. Massage • Acute stages: Can help with lymph circulation to address edema • Later stages: STM is appropriate in addressing soft tissue restriction in joint ROM. Exercise: To regain strength lost in the affected lower extremity caused by immobilization.
CONTRIBUTING FACTORS • Systemic inflammatory diseases and disorders (RA, SLE) • Repetitive loading injury at the toes (e.g., jumpers, dancers, sprinters) • Long-term steroid use • Forefoot equinus • Medial column instability • Severe calcaneovalgus deformity
PROGNOSIS Depending on severity and treatment of initial injury: A less severe sprain with immediate treatment has better long-term results.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant unrelenting foot pain:Infection or tumor • Pain that does not change with position or weight bearing: Infection or tumor • Allodynia, hyperesthesia, sympathetic changes: Reflex sympathetic dystrophy (RSD) • Streaking along skin toward lymph nodes: Infection • Purulent exudate from surgical site: Infection • Significant and unexplained weight loss: Tumor • Nocturnal pain:Tumor • Worsening or no improvement of symptoms: Fracture, infection • Major trauma: Fracture • Fevers and chills: Infection or tumor
SUGGESTED READINGS Bouche RT, Heit EJ. Combine plantar plate and hammertoe repair with flexor digitorum longus tendon transfer for chronic,
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severe sagittal plane in stability of the lesser metatarsophalangeal joints: preliminary observations. J Foot Ankle Surg. 2008;47(2):125–137. Coughlin MJ. Common causes of pain in the forefoot in adults. J Bone Joint Surg (Br). 2000;28-B(6):781–790. Coughlin MJ, Grimes JS, Schenck RC. Lesser toe deformities. In: Porter DA, Schon LC, eds. Baxter’s The Foot and Ankle in Sport. Philadelphia: Mosby; 2008.
Leung WY, Wong SH, Lam JJ, Ip FK, Ko PS. Presentation of a missed injury of a metatarsophalangeal joint dislocation in the lesser toes. J Trauma. 2001;50:1150–1152. Prisk VR, O’Loughlin PF, Kennedy JG. Forefoot injuries in dancers. Clin Sports Med. 2008;27:305–320. Sferra JJ. Lesser toe deformities, Freiberg’s infraction and bunionette deformity. In: Richardson EG, ed. Orthopedic Knowledge Update: Foot and Ankle. Rosemont,
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IL: American Academy of Orthopedic Surgeons; 2004. Thornton GM, Schwab TD, Oxland TR. Fatigue is more damaging than creep in ligament revealed by modulus reduction and residual strength. Ann Biomed Eng. 2007;35(10):1713–1721. AUTHOR: MILDRED V. LIMCAY
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Metatarsal Stress Fractures
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BASIC INFORMATION DEFINITION Metatarsal stress fractures are closed incomplete fractures through the cortex and into the trabecular bone matrix in the shaft of a metatarsal bone. Stress fractures and stress reactions, both RSIs of bone, are a reaction of bone to repetitive and abnormal forces.
SYNONYMS • • • • •
Fatigue fracture Insufficiency fracture Chronic RSI of bone Stress reaction March fracture
ICD-9CM CODES 733.94 Stress fracture of the metatarsals
OPTIMAL NUMBER OF VISITS Physical therapy for this condition depends on the intervention chosen by the physician. Generally, a boot is used for a period of time and a home exercise program can be initiated. Return to function may require 4 to 8 visits over a number of weeks.
MAXIMAL NUMBER OF VISITS 300% of body weight. Normal function is to provide shock absorption to the first MTP joint and provide increased mechanical leverage to the great toe flexors and to protect the FHL tendon. • The following disorders may occur to the sesamoid bones: Sesamoiditis is a general term for pain around the sesamoid region as a result of soft tissue (bursa, flexor tendon) pathology with normal radiographs and MRI; this is a diagnosis of exclusion. Sesamoid fracture most often occurs to the tibial (most medial) sesamoid. Sesamoid degeneration is associated with chondromalacia, osteophytes, and gout. Avascular necrosis of the sesamoid: Traumatic or nontraumatic Osteomyelitis of the sesamoid: Direct relation to plantar wound or ulcer or puncture wound
• Avascular necrosis of the sesamoids: Each sesamoid bone receives its blood supply mainly from one sesamoid artery off the medial and/or lateral plantar artery. With trauma, blood flow can be disrupted, leading to avascular necrosis. • The patient experiences pain as a result of the following: Sesamoiditis: Inflammation of soft tissue structures leads to pain and edema Fractures: Nociceptors within the bone stimulated with fracture of either type, especially when weight bearing Avascular necrosis: Pain caused by bone deterioration and collapse
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• In later stages of avascular necrosis and with infections, there is constant pain throughout the day.
TREATMENT
PAST HISTORY FOR THE REGION
• • • •
• For acute fracture: Traumatic event without previous incident or injury to the foot or ankle. • For stress fracture and avascular necrosis: May have previous history of pain over the plantar surface of the first MTP. • Osteomyelitis: History of plantar pressure ulcer (and neurological deficit) or puncture wound that would account for the introduction of infection.
PHYSICAL EXAMINATION • Avoidance of weight-bearing or asymmetrical weight-bearing activities that favor the involved foot. • During gait, patients may reveal lack of trailing limb posture and a shortened stance phase on the affected side • Flexor hallicus brevis and longus may be tender to palpation or may even elicit pain at the sesamoids because of the close anatomical relationship of their distal tendons and the sesamoids.
IMPORTANT OBJECTIVE TESTS • No specific physical tests for sesamoids: Because of the close and intricate relationship between the sesamoids, the first MTP joint, and the flexor tendons, it is difficult to isolate a sesamoid pathology, which is why radiographs are often recommended to rule out fracture, osteoarthritis, and avascular necrosis. • First ray ROM Symptoms may be reproduced with passive dorsiflexion of the first ray. • First MTP joint mobility or stability Differentiates between first MTP instability or rigidus versus sesamoid injury • Compression of the sesamoids to provoke symptoms Reproduction of grinding may indicate osteoarthritis • Palpation of region for edema and warmth
DIFFERENTIAL DIAGNOSIS • • • • • • • • • •
Flexor tendinitis Turf toe Interdigital neuroma Gout RA Intractable plantar keratosis Osteoarthritis of the first MTP joint Osteonecrosis of the sesamoid Absent sesamoid Bipartite sesamoid
SURGICAL OPTIONS Sesamoidectomy Curettage and grafting Bone graft for midwaist fractures Internal fixation
SURGICAL OUTCOME • Sesamoidectomy • Literature reports between 42% and 50% complete pain relief after sesamoidectomy. • Although sesamoidectomy may relieve symptoms, the literature reports several complications postsurgically, as follows: Intrinsic minus or cock-up deformity of the great toe Hallux varus deformity Exacerbation of a hallux valgus deformity Hallux rigidus Overload to the first MTP leading to osteoarthritis • Curettage and grafting has been reported to be 89% successful without report of these complications.
REHABILITATION • First course of action is nonsurgical treatment for at least 3 months for most sesamoid injuries. Usually this involves a period of casting or splinting and limited weight-bearing activities, depending on severity and type of disorder. • Acute disorders should be treated using activity modification and RICE to relieve symptoms. • Focus is on offloading the sesamoids with activity via orthoses, metatarsal pads, or devices to limit hallux dorsiflexion. • Strengthening and proprioceptive or balance training address loss caused by immobilization and disuse. • To decrease inflammation, the clinician may consider the following: Pain-free AROM Cold pack Ultrasound: If no fracture or tumor is present Electrical stimulation • Once the inflammation process has decreased, the focus of rehabilitation should be on the following: Eliminating the source of repetitive stress External considerations such as taping, pads to offload sesamoids (placed proximal to sesamoids), and/or orthoses • Early exercises in non–weight-bearing positions that actively go through painfree ROM to promote circulation and reduce edema.
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• Joint mobilization and manipulation are appropriate in the later phases of rehabilitation to address limitations in first MTP motion, specifically hallux dorsiflexion. • Massage can be used in early rehabilitation (lymphatic massage or myofascial release) to reduce edema. • In later stages, STM is appropriate for addressing soft tissue restrictions in mobility. • Exercise plays a significant role in regaining strength and proprioceptive loss caused by disuse and immobilization.
CONTRIBUTING FACTORS • Failure to incorporate modifications to footwear and activity • Factors that contribute to nontraumatic sesamoid disorders are as follows: Blood disorders that facilitate ischemia such as sickle cell anemia Long-term steroid use Long-term alcohol use Systemic inflammatory disorders Diabetes (neuropathic pressure ulcers) Those who are immunosuppressed
PROGNOSIS • Prognosis depends on type and severity of disorder such as the following: Sesamoiditis and disorders responding to conservative care should continue to be asymptomatic with continued modification of activity and footwear. Avascular necrosis or infection will likely require sesamoidectomy, which can resolve pain; however, iatrogenic complications are likely to cause other symptoms in patients.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant unrelenting pain: Infection or tumor • Pain that does not change with position: Infection or tumor • Major trauma: Fracture • Fevers, fatigue, and chills: Infection or tumor • Purulent exudate: Infection • Allodynia, hyperesthesia, or sympathetic changes: Complex regional pain syndrome
SUGGESTED READINGS Anderson RB, Shawen SB. Great-toe disorders. In: Porter DA, Schon LC, eds. Baxter’s the Foot and Ankle in Sport. Philadelphia: Mosby, Inc; 2008. Dedmond BT, Cory JW, McBryde A.The hallucal sesamoid complex. J Am Acad Orthop Surg. 2006;14(13):745–753. Kanatli U, Ozturk AM, Ercan NG, Ozalay M, Daglar B, Yetkin H. Absence of the medial sesamoid bone associated with
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metatarsophalangeal pain. Clin Anat. 2006; 19:634–639. Karasick D, Schweitzer ME. Disorders of the hallux sesamoid complex: MR features. Skeletal Radiol. 1998;27:411–418.
Mandracchia VJ, Mandi DM, Toney PA, Halligan JB, Nickels WA. Fractures of the forefoot. Clin Podiatr Med Surg. 2006;23:283–301. Vanore JV, Christensen JC, Kravitz SR, et al. Diagnosis and treatment of the first meta-
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tarsophalangeal joint disorders. Section 4: sesamoid disorders. J Foot Ankle Surg. 2003;42(3):143–147. AUTHOR: MILDRED V. LIMCAY
Section III ORTHOPEDIC PATHOLOGY
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Sinus Tarsi Syndrome BASIC INFORMATION DEFINITION Sinus tarsi syndrome results in pain over the sinus tarsi and the sensation of rearfoot instability that is thought to be the result of a combination of neuromuscular proprioceptive loss and compromise of the ligaments of the subtalar joint.
SYNONYMS Subtalar joint instability ICD-9CM CODES 726.79 Other enthesopathy of ankle and tarsus
OPTIMAL NUMBER OF VISITS 6 or fewer
MAXIMAL NUMBER OF VISITS 24
ETIOLOGY • Sinus tarsi syndrome is usually a result of chronic inversion ankle sprains, leading to instability of the subtalar joint. Instability can result from disruption of the passive supportive structures of the joint (specifically the cervical ligament and interosseous talocalcaneal ligaments) or from loss of active support (neuromuscular proprioception). • The source of pain has been disputed. Possibilities include the following: Tears and/or fibrosis of the cervical or interosseous talocalcaneal ligaments Hyperplasia of the synovial membrane Neurogenic inflammation of the nociceptive and mechanoreceptors present in synovium Synovitis Posttraumatic fibrous changes in veins resulting in the impaction of venous outflow Bleeding into the sinus tarsi • Physiologically, the sinus tarsi is the talocalcaneal joint space formed by the sulcus of the talus and calcaneus. Contained in the sinus tarsi are the interosseous talocalcaneal ligament; the cervical ligament; the subtalar joint capsule; synovium; and medial, inferior, and lateral roots of the inferior lateral retinaculum and neurovasculature. • There is general agreement on how sinus tarsi syndrome first occurs. An inflammatory event—most commonly an inversion ankle sprain—creates trauma or microtrauma to the ligaments and synovium within the sinus tarsi. The subsequent remodeling of the previously mentioned ligaments, synovium, and tissues is blamed for the etiology of pain and pathology. Inflammatory
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diseases, such as RA and gout, have also been identified as predisposing factors in the development of sinus tarsi syndrome. Significant ligamentous instability of the subtalar joint need not be present in sinus tarsi syndrome. • In neurohistological studies of synovial samples of those with sinus tarsi syndrome as opposed to a control subject, Akiyama et al found nociceptive free nerve endings and three mechanoreceptor variants: Pacinian, Golgi, and Ruffini corpuscles. The area of most neurodensity was present within the synovium located in the sinus tarsi in both controls and symptomatic individuals. Because of this finding, the authors hypothesized that the sinus tarsi is a region of great proprioceptive and nociceptive ability. Therefore inflammation or irritation here would produce pain, and altered proprioception would result in feelings of instability caused by altered neuromuscular control. In the same study, findings of chronic synovitis with hypervascularization and lymphocytic infiltration were also reported. Feelings of instability can be the result of actual ligamentous laxity or rupture (mechanical instability) and proprioceptive changes; thus neuromuscular insufficiency (functional instability) results.
EPIDEMIOLOGY AND DEMOGRAPHICS • The most common age group for patients with sinus tarsi syndrome are those in their twenties and thirties. • There are no gender and cultural predispositions to sinus tarsi syndrome.
MECHANISM OF INJURY • Typically occurs after acute traumatic or chronic inversion injury to the ankle complex resulting in inflammation, microtrauma,and/or macrotrauma to the ligamentous or articular components. • Inflammatory diseases, such as RA and gout, have been linked to sinus tarsi syndrome as predisposing factors.
COMMON SIGNS AND SYMPTOMS • • • •
Pain Feeling of instability Possible edema over sinus tarsi Typically, pain is localized over the sinus tarsi.
AGGRAVATING ACTIVITIES • • • • •
Walking, especially on uneven ground Standing Running Jumping Wearing shoes with narrow base of support (heels)
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EASING ACTIVITIES • Sitting • Limiting weight-bearing activities on affected side • Wearing more stable shoes • Use of orthotics • Pain relievers
24-HOUR SYMPTOM PATTERN Symptoms usually depend on aggravating factors.
PAST HISTORY FOR THE REGION • History of inversion ankle sprain(s): Estimated that 70% of those with sinus tarsi syndrome have had an inversion ankle injury. • Systemic inflammatory diseases affecting the foot include gout and RA.
PHYSICAL EXAMINATION • Common physical findings: Point tenderness over the sinus tarsi Passive abduction and pronation of the heel and midfoot may reproduce symptoms Swelling over the sinus tarsi may or may not be present.
IMPORTANT OBJECTIVE TESTS • Talar tilt test (inversion) A positive test indicates disruption of the interosseous talocalcaneal ligaments; it does not, however, confirm the presence of sinus tarsi syndrome, it only suggests the predisposing mechanism to the disorder and allows the clinician to determine if reported instability is due to ligamentous compromise. • Anterior drawer test Test of the talocrural joint and laxity of the anterior talofibular ligament.A positive test does not confirm the presence of sinus tarsi syndrome, it only suggests the predisposing mechanism to the disorder and allows the clinician to determine if reported instability is due to ligamentous compromise.
DIFFERENTIAL DIAGNOSIS • • • • •
Anterior talofibular sprain Subtalar instability Superficial peroneal nerve irritation L5 or S1 nerve root irritation Osteochondral lesion of the talus
CONTRIBUTING FACTORS • Functional or mechanical instability of the foot and ankle • Previous foot and ankle sprain • Autoimmune or chronic inflammatory disorders (RA or gout) • Impaired neuromuscular control in the ankle and hip
Sinus Tarsi Syndrome
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TREATMENT SURGICAL OPTIONS • Arthroscopic debridement • Arthroscopic synovectomy • Interosseous talocalcaneal reconstruction
ligament
SURGICAL OUTCOMES • Pisani reported that postsurgically, the amount of passive instability is reduced and the patient’s ability to single limb balance is improved. • Surgical indicators include the following: Failure of conservative interventions (injection, orthotic therapy, physical therapy) to manage symptoms and instability Instability of the subtalar joint as the result of compromised passive stabilizers
REHABILITATION
PROGNOSIS Because the mechanism of injury is related to an inversion sprain injury, the patient is more likely to have recurrent inversion
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SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Pain that does not change with position: Infection or tumor • Significant and unexplained weight loss: Tumor • Major trauma: Fracture • Inability to bear weight: Fracture • Fevers and chills: Infection or tumor
SUGGESTED READINGS Akiyama K, Takakura Y, Tomita Y, Sugimoto K, Tanaka Y, Tama S. Neurohistory of the sinus tarsi and sinus tarsi syndrome. J Orthop Sci. 1999;4:299–303. Chao W. Interdigital neuroma and tarsal tunnel syndrome. In: Richardson EG, ed. Orthopedic Knowledge Update:Foot and Ankle.Rosemont, IL:American Academy of Orthopedic Surgeons; 2004. Hertel J. Functional instability following lateral ankle sprain. Sports Med. 2000;29(5):361–371. Pisani G, Pisani PC, Parino E. Sinus tarsi syndrome and subtalar joint instability. Clin Podiatr Surg Med. 2005;22:63–77. Sauer ST, Hanson TW, Marymont JV. Disorders of the subtalar joint, including subtalar sprains and tarsal coalitions. In: Porter DA, Schon LC, eds. Baxter’s The Foot and Ankle in Sport. Philadelphia: Mosby, Inc; 2008. Swarzenbach B, Dora C, Lang A, Kissling RO. Blood vessels in the sinus tarsi and sinus tarsi syndrome. Clin Anat. 1997;10:173–182. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985;13:259–262. AUTHOR: MILDRED V. LIMCAY
ORTHOPEDIC PATHOLOGY
• Proprioceptive training is an important consideration in the rehabilitation of sinus tarsi syndrome. • To decrease inflammation, the clinician should consider the following: Cryotherapy Joint mobilization Ultrasound Therapeutic exercises Lymphatic massage • Once the inflammation process has decreased, the focus of rehabilitation should be on the following: Neuromuscular reeducation: Balance and proprioceptive training to restore dynamic stability of the foot and ankle. Balance training has been shown to decrease deficits in postural control.
injuries without proprioceptive training. Increased occurrence of this type of injury only contributes to recurrent episodes of sinus tarsi syndrome.
Section III
Taping or bracing has been shown to help with postural control in those who have already sustained one lateral ankle sprain. In those who have never sustained a lateral ankle sprain, it has been shown to be ineffective or even diminishes the response to perturbations in balance. Foot orthoses have also been reported to assist in alleviating symptoms of pain and instability in a person with sinus tarsi syndrome. Hertel discusses previous studies regarding orthoses and alleviation of pain and instability and notes improvement in symptoms without details in posting or orthotic specifics. • Balance exercises progressing to return to sport or activity should target both ankle and hip strategies with perturbations in balance. • Long-term exercises Proprioceptive and balance training helps prevent recurrent inversion ankle injury, which is the most common cause of sinus tarsi syndrome. This training helps prevent and address dynamic instability of the talocrural and subtalar joint, which can also lead to other foot and ankle disorders. Exercises targeting the proximal hip musculature would assist in prevention, according to Bullock-Saxton, who identified a delay in hip muscle function after severe ankle sprain. For those who are active in sports, external bracing should be considered.
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Talar Dome Damage
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BASIC INFORMATION DEFINITION • Damage to the articular cartilage and/ or underlying bone of the superior articular surface of the talus within the ankle mortise is described as chondral only, subchondral only, or chondralsubchondral. • Berndt and Harty classification system is as follows: Stage I: small compression fracture of the talar dome Stage II: Incomplete avulsion Stage III: Complete avulsion Stage IV: Displaced fragment • Pritsch (arthroscopic classification) system is as follows: Grade I: Intact, firm cartilage Grade II: Intact, soft cartilage Grade III: Frayed cartilage
SYNONYMS • • • • • •
Osteochondral lesion Avascular necrosis of the talar dome Transchondral fracture Osteochondritis desiccans Talar dome fracture Flaked fracture
ICD-9CM CODES 732.7 Osteochondral desiccans 733.44 Aseptic necrosis of talus 718.07 Articular cartilage disorder involving ankle and foot
OPTIMAL NUMBER OF VISITS 6 or fewer
MAXIMAL NUMBER OF VISITS 18
ETIOLOGY • The origins of injury and areas of the talar dome that are most often injured are as follows: Traumatic origin: Anterolateral (98% ) or posteromedial (78%) aspect of the talar dome Atraumatic origin: Posteromedial aspect of the talar dome Anterolateral lesions tend to be more shallow, wafer-like, and more apt to become displaced. Posteromedial lesions tend to be deeper lesions that do not get displaced. • Damage to the talar dome occurs because the talar dome has poor vascularity. An osteochondral lesion occurs when blood supply is disrupted (through trauma, emboli, etc) and the involved bone fragment is left without direct vascularization. With continued weight bearing, the fragment may
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not heal and collapse, lead to cartilage defect, and/or break away from the parent bone and remain loose within the talocrural joint. • Patients experience pain because of the following: Local inflammation and edema in a confined space Bone has nociceptive afferents, therefore if the lesion is subchondral, nociceptors are stimulated. If the lesion becomes displaced, it can become trapped between the talus and mortise, thus stimulating the nociceptors on these structures.
EPIDEMIOLOGY AND DEMOGRAPHICS • Most common presentation is a man, 25 to 35 years of age, who is participating in activities that would predispose to ankle sprains (jumping sports, cutting sports). • Others affected are as follows: Those with genetic predisposition Those with systemic inflammatory diseases • Most people experience pain, which is often how the lesion is found:The complaint of persistent pain after an ankle sprain is usually what brings the patient in for further work-up.
MECHANISM OF INJURY • Trauma is the primary cause of talar dome damage. Anterolateral lesions: Inversion trauma in dorsiflexion causes abutment between the anterolateral aspect of the talar dome with the fibula. It can occur in conjunction with a distal fibular fracture. Posteromedial lesion: Inversion trauma in plantar flexion with tibial external rotation leads to compression of the posteromedial talus with the tibial plafond. Some believe lesions can occur with recurrent inversion ankle sprains, resulting in unresolved instability. • Atraumatic causes, with proposed theories, are as follows: Infarct caused by fat emboli, sickle cell anemia, or corticosteroid use Endocrinologic conditions Systemic inflammatory conditions such as RA, SLE, or ankylosing spondylitis Genetic predisposition
COMMON SIGNS AND SYMPTOMS • History of an ankle sprain with persistent pain local to area of lesion with or without swelling • Duration of symptoms lasts well beyond time frame for ligamentous healing (several months to years).
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• Complaints of “catching,” “locking,” or “grinding” that may suggest presence of a loose fragment • Complaints of the ankle being “unstable” or “giving way” with pain
AGGRAVATING ACTIVITIES • • • • • • • • •
Prolonged standing Walking Ascending and descending stairs Activities requiring dorsiflexion, especially with anterolateral lesions, such as squatting or lunging Activities requiring plantar flexion, especially with posteromedial lesions, such as going up onto toes or reaching Running Cutting (running with sudden change of direction) Compression of joint surfaces Activities, such as running and cutting, cause shear forces of talus within mortise
EASING ACTIVITIES • • • •
Non–weight-bearing activities Antiinflammatories Ice Non–weight-bearing activities allow space between the talus and mortise. Antiinflammatories and ice address inflammation and edema.
24-HOUR SYMPTOM PATTERN • Stiffness caused by inflammation in the morning with gradual resolution • Worsening depends on activity with cumulative effect throughout the day.
PAST HISTORY FOR THE REGION • History of one or multiple ankle sprains of the involved side • Of all ankle sprains, it is estimated that osteochondral lesions occur in 6.5% of these incidents.
PHYSICAL EXAMINATION • Patients often limit weight-bearing activities over the involved limb.This may be seen as a reduction in stance time during gait or a weight shift away from the involved side with standing. • During non–weight-bearing activities, the involved side takes up the loose pack position of the talocrural joint, approximately 30 degrees plantar flexion.
IMPORTANT OBJECTIVE TESTS • Talar tilt test To assess for medial or lateral instability that would predispose to this type of injury. • Anterior and posterior drawer testing To assess for anterior to posterior stability and for any crepitus or grinding that may indicate a loose body.
Talar Dome Damage
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• Talocrural ROM Active versus passive with attention quantity of each (similarity versus discrepancy), crepitus or catching, and end-feel with PROM. It may indicate loose body within joint.
DIFFERENTIAL DIAGNOSIS • Talar fracture • Syndesmotic sprain or rupture • Anterior or posterior talocrural impingement • Osteoarthritis • FHL, flexor digitorum profundus, or posterior tibialis tendinopathy (for posteromedial lesions) • Anterior talofibular ligament sprain (for anterolateral lesion) • Sinus tarsi syndrome • Seronegative systemic arthropathy • Localized infection
TREATMENT SURGICAL OPTIONS Debridement Mosaicplasty Autologous chondrocyte transplant Drilling or microfracture to stimulate bleeding in the area • Internal fixation • Bone grafting
• Pritsch et al found good results in 13 of 14 patients who underwent arthroscopic debridement. • Tol et al performed a systematic review of treatment options for osteochondral lesions based on 54 studies (684 subjects, average age 26 years, male-to-female ratio not reported).A successful treatment was classified as one that produced a good or excellent result, although there was no information regarding what quantified a “good” or “excellent” result. Calculated surgical success (overall): 75% Fragment excision: 39 patients total, 38% reported successful treatment Excision and curettage: of 11 studies and 141 patients, 78% reported successful treatment Excision, curettage, and drilling: Unable to determine • Nonoperative: In 14 studies with 201 patients, 45% reported successful treatment.
REHABILITATION • Nonoperative treatment • Based on literature, casting with non– weight-bearing or partial weight-bearing status from 3 weeks to 4 months and cessation of sport or activity.
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CONTRIBUTING FACTORS • Structural or functional instability of the ankle complex • Diseases or conditions that would slow the healing process (e.g., diabetes, longterm steroid use, systemic inflammatory disorders, smoking, or sickle cell anemia)
PROGNOSIS • Finger et al reported that 12 out of 41 medial osteochondral lesions developed into arthritis. 34.5 months after autologous cartilage transplant, 85% of patients had good-to-excellent follow-up.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant unrelenting pain: Infection or tumor • Pain that does not change with position: Infection or tumor • History of cancer: Metastatic disease • Fevers and chills: Infection or tumor • Purulent exudate (after surgery): Infection • Allodynia, hyperesthesia, or sympathetic changes: Complex regional pain syndrome
SUGGESTED READINGS Berndt A, Harty M. Transchondral fractures (osteochondritis desiccans) of the talus. J Bone Joint Surg. 1959;41A:988–1020. Bowman M. Osteochondral lesions of the talus and occult fractures of the foot and ankle. In: Porter DA, Schon LC, eds. Baxter’s The Foot and Ankle in Sport. Philadelphia: Mosby, Inc; 2008.
ORTHOPEDIC PATHOLOGY
SURGICAL OUTCOMES
In both nonoperative and operative treatments, immobilization with non– weight-bearing status is part of the protocol, with immobilization lasting anywhere from 6 weeks to several months. Exercise is significant in regaining strength to those muscles that have undergone disuse atrophy not only around the foot and ankle but also along the entire affected lower quarter. • Long-term exercises: Proprioceptive and balance training to prevent inversion ankle injury, which is the most common cause of osteochondral lesions.Also, this helps prevent dynamic instability of the talocrural joint, which can also lead to other foot and ankle disorders. Exercises targeting the proximal hip musculature would assist in prevention, according to Bullock-Saxton, who identified a delay in hip muscle function after severe ankle sprain. For patients who are active in sport, external bracing should be considered.
Section III
• • • •
• After pain resolves, focus is on restoration of ROM and strength. • Postoperative Weight-bearing status and progression of weight-bearing depends on surgical intervention and severity of lesion. Generally, procedures that require regeneration or repair of articular cartilage have a longer period of non–weight-bearing or partial weightbearing status. AROM: Degree of which depends on procedure and healing times Gait training: With and without assistive devices Proprioceptive or neuromuscular reeducation Strengthening Joint mobilization and STM to restore mobility • To decrease inflammation, the clinician should consider the following: Lymphedema massage Myofascial release Joint mobilization AROM in a pain-free range Cold pack Ultrasound Electrical stimulation • Once the inflammation process has decreased, the focus of rehabilitation should be on the following: Restoration of mobility via STM and joint mobilization Restoration of normal gait (within weight-bearing precautions) Balance and proprioceptive training Trop and associates identified rehabilitation using balance discs to prevent occurrence and recurrence of inversion ankle injuries by addressing functional instability and impaired postural control after ankle sprain. • Strength training: Around the ankle and proximal hip musculature Mediolateral sway is controlled primarily at the foot and ankle, secondarily by the hip. • Initial exercises in non–weight-bearing position that actively go through painfree ROM to promote circulation and reduce edema. Must take into consideration any precautions with ROM. • Joint mobilization or manipulation are appropriate in the later phases of rehabilitation to address joint-specific mobility restrictions after immobilization at the talocrural joint, distal tibiofibular joint, and subtalar and tarsal joints. • Massage can be used in early rehabilitation (lymphatic massage or myofascial release) to reduce edema. • In later stages, STM is appropriate to address soft tissue restrictions in mobility. • Exercise has a significant role in preventing recurrence of inversion ankle injuries, specifically those that target proprioceptive and balance training.
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Talar Dome Damage Bullock-Saxton JE. Local sensation changes and altered hip muscle function following severe ankle sprain. Phys Ther. 1994;74:23–37. Finger A, Sheskier M. Osteochondral lesions of the talar dome. Hosp Joint Dis. 2006; 61(3&4):155–159. Hertel J. Functional instability following lateral ankle sprain. Sports Med. 2000; 29(5):361–371.
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Pritsch M, Horoshovski H, Farine I.Arthroscopic treatment of osteochondral lesions of the talus. J Bone Joint Surg Am. 1986;68:862–865. Takao M, Ochi M, Uchio Y, Naito K, Kono T, Oae K. Osteochondral lesions of the talar dome associated with trauma. Arthrosc: J Arthrosc Relat Surg. 2003;19(10):1061–1067. Tol J, Struijs P, Bossuyt P, Verhagen R, van Dijk C. Treatment strategies in osteochondral defects
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of the talar dome: a systematic review. Foot Ankle Int. 2000;20(2):119–126. Tropp H, Askling C, Gillquist J. Prevention of ankle sprains. Am J Sports Med. 1985; 13:259–262. AUTHOR: MILDRED V. LIMCAY
Turf Toe
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BASIC INFORMATION DEFINITION • Turf toe is a sprain of the ligamentous and capsular support structures of the first MTP joint, with or without involvement of the tendons of the great toe flexors and extensors, as well as the two sesamoid bones embedded in the flexor tendons. • Classified as the following: Grade I: Strain of the joint capsule, all soft tissue components remain intact. Grade II: Partial thickness tearing of the plantar plate and capsular structures, sesamoids remain in normal position. Grade III: Complete disruption of joint capsule, plantar plate, and collateral ligaments. The plantar plate may have avulsed from its proximal attachment at the distal metatarsal. Sesamoid bones may fracture or displace proximally; and because of the complete disruption of capsule and ligaments, fracture of the metatarsal is possible as a result of impaction.
SYNONYMS
ICD-9CM CODES 845.12 Metatarsophalangeal (joint) sprain
•
•
•
EPIDEMIOLOGY AND DEMOGRAPHICS • Childs reports that there are no age-, gender-, or race-related predispositions to turf toe. • Most patients do experience pain with this injury.
AGGRAVATING ACTIVITIES • Depending on grade of injury Weight bearing Dorsiflexion of the first MTP, passively or actively Plantar flexion of the first MTP, passively or actively Compression of the forefoot, type of shoe worn (tight shoe box) Walking, especially barefoot or in flexible-soled shoes Running Rising up onto toes (heel raise) • Activities and positions that require MTP dorsiflexion place stress on the attenuated or torn plantar support structures. MTP plantar flexion places stress on the attenuated or torn dorsal support structures. In the presence of interarticular edema, symptoms can be aggravated with either position. • With walking, symptoms are exacerbated with weight bearing and progression of the body over the forefoot, thus forcing the great toe into dorsiflexion.
EASING ACTIVITIES
OPTIMAL NUMBER OF VISITS
MECHANISM OF INJURY
3 or fewer
The capsular, ligamentous, and tendinous stabilizers of the first MTP is most commonly injured by hyperextension of the great toe with an axial load (85% of cases). Less common mechanisms include hyperflexion and varus and valgus stress loads to the first MTP.
24-HOUR SYMPTOM PATTERN
COMMON SIGNS AND SYMPTOMS
PAST HISTORY FOR THE REGION
MAXIMAL NUMBER OF VISITS 36
ETIOLOGY • With a hyperextension injury, which makes up approximately 85% of cases of turf toe, the plantar plate, MCL and LCL, and joint capsule are most injured. • Usually the injury is associated with sports activity involving play on artificial turf versus grass. It is more commonly seen with football, baseball, wrestling, basketball, and soccer athletes. • Acute hyperextension injury was reported as 85% of turf toe injuries by Allen et al. Injury occurs during weight bearing with the forefoot planted and first MTP in dorsiflexion when an axial load through the heel, either through pushoff or via external force of another person, drives the first MTP into excessive dorsiflexion. This results in attenuation or tear of the joint capsule and plantar plate off its proximal, looser attachment to the first metatarsal and compression of the dorsal articular surface of the metatarsal head. Severity of damage to these support structures, as well as
• The common presentation for turf toe is as follows: Grade I: Usually no discoloration, but swelling in the dorsum of the forefoot is evident. The patient should be able to bear weight and has mild limitation in motion, especially into dorsiflexion, since this is painful. Grade II: Pain with ecchymosis and moderate edema, especially over the dorsum of the first MTP joint. Patients may avoid full weight bearing on the affected side due to pain, resulting in a limp with gait. ROM is limited, especially into dorsiflexion with pain. Grade III: Severe pain and tenderness with significant loss of ROM, ecchymosis, and edema. Because of severity of pain, patient may not bear weight on the affected side.
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Symptoms depend on use and if swelling is present, and therefore are usually more prominent by the end of day, with time spent on feet and time spent with foot in a gravity-dependent position.
• No history of injury to the foot and ankle to predispose to this injury. • Chronic cases do involve a previous history of one or repeated injury to the first MTP support structures that has caused complete disruption of the capsuloligamentous structures. • In chronic cases as a result of systemic inflammatory disorders, other joints of the foot can be involved.
PHYSICAL EXAMINATION • The patient may avoid weight bearing on the affected side. • With a chronic injury that has resulted in disruption of first MTP stabilizers, deviation or deformity of the great toe may be seen, including angulation medially or laterally, hammer toe, or subluxation. • Intrinsic minus position: MTP extension with interphalangeal flexion may indicate
ORTHOPEDIC PATHOLOGY
• Non–weight-bearing or partial weightbearing activities • Antiinflammatory medication • Pain-relieving medications • Wearing firm-soled or rocker-bottom shoes can prevent extension at the MTP during walking, thus not allowing attenuation of plantar support structures. • Ice:In the presence of acute injury,ice and medication can address inflammation.
Section III
• Sprain of the first MTP • Sand toe
•
additional damage to the sesamoids, proximal phalanges, distal metatarsals, and flexor and extensor tendons, depends on the intensity of the applied load. Acute valgus injury is less common than hyperextension. Mechanism of injury is thought to be the presence of an excessive valgus stress during push-off with the first MTP in a dorsiflexed position. With this mechanism, the MCL, in addition to the joint capsule and plantar plate, is affected. Acute hyperflexion injury, the least common as reported by Childs, occurs with forcible flexion of the first MTP while in a position of first MTP plantar flexion, causing attenuation or disruption of the dorsal joint capsule and compression of the plantar articular surface of the metatarsal head. In acute injuries, nociceptors within ligaments and joint capsule are stimulated with attenuation or tear. Inflammation resulting from ligamentous injury bathes the area in chemical mediators (substance P, bradykinin, etc) that can sensitize neurons, thus perpetuating pain. Edema within the joint can produce feelings of pressure and ache.
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Turf Toe plantar plate avulsion or rupture of the flexor hallicus brevis on one or both of the sesamoids. • Possible tenderness to palpation of the toe flexors and/or extensors caused by guarding, but symptoms are not reproduced.
IMPORTANT OBJECTIVE TESTS • First MTP testing: AROM and PROM In acute injury, both dorsiflexion and plantar flexion is limited, more so, however, toward the direction of the mechanism of injury caused by pain. In subacute and especially chronic phases, hypermobility may be noted toward direction of injury caused by attenuation of capsule and ligaments. If a the toe has a hard or blocked endfeel one should suspect a foreign body within the joint. • Varus and valgus testing assesses for compromise of MCL and LCL of the first MTP. • Accessory mobility: Depending on severity of injury and capsuloligamentous damage, laxity in end-feel and hypermobility in the arthrokinematic motion associated with direction of injury. For example, with the hyperextension mechanism, there may be laxity in end-feel and hypermobility in dorsal glide of the proximal phalanx relative to the metatarsal.
DIFFERENTIAL DIAGNOSIS • • • • • • •
Sesamoiditis Stress fracture Septic arthritis of the first MTP Osteoarthritis of the first MTP Gout RA Intermetatarsal bursitis
TREATMENT SURGICAL OPTIONS • Surgical indicators are as follows: Loose body in the joint Large cartilage flaps Sesamoid fracture or retraction Gross instability of the first MTP Traumatic hallux valgus Significant plantar plate avulsion
SURGICAL OUTCOMES • Surgery is indicated in cases with instability at the first MTP joint and with sesamoid fracture or retraction. In cases of instability, Mullen describes surgery that may involve attempts to repair the capsule directly, or if it cannot be repaired, transposition of the abductor hallicus to stabilize the joint. With a sesamoid
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fracture, removal of the affected sesamoid is performed. • Mullen reports a good result postsurgically and recommends surgery with instability or in cases where conservative care is ineffective.
REHABILITATION • Acute injury RICE Modalities, such as pulsed ultrasound, may be used to help control edema as long as fracture has been ruled out. • Dependent on grade of injury Grade I: The patient should be able to resume sports or activity participation with use of a stiff insole or taping during activity until irritation has subsided. Once pain is reduced, focus shifts to regaining AROM and PROM of the first MTP via joint mobilization, stretching, and exercises. Balance also needs to be evaluated and addressed, especially in the context of the activity the patient would like to return to. Grade II: Requires up to 2 weeks of rest (stopped sports or activity) with more time with toe taped or use of stiff insole as the result of more severe injury to the capsule and ligaments of the first MTP joint. Rehabilitation is similar to that of grade I injury after pain has subsided. Grade III: Rehabilitation usually begins after 4 to 6 weeks of immobilization or postsurgically. Because of the longer period of immobilization, expect adjacent joints to also lose ROM. Until the first stabilizers heal postsurgically or via immobilization, rehabilitation should focus on regaining or maintaining ROM at the talocrural and subtalar joints, protective weight bearing, and prevention of strength loss of the proximal musculature. If tendon transfer was performed, active contraction of the parent muscle is contraindicated until cleared by the surgeon. Once cleared, progression of rehabilitation is similar to that as described. • Return to activity should progress from walking to running to cutting to plyometrics, depending on the type of sport. • To return to the activity or sport, the patient should have painless first MTP dorsiflexion of 50 to 60 degrees. • To decrease inflammation, the clinician should consider the following: Joint mobilization Exercises that promote movement of the region in a pain-free range Cold or hot pack Ultrasound Electrical stimulation Lymphatic massage • Once the inflammation process has decreased, the focus of rehabilitation should be on the following:
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Restoring ROM, balance, and strength Progression to return to sport or activity • Initial exercises In grade I and II exercises, active ROM exercises within pain-free ROM can help reduce inflammation in the region.
CONTRIBUTING FACTORS • Childs identified the following predisposing factors: Previous history of first MTP injury Artificial turf and playing surface Type of sport played (football players more susceptible) Flattened first MTP Foot pronation Hallux degenerative joint disease Increased toe box flexibility and decreased number of cleats in the shoe Pes planus Hypermobility of the talocrural joint
PROGNOSIS • Most recover from turf toe and can return to activity with or without modification in footwear, custom orthoses, or use of a firm plate in the forefoot of the shoe to prevent hyperextension. • Previous episodes can predispose a patient to turf toe again in the future.
SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant unrelenting foot pain: Infection • Pain that does not change with position or weight bearing: Infection • Allodynia, hyperesthesia, sympathetic changes: Complex regional pain syndrome • Streaking along skin toward lymph nodes: Infection • Worsening or non improvement of symptoms: Fracture or infection • Major trauma: Fracture • Fevers and chills: Infection or tumor
SUGGESTED READINGS Allen LR , Flemming D, Sanders TG. Turf Toe: ligamentous injury of the first metatarsophalangeal joint. Mil Med. 2004;169 :14 –24 . Childs SG.The pathogenesis and biomechanics of turf toe. Orthop Nurs. 2006;25(4):276–282. Mullen JE, O’Malley MJ. Sprains—residual instability of the subtalar, Lisfranc joints and turf toe. Clin Sports Med. 2004;23:97–121. Padanilam TG. Disorders of the first ray. In: Richardson EG, ed. Orthopedic Knowledge Update: Foot and Ankle. Rosemont: American Academy of Orthopedic Surgeons; 2004. AUTHOR: MILDRED V. LIMCAY
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Lower Extremity
CHAPTER 6
AUTHORS: KEITH MAHLER and JACKLYN H. BRECHTER
INTRODUCTORY INFORMATION The lower extremities function as the interface between the ground and the rest of the body.They are responsible for propulsion; positioning the head, arms, and trunk; and shock absorption. Mostly, the lower extremities function in a closed-chain manner and are under weight-bearing forces that frequently exceed a person’s body weight. When the lower extremity is injured, patients use compensatory strategies to maintain function. These compensatory strategies place increased stress on other joints in the kinetic chain, even up into the trunk. Frequently, a patient’s dysfunction is the result of these compensatory motions.27 What factors should you consider when rehabilitating lower extremity dysfunctions? Mostly, the lower extremities function in a load-bearing, closedchain manner with forces that range from 1.3 to 5.8 times a person’s body weight.35 These forces can cause compensatory motions, placing abnormal stress on other structures in the kinetic chain and thus causing tissue failure. A patient’s age, gender, static and dynamic postures, biomechanics, morphology, strength-to-weight ratio, and systemic factors all must be considered. Patients who seek care rarely have a dysfunction without multiple contributing factors. Clinicians therefore need to examine the entire lower extremity when there is damage to a single joint. How do these factors affect the rehabilitation process? Abnormal stresses on the lower extremities cause tissue failure to exceed the body’s rate of repair. Clinicians must seek to limit the stress on the affected tissue, allowing for optimal repair. Traditional examples include use of assistive devices, such as canes, crutches, and walkers. Other strategies may include adding cushions in shoes to dissipate shock from ground reaction forces, limit multiplanar motions during an activity (including with tape or bracing), limit dysfunctional postures, and improve motor control and strength. Some patients may need to avoid certain activities for a time as the involved tissue heals. Older individuals can have decreased healing time, altered gait, decreased strength/endurance, decreased tendon and ligamentous extensibility, and decreased neural response related to spatial awareness and joint proprioception. These factors can increase the rehabilitation time and will tend to alter the clinician’s choice of intervention. At the microscopic level, aging causes changes in cartilage or subchondral bone and decreased fluid retention in tendons and ligaments, all resulting in increased tissue stress.These microlevel changes can cause tissue failure at the site, as well as increase stress on proximal and distal joints. For example, a reduced fat pad on the calcaneus causes increased joint reaction forces up the kinetic chain. In addition, cartilaginous changes, including decreased glycosaminoglycan (GAG) binding, decreased fluid retention in matrix, and subchondral stiffening, decrease the lower extremities’ ability to dissipate force.42a Younger individuals may require consideration of issues with bone formation, strength-to-weight ratios, and structural changes. As the long bones are still growing, the clinician needs to consider the effect of the injury on the bones, as well as other tissue. The growth may be what is causing the injury. Furthermore, the exercise selection during rehabilitation should keep in mind the developing state of the musculoskeletal structure. Many parents are pushing children into competitive sports at earlier ages. The clinician should be firm and articulate to educate parents on the results of this excessive stress on the growing bodies.
Females demonstrate a significantly higher incidence of knee injuries. Research points to structural differences such as increased Q angle, decreased strength-to-weight ratios, pelvic position, and increased incidence of genu recurvatum as possible causes for the increased injury rates. Recent evidence links hormonal changes to cruciate ligament damage. This evidence means that clinicians should include some structural measures and cycle information as part of the examination of the female patient. Patients with systemic dysfunction can experience limited tissue repair. These systemic dysfunctions may instead be the cause of tissue failure as well. Patients with diabetes have decreased healing time secondary to the body’s decreased ability to supply oxygen to the tissues and decreased afferent input and efferent response. Patients with autoimmune disorders, such as rheumatoid arthritis (RA) and lupus, can present with multiple joint involvement and decreased ability to participate in regular exercise. Identification of the autoimmune disorder is critical if not already done. If identified, then the rehabilitation process for those with such an autoimmune disorder should be specific to the resulting presentation while respecting the limitations of the disorder. What role does acuteness versus chronic injury play in rehabilitation in a patient with lower extremity dysfunction? Acute injury treatment must first focus on decreasing the inflammation and removing the source of the lesion. Strategies for managing the inflammatory process include removing local swelling with the use of modalities, relative rest to the area, and the maintenance of pain-free passive and active range of motion (ROM). Rest, ice, compression, and elevation (RICE) have been beneficial in decreasing local swelling. Care must be taken, however, when using compression. If the swelling is intraarticular, compression of the affected joint is minimally beneficial and may even be detrimental. Compression at the knee can limit range of motion and irritate extra-articular structures such as bursa along the iliotibial track and hamstrings. A trial of compression may usually be indicated, with individual response guiding the decision-making. During this inflammatory phase, manual therapy techniques also may be used. These should focus on decreasing pain and inflammation, as well as maintaining ROM. Stretching is appropriate in patients demonstrating onset of resistance before onset of pain during ROM testing.With regards to strength, it is the recruitment and motor control that are far more important at this phase than the actual strength.The clinician should remember that pain is inhibitory to muscle function and joint swelling can also be inhibitory to muscle function. Patient education is a critical component of rehabilitation during acute injuries. Patients should be made aware of their own dysfunction, as well as the biomechanical issues related to their particular situation. This patient awareness and understanding of how movements can impact the problem is one of the most important tools a therapist can use to promote a positive outcome. Patients will also benefit from education regarding the phase of healing they are experiencing and how they can help provide the optimal healing environment. Chronic conditions require a closer look a patient’s biomechanics.The therapist must identify compensatory motions either proximal or distal to the area of dysfunction that may contribute to the problem. Further systemic dysfunction must be considered as well. The goal and difficulty for the therapist treating patients with chronic conditions is to identify those factors that are placing excessive loads on the injured tissues. This is often accomplished through motion analysis and primary observation and confirmed through tests and measures during the objective examination.
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Lower Extremity
CHAPTER 6
What factors make treating patients with lower extremity dysfunctions challenging? The lower extremities are subjected to constant repetitive high load on the joints. A patient’s hip joint is subjected to nearly three times the compressive load at the hip during single-limb stance as opposed to double-limb stance. This is due to the increased abductor stabilization force produced to stabilize the contralateral hip. The knee and patellofemoral joints have the highest loads in the body and the thickest cartilage. The ankle and foot must take the initial impact of loading and absorb the shock or transmit the load up the chain. All of the lower extremity joints must be involved for any weight-bearing activity. Therefore the clinician must assess the concert of motions between the foot, ankle, knee, hip, and pelvis during dynamic tasks. Deficits in strength and/or ROM in the lower extremities can cause issues proximal or distal to the affected joint. For example, patients with weak plantar flexors may demonstrate excessive dorsiflexion (DF) during loading in gait requiring excessive knee joint muscle activity for control and excessive internal rotation (IR) of the lower extremity as the end-range of DF is exceeded. Alternately, patients with inadequate DF may demonstrate rapid subtalar joint pronation during loading in gait, causing increased tibia and/or hip internal rotation (IR). Both of these problems and the resulting compensations can lead to abnormal loading at joints other than the one primarily involved and result in further complaints at secondary locations.
The job of a clinician is to restore mobility and function, prevent further deterioration, provide an optimal healing environment, and enhance performance. Treatment should encompass as many of these categories as possible to achieve a good prognosis. The following list of questions should be asked to maximize treatment. • What region is affected? Is the pain coming from that site or is it referred? • Does the patient have a history of lumbar, radiculopathy, or urogenital issues? • Why is that region affected? Is the patient’s tissue failure the result of systemic issues, biomechanical, traumatic, etc.? • What are the contributing factors that lead to the patient’s current condition? Treatment must address ALL of these questions to achieve a successful outcome. In addition, weight is particularly important to rehabilitation of the lower extremities. Since the lower extremities are required to undergo loading in excess of body weight with every step during gait, prognosis is heavily associated with body weight.
PROGNOSIS
EVIDENCE-BASED MEDICINE
How successful is rehabilitation in treating acute lower extremity pain? Rehabilitation of patients with acute or subacute complaints in the lower extremity after first onset have the greatest chance for successful lower extremity rehabilitation. Patients with advanced age, obesity, or significant lower extremity mechanical alignment deviations from normal (among other factors) will have a reduced prognosis than those patients who are younger and fit and have small or no mechanical alignment deviations.
What trends are currently being seen in research regarding rehabilitation of patients with lower extremity pain? Current trends in the literature indicate that researchers are examining treatment effects by gender or age characteristics.* It is heartening to see clinical efficacy studies for children and for female populations.
INTERVENTION Therapists use many techniques to restore a patient’s function. Manual therapy, strengthening stretching, neural mobilization, and modalities are very important tools used in the rehabilitation process. However, every treatment technique has limited benefit if the patient continues to place abnormal stress on the healing tissues. Patient education is one of the most important interventions a therapist can provide. The clinician’s main job is to inform, instruct, and train. It is important to never underestimate a patient’s capacity to learn even complex concepts such as biomechanics, the phase of healing, and the physiological rational for exercise. Furthermore, patients’ compliance will be enhanced if they understand why they must perform home exercises and correct abnormal movement patterns. What interventions have proven the most successful in treating patients with lower extremity dysfunction? Although patient education can be one of the most beneficial interventions a therapist can use, patients may not progress without the addition of manual therapy. Restricted tissue and/ or joints will require manual therapy to restore optimal performance. In general, manual therapy can be beneficial in controlling inflammation, restoring joint motion, and optimizing tissue function. Common techniques include soft tissue mobilization (STM), joint mobilization, manual stretching, and neural mobilization.
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*References 10-12, 22, 24, 25, 28, 29, 46, 47, 51, 56, 58, 61.
REHABILITATION AND COMMON CLINICAL QUESTIONS
Which patients with lower extremity pain derive the greatest long-term benefits from rehabilitation? Patients without the goal of significantly high levels of weightbearing exercises (marathoners, triathletes, etc) derive the greatest long-term benefits from rehabilitation. To achieve optimal outcomes with patients requires careful thought and planning.
What other regions of the body are most likely to contribute to lower extremity pain and dysfunction? Lower extremity pain may be caused by referred pain from the lumbar spinal nerve roots or facets. Lower extremity complaints may also be either caused by or have contributions from the peripheral nerves (neurodynamic tension, peripheral neuropathy, etc.).
Section IV
How successful is rehabilitation in treating chronic lower extremity dysfunction? Treatment of lower extremity complaints can be very successful, even with chronic complaints, providing the clinician can identify the factors that contribute to the complaint. Furthermore, those factors that clinicians identify need to be treatable as opposed to bony or other permanent malalignments. Most often, the chronic complaint has been inadequately treated in the past or some associated factor has not been addressed. As such, patients with chronic complaints that have not responded to rehabilitation should be reexamined (or sent for consult) or the plan should be revised. Factors to consider in this reexamination or revision of treatment intervention include the following: • Referral from other sources (neurodynamic influence, low back pain) • Associated factors such as lower extremity postural alignment (rear foot pronation, hip muscle weakness, etc.) • Activities of daily living (ADLs) required by the patient • Is successful unloading of the joint occurring in a fashion that is sufficient to allow tissue healing?
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CHAPTER 6
What is the physiological rationale behind the use of manual therapy in treating patients? Manual therapy is used to relieve symptoms, increase mobility, and restore biomechanically correct functions. Joint mobilization techniques can be used to increase ROM and decrease painful motions. Grades I and II mobilizations are beneficial in treating painful and inflamed joints. Grades III and IV mobilizations can be used for improving the ROM in hypomobile joints. Grade V mobilizations can be used to restore motions in hypomobile joints, including those joints in which the patient cannot tolerant sustained or oscillatory grade III or IV mobilizations or when the joint has reached a plateau in treatment. Mobilization with movement is another useful technique for treating lower extremity complaints. For these techniques, the mobilization is accompanied by active motion to restore normal joint mobility. Joint mobilizations used for stretching are indicated when the ROM of the joint is limited with a capsular end-feel, or accessory motion testing indicates limited accessory glide in the joint. Soft tissue techniques can be useful for restoring integrity of contractile tissues, decrease fascial restrictions, aid in stretching, and promote blood flow. Further manual stretching can be used to help restore length. Soft tissue techniques for improving ROM are especially useful when there is a muscular end-feel, and the clinician has identified focal restrictions in the muscle tissue. Manual or physiological stretching is indicated if there is a muscular end-feel causing motion restriction and there are no focal restrictions to the muscle tissue.
CLINICAL PEARL How is the treatment intervention selected when ROM is limited? During ROM assessment, determine what structure feels like it is causing the motion restriction (end-feel). Alternately, additional testing for muscle length and accessory mobility can be completed. If the muscle is the limiting factor to ROM, then palpate the muscle for areas of tightness and focal restriction. If focal restrictions are present, treatment should begin with STM to the area of restriction. If focal restrictions are not present, treatment may commence with a physiological stretch or a muscle energy technique. If the accessory mobility is limited a joint mobilization is indicated. Grades III and IV oscillatory techniques are used for stretch, or alternately, a grade V mobilization may be attempted (or may be used if progression from grades III and IV is not sufficient).35a To change the impairment or complaint, the clinician’s choice of treatment must reach the targeted tissue. To this end, trial treatments with subsequent reevaluation are helpful in determining the course of treatment. It is recommended that the clinician use an assess, treat, reassess philosophy to prove that the treatment is justified. With reassessment, a joint restriction may present with a different end-feel, making a new treatment choice ideal. Table IV-6-1 lists some common presentations for the lower extremity. Is joint manipulation recommended for patients with lower extremity complaints? Little research has been completed on the role of manipulation in rehabilitation of lower extremity complaints. However, what has been reported speaks favorably to the use of joint manipulation for the hip, knee, ankle, and cuboid.*
What does evidence reveal regarding the use of massage for the treatment of patients with lower extremity complaints? Massage may be used as STM to improve focal limitations within the muscle.The use of STM has not been well-documented in the literature.† Friction massage is another form of massage that is used to treat tendonitis injuries. Friction massage has some supporting evidence.6,57 Is stretching beneficial or indicated for patients with lower extremity complaints? Stretching is well-documented for its beneficial effects on individual joint ROM and on functional activity. Stretching is being evaluated in the literature for its beneficial effects on injury prevention as well.‡ How should a clinician decide which manual therapy intervention is most appropriate for a patient with lower extremity pain? In determining the appropriate manual therapy intervention, the clinician should use the results of tests and methods from the clinical examination. In particular, when ROM is limited, the clinician should determine what is the limiting factor. Using end-feel assessment is one method and using confirmatory tests is another. Confirmatory tests include muscle length assessments and accessory glide mobilizations. When ROM is limited by muscle length, the clinician should palpate the muscle itself for focal areas of limitation. When such areas are found, the clinician should use STM to improve the tissue mechanics. Physiological stretching is then the treatment of choice to improve ROM. When ROM seems to be limited by the capsule or accessory mobility glides are limited, then the treatment of choice should be an accessory mobility glide. Accessory glides should be performed in the direction of the greatest mobility limitation. Table IV-6-1 indicates the normal direction of accessory glides for movement restrictions in the major joints of the lower extremity and can be used as a guide to selection of joint mobilization direction or direction of stretch.
THERAPEUTIC EXERCISE Manual therapy techniques contribute to restoring ROM of a specific segment whether it is the main complaint or a contributing factor. However, they do not directly address muscular control or weakness that may result in suboptimal function. Therapeutic exercise is the treatment of choice to accomplish this change in muscular control or strength and can be of great benefit for lower extremity function. What is the physiological rationale behind the use of exercise in treating patients with lower extremity complaints? Muscles in the lower extremities contribute to a variety of functions. Muscles are responsible for maintaining static postures such as standing, they must produce motion, they work to attenuate force during loading, and they act to alter bone loading to avoid detrimental forces on the skeleton during function. For ideal performance, muscles must be able to contract in a variety of fashions, isometric and isotonic, fast and slow, and in a coordinated effort to allow force increments as needed. Muscles in the lower extremity also must be able to generate extreme forces sometimes quickly as during direction changes at high speed or in landing and taking off again from a rebound and subsequent shot. Muscular weakness in the lower extremities or inadequate muscle coordination or velocity of contraction may set the patient up
†
*References 5, 13, 14, 33, 40, 41, 43.
‡
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References 6, 18, 20, 23, 26, 34, 39, 42, 44, 57, 62. References 2, 16, 19, 31, 36, 38, 50, 60.
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TABLE IV-6-1 Motion Restrictions Presentation
Motion Restrictions
Posture
Hip flexion
Reduction of lumbar lordosis
Hip extension
Increased anterior pelvic tilt, knee hyper extension, plantar flexed stance
Hip internal rotation
Toe out stance and frequently hip abduction stance
Hip external rotation
Primary Observational Plane/ Compensation Motions
Functional Loss
Sagittal plane: Early lumbar flexion during hip flexion tasks. Sagittal plane: Excessive lumbar extension during hip end-range extension tasks
Early lumbar flexion with gait, sit to stand, and forward bending tasks Excessive lumbar extension with stance and gait, increased pelvic motions during gait
Transverse plane: Lack of contralateral pelvic motion during gait Toe-in stance, squinting patella Transverse plane: motions limited at hip
Treatment plane for the hip is the acetabulum. Knee flexion Hyper extension (if motion loss extreme) else limited knee flexion during ADL’s Knee extension
Sagittal plane: Early lumbar and hip flexion Compensate with frontal plane motions like hip abduction Sagittal plane: compensation seen in frontal plane such as unequal hip height, trunk lean, contralateral abducted stance.
Sagittal plane: Flexed knee, ipsilateral foot pronation, contralateral supination, iliac crest height difference with compensatory lumbar side bend Treatment plane in the knee is the tibial plateau. Ankle dorsiflexion Anterior pelvic tilt, knee hyper Sagittal plane: early heel off, extension, decreased arch excessive/early pronation, hip height internal rotation (loading) then external rotation during swing Sagittal plane: compensation knee flexion
Stretch into hip flexion (knee flexed) / gluteal muscle limited Stretch hip extension if psoas limited, knee flexion with hip extension if rectus femoris is limited Stretch into hip IR if external rotators are limited
Anterior to posterior glide of femur on acetabulum Posterior to anterior glide of femur on acetabulum
Decreased hip rotation in gait, knees Stretch into ER if internal rotators together with sit to stand, may are limited also see excess pronation.
Posterior to anterior glide of femur on acetabulum
Decreased hip rotation in gait, wide based with sit to stand
Stooping and squatting demonstrates staggered stance (affected leg forward), hip hike with step up Decreased dorsiflexion in initial stance, decreased stance time on ipsilateral limb, trunk lean with sit to stand, contralateral hip hike with ascending stairs
Early heel off in gait and squatting activities, excessive rearfoot pronation, hip internal rotation
Stretch knee flexion if quadriceps Anterior to posterior glide of are limited, knee flexion with tibia on femur hip extension if rectus femoris is limited Stretch knee extension, single joint Posterior to anterior glide of knee flexor hypomobility or hip tibia on femur flexion with knee extension if Hamstrings are limited.
Stretch into dorsiflexion (control subtalar joint mobility) with knee flexion if soleus is limited, knee extension with gastroc limited Late heel off in gait, abducted stance Stretch into plantar flexion if with descending stairs. pretibial muscles are limited
ER, external rotation; IR, internal rotation.
Anterior to posterior glide of femur on acetabulum
Anterior to posterior glide of the Talus on the mortise.
Posterior to anterior glide of the Talus on the mortise.
Lower Extremity
Ankle plantar Flexed knee with posterior flexion pelvic tilt Ankle treatment plane is the mortise.
Direction of Joint Mobilization: Moving Bone Direction of Physiological If Capsule or Accessory Stretch/Muscle Limiting Motion Mobility Is Limited
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for joint, bony, soft tissue, or muscular damage. Furthermore, the normal function of the muscle is compromised and may lead to compensatory motions. During the examination, the functional demands of involved or related muscles must be assessed and the choice of therapeutic exercise must match the demands. Therapeutic exercise may be used to improve the muscular control, muscular coordination, and multisegment coordination or for actual strength or endurance, as well as to maintain or improve ROM as part of the rehabilitation process. The muscular control or coordination may be as or more important than the ultimate strength of the muscle. Restoration of muscle function is essential for avoidance of tissue damage and for return to activities. In the event that muscle function cannot be restored, patients should be taught compensatory actions and should develop the muscles required for those compensations. Are exercise programs beneficial in treating patients with lower extremity complaints? Every patient with a lower extremity complaint should be involved in some form of therapeutic exercise. If the involved lower extremity is unable to participate, then the contralateral limb and/or the torso and upper extremities should be involved in some general exercise to maintain or improve overall fitness as the involved joint recovers. Which exercise programs are effective in treating patients with lower extremity complaints? Therapeutic exercise intervention for patients with lower extremity complaints are varied and many. They include interventions that help with stretching, interventions with equipment such as may be found in a health club, or interventions that use Thera-band or Thera-tube for resistance, bodyweight for resistance, functional activities, Swiss ball or weighted-ball exercises with or without a rebounder, etc. Selection should be determined based on what the patient is already using as a work-out method, together with an examination of the current and desired levels of function of the patient. It is critical during the selection process of exercises for the lower extremity to address multiple dimensions of the muscular limitations, as opposed to selecting exercises that each accomplishes only one outcome.
CLINICAL PEARL How can one exercise be used to affect multiple areas of muscle dysfunction in the lower extremity? Since the segments of the lower extremity are connected, what happens to one joint affects other joints. Abduction or external rotation (ER) of the hip places the knee in a more varus alignment. Supination of the foot may do the same via its effect on the tibia. Examining the exercise used for the following case study, the patient is abducting and externally rotating the thigh into the wall (loading the hip abductor muscle and external rotators). The stance limb is being stressed for increasing hip abduction, quadriceps strength, and foot musculature. Quad involvement may be increased by adding a partial squat as DF ROM increases.
CASE STUDY Your patient is a 29-year-old female who reports right anterior knee pain during running (10 minutes). Onset was insidious but reached the 6/10 pain level last week. She reports being unable to run now and is complaining of pain with sustained sitting (after 10 minutes) and going downstairs (every step). Pain has been worsening over the past 5 weeks as she trains for a marathon. Normal or premorbid running mileage is 3 to 5 miles 3 to 4 times per week.
Objective findings include the following: • Step down: Lack of hip control (IR/ER), pelvic drop, and excessive subtalar pronation, with reproduction of pain • Vastus medialis oblique muscle is visibly atrophied. • Hip: Postured in internal rotation right>left, foot in pronation on right • ROM: Knee flexion lacks 20 degrees, prone knee bend reveals rectus tight with knee flexion of 45 degrees and reproduction of pain • Thomas test: Hip 25 degrees F, knee −60 degrees, hip −15 degrees with knee extension • Knee extension full with pain on overpressure • Patella positioned laterally into glide and tilt • Swelling observed around patella and knee joint. • DF limited at −10 degrees with muscular end-feel, no change with knee flexion (soleus limit) • Manual muscle test (MMT): Quads 4/5, hip abductor 3+/5, hip ER 3/5 • Pain to palpation retropatellar and lateral patellar border, lateral soleus thick and knotted with tenderness, rectus femoris thick and sore to palpation distal one-third. Answer This patient exhibits related findings at the foot/ankle, the knee, and the hip. In this case the author elected to treat with the following: • Medial glides and medial tilts (grade IV × 4 at 40 seconds each), followed by reeducation using active assist contractions while maintaining the medial tilt and glide. • DF was addressed beginning with STM to lateral soleus, followed by instruction in home exercise for soleus stretch (controlling for rearfoot position) • Rectus femoris STM to distal one-third, followed by heel to bottom stretch (30 second × 4 with contract relax), followed by home exercise stretch. • Patella taping was used and patient pain complaints were 0/10 during step down. • Exercise was given using standing on contralateral limb with involved knee pressing into wall (ER and abduction) with patient maintaining control of stance foot. Exercise was repeated on the involved leg with the stance limb (involved) controlled for hip, knee, and foot position to restore lower extremity alignment. Patient symptoms and findings were mainly resolved within 3 visits, and she returned to running. Which muscles should be strengthened in treating patients with lower extremity complaints? The clinician should determine the impact of the complaint on the musculature. Of primary importance to the lower extremity are the postural muscles or the antigravity muscles, including the gastrocsoleus, quadriceps, hip abductors, and extensors. However, any muscle, including the foot intrinsic muscles, may be targeted as part of the rehabilitation program. Muscle weakness or other deficits and frequently seen clinical findings that indicate that muscle involvement have been presented (Table IV-6-2). How should a clinician decide which exercise is most appropriate for a patient with lower extremity complaints? Early rehabilitation of muscles should focus on motor control through pain-free ranges beginning with isometric contractions and progressing to concentric motions. Eccentric motions should be limited until the patient is able to use 80% of the joint’s ROM.30 When beginning eccentric strengthening, a patient should begin with slower velocity activities (60 to 120 degrees per second is generally considered a safe velocity). As the patient achieves appropriate control, he or she can progress to full ROMs and functional activities, then increase the velocity of action during the
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TABLE IV-6-2 Muscle Weakness Presentation Affected Joint
Posture
Hip flexion weakness
Anterior pelvic tilt (limited length and/or weakness), posterior pelvic tilt Posterior pelvic tilt, with crouched stance, observed decreased gluteal mass Toe-out stance
Hip extension weakness
Hip internal rotation weakness Hip external rotation weakness
Toe-in stance
Hip abduction weakness
Trunk shift toward ipsilateral side, wide base
Knee flexion weakness
Hyper extension with anterior pelvic tilt Hyperextended in stance
Knee extension weakness
Ankle dorsiflexion weakness Ankle plantar flexion weakness
Ankle plantar flexed Ankle plantar flexed due to decreased use
Primary Observational Plane/ Compensation Motions
Functional Loss
Sagittal plane: Excessive lumbopelvic motions
Decrease stride/velocity in gait, circumduction in swing phase, excessive pelvic motions Sagittal/frontal: Limited hip extension with Stair ambulation, excessive trunk lean frontal plane hip hike to compensate with sit to stand, excessive heel strike in terminal stance (weak hamstrings) Frontal: With wide based tasks, hip Toe-out gait with limited hip rotation, external rotation with hip flexion Frontal: Narrowed stance, hip internal Gait demonstrates limited stance time rotation with hip flexion to extension with adduction in stance phase, knees touch with sit to stand. Frontal:Trunk leans toward affected side Gait demonstrates contralateral hip drop or trunk lean on stance leg. Hip adduction and internal rotation with sit to stand. Sagittal plane: Rapid hyper extension Gait demonstrates pronounced heel strike knees with excessive pelvic motions and rapid knee extension. Sagittal plane: Hyperextension in gait Gait demonstrates limited loading response and limited control in preswing. Sagittal plane: Foot drop during swing Increased hip flexion or toe dragging phase of gait during swing phase of gait Sagittal plane: decreased dorsiflexion Decreased stride length and shorter during terminal stance or knee hyper terminal stance phase of gait extension to compensate for lack of ankle dorsiflexion
functional activities. Competitive level of function is an extremely high level of function and clinicians should retrain for the competition and not just for the motions because competition will increase the magnitude and velocity of the muscle contraction. In the lower extremity, the focus should be on exercises that use multiple joints in functional positions as appropriate for the level of the patient.
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How should a clinician progress an exercise program for the lower extremity complaints? Muscle impairments are frequently measured clinically with MMT. However, MMT does not have the sensitivity to differentiate subtle differences in muscle function. At the knee, a grade 5 MMT may be given when the actual muscle function is as little as 53% of the normal strength of the quadriceps muscle group. At the hip a grade 5 MMT may be given when the actual muscle is only 65% of normal.45 Whereas MMTs are appropriate outcome measures, additional information should be gathered during the examination of patients with lower extremity complaints. Observation of functional tasks will be helpful in determining muscular deficits, as will endurance tests and outcome measures, including function, such as the knee walk test (self-paced), timed “up & go” test, 6-minute walk test,54 hop test,48 or self-report scales such as the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC),54 the Patient Specific Functional Score (PSFS),53 Oswestry Disability Index,17 Lower Extremity Functional Scale (LEFS),4 and others. It is important that function be documented at the onset of treatment so changes with intervention can be measured and monitored. As the patient progresses with an exercise program, the clinician should initially monitor the patient frequently for changes in MMT grades or for observational indicators of quality in performance of the exercises. Progression should be rapid in these early phases as the patient becomes proficient in the activity.The exercise should always be performed correctly but should remain difficult for the patient. If the patient is unable to perform the exercise correctly, then either further explanation or instruction
is required, or alternately, another exercise should be selected. Once the patient is too comfortable with the exercise (exercise is too easy), then there is little further therapeutic benefit and the exercise should be progressed. Functional or subjective outcome measures should be completed weekly or bi-weekly to indicate functional changes and help guide progression as well. Progression may be accomplished in a variety of methods, some options are as follows: • Increase in the number of repetitions (or sets) • Increase in the time of contraction for isometric activities (or exercises involving equipment like the body blade) • Increase in the ROM of the action • Increase in the amount of resistance (including depth in the water or resistance tools in the water) • Increase in the velocity of the action • Increase in the number of participating joints or the complexity of the activity (functional activities) • Increase in the change in directions (adding cutting or increasing the competitive level of the activity) • Addition of unstable surfaces on which to exercise, or other unexpected perturbations The exercises for patients with lower extremity injury must be selected not only to appropriately prepare the musculature for activity but also to prepare the other tissues of the musculoskeletal system for the expected loads of the desired activities. For example, if the patient desires to return to pick-up basketball games 2 to 3 times per week, then the appropriate exercise selection should not be an aquatic exercise program.Although an aquatic program may restore strength and flexibility to the joint, it lacks the impact required to prepare the cartilage and bony tissue for the loads demanded during basketball. A general rule of thumb is to keep the exercise selection and progression as close to the desired activity as possible for optimal rehabilitation times. The exception to this is the patient who requires unloading of a tissue as part of the treatment progression. In these cases, where the activity desired is in excess of the capacity of the tissues, the
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therapist should modify the exercise program until the patient is successful (no increase in symptoms or swelling during or after the exercise activity). At this time, the exercise may be progressed back to the desired level of function. Which modalities have proven most successful in treating patients with lower extremity complaints? The lower extremity has been a frequent source of pathology for the study of treatment modalities. Modalities that are known to be beneficial in the rehabilitation of the lower extremity include heat, cold, electricity, biofeedback, taping, and others. How should a clinician decide which modality is most appropriate for a patient with lower extremity complaints? Cold or electrical therapy in various forms may be used to manage swelling or pain. Heat (hot packs, ultrasound, or general exercises) may be used to assist with tissue extensibility and avoidance of muscle strain or reduction of muscle spasm. Biofeedback may be used to retrain movement patterns. Taping may be used for stability, swelling control, tactile cues, assessment (i.e., for orthotic intervention), and unloading of painful structures. What is the role of bracing or taping in treating patients with lower extremity complaints? In general, joints that are presenting with excessive ROM may require some type of taping or bracing to improve stability. This assistance with stability may be temporary, as the joint recovers (as with knee braces and ankle braces with lateral stays) or it may be permanent as seen with orthotic intervention to control excessive subtalar joint mobility in some patients. Taping for altering the pain presentation of the patellofemoral joint, for Achilles, plantar fascia, or patellar tendon unloading or for navicular lifts is frequently used, but this is not nearly an exhaustive list. Taping may use the McConnell techniques1,9,37,49 or clinicians may use Kinesiotaping.21,52,59 Rehabilitation of the lower extremity may also be enhanced by the appropriate use of orthotic intervention. Current research supports the use of orthotics for altering lower extremity mechanics during interaction with the ground.* What is the role of treatment aimed at neurodynamics in treating patients with lower extremity complaints? Many pathologies in the lower extremity exist together with neurodynamic findings. In general, during an examination of patients with acute traumatic injuries of obvious origin, a neurodynamic examination in not required. However, a large number of patients indicate an insidious onset to the lower extremity complaint. In these patients, the affect of neurodynamic tension on the complaint should be determined. For those patients with chronic or repeat involvement, the neurodynamic component is more strongly suggested. Regardless of the origin of the pathology, the clinician should be aware of the status of the neurodynamic tension in those with lower extremity complaints. The entire kinetic chain becomes involved when any portion of the chain experiences a problem. Over time, as with chronic conditions or with a plateau in treatment progression, the neurodynamic tension should be addressed and included in the treatment plan. Which home exercises are the most beneficial to give patients with lower extremity complaints? Clinicians should carefully select two or three exercises as a home program for patients with lower extremity complaints.
*References 3, 7, 8, 15, 32, 55.
These exercises should be adjusted on a regular basis according to the recovery process and healing timeline. Home exercises should be those that have been completed successfully in the clinic, yet are still difficult for the patient to perform. Examples of home exercises include those designed for muscle strengthening, for maintaining ROM, and for swelling management (as appropriate), or for breaking habitual postures that have been identified as detrimental. As the functional status of the patient increases, the home program should include a partial return to activity to see the affect of the target function on the complaint.
REHABILITATION CLINICAL REASONING How should a clinician decide which intervention is most appropriate for a patient with lower extremity complaints? Intervention is determined according to two factors. The clinician should initially determine what is causing the lower extremity complaint (what tissue is involved) and then determine why that tissue is involved. Intervention is then initially selected to unload the damaged tissue and then to selectively load the tissue in a fashion that continues to produce an increase in the tissue tolerance to load and to change the factors that contribute to the why of the involvement. Monitoring pain or swelling, as well as functional outcome measures, will provide the clinician with an understanding of whether the tissue is improving in its functional capacity. For example, when loading a tissue and pain is reproduced immediately, the clinician should understand that the load is excessive for the present status of the tissue capacity. If pain or swelling are onset latently, it is an indication that the capacity of the tissue has been exceeded or the number of repetitions is too great for the capacity. In this instance, the duration or magnitude of the load or treatment should be reduced but not eliminated. Similarly, with appropriately applied treatments, the functional outcome measures should indicate consistent increase in function. Tissue injury and the intervention of choice have been compiled for reference (Table IV-6-3). Please keep in mind that significant ligament or tendon ruptures will involve surgical intervention and are not represented on this table. After surgical repair, the patient may have a period of immobility required to prevent tearing of the repair, but otherwise, the treatment can progress as shown. What red flags should a clinician be aware of regarding rehabilitating a patient with lower extremity complaints? Clinicians treating patients with musculoskeletal complaints should be certain that those complaints are mechanical. Tests and measures of the musculoskeletal system should be conducted, and the results compiled to reveal such mechanical complaints. Complaints that are not reproduced by mechanical testing should be further examined for systemic or organic involvement. Patients with pathologies of this nature should be referred to the appropriate health care practitioner for further testing. Patients with mechanical lower extremity complaints should also be monitored regularly for cardiopulmonary status. Heart rate and blood pressure should be assessed at base line and at regular intervals during the rehabilitation program. In patients with positive indicators of cardiac dysfunction or elevated blood pressure, the response to any exercise program must be determined and monitored. Should abnormal response to exercise be observed, the patient should be referred to his or her physician for management.
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TABLE IV-6-3 Tissue Injury and Intervention Choice What are the best interventions for the acute phase (0-14 days postinjury)?
What are the best interventions for the When to progress reparative phase When to progress to next phase (15-21 days postinjury)? to next phase
Muscle strain Avoid contraction that Progression is Functional exercises causes complaints, determined by to maintain quality static, or partial ROM the quality and and begin increasing contraction below the magnitude of magnitude of level of complaint. Assess the contraction. contraction as able. muscle mobility and Keep contraction Lengthening of muscle use tack and stretch or below the level as needed, short of STM to improve muscle of pain. pain. extensibility. Muscle Muscle electrical electrical stimulation may stimulation may be used, as can modalities be utilized, as can for inflammation. modalities for inflammation. Ligament sprain Protection of the damaged tissue, maintenance of all other ROM. Gentle maintenance or increase in ROM controlled by target tissue. Modalities for inflammation.
As new collagen tissue is laid down, the tissue needs to be exposed to gentle tension stress.
Tendon pathology Cross-friction massage and Static test indicates unloading. resolving Ice massage after. complaints. Contraction below the level of pain. See muscle tissue as well.
When to progress to next phase
What are the best interventions for the maturation phase (60-360 days postinjury)?
When to progress to next phase
Rapidly increase the level of exercises until there is full asymptomatic ROM and functional activities, either concentric or eccentric.
Side-to-side Include unstable surfaces, differences are velocity retraining, within 20% and cutting or power or muscle has exercises. no negative response to highlevel activities.
STM to assist new tissue Controlled use of in laying down in the the joint with the appropriate direction ligament protected (direction of the force to allow tension the ligament controls). stress to gradually ROM should be full or increase in the near full. healing tissue. Proprioceptive retraining continues throughout rehabilitation program.
Pain and swelling in the tissue are not elicited by the treatment activities, function is improving.
Return to functional As needed functional Continued activities as activities, with or improvement of tolerated by an without external tissue mechanics absence of pain stabilization as required. and absence of and swelling pain or swelling in the involved in the ligament. tissue. Avoid No compensatory compensatory movements are movements. observed.
Eccentric exercises: See muscle Goal of this progression. rehabilitation is to increase the tendon tolerance to force until capacity exceeds demand. See muscle progression.
See muscle progression.
See muscle progression.
See muscle progression.
See muscle progression.
Address soft tissue damage associated with the fracture.
Resolve any range of motion deficits, begin increased compressive loading on the bone below the level of complaint.
Asymptomatic and full range of motion.
Return to full activity as desired.
Asymptomatic in involved tissue.
Cast removal.
Monitor muscle response to exercise using pain and swelling. Should either occur, then the capacity has been exceeded.
Continued on following page.
Lower Extremity
Bone fractur e Stabilization of fracture Fracture site is (refer to physician). asymptomatic or Maintain all other motion at x-rays indicate adjacent segment, unload good bone bone by altering activity healing. level.
Asymptomatic muscle contraction within the available ROM.
What are the best interventions for the remodeling phase (22-60 days postinjury)?
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What are the best interventions for the acute phase (0-14 days postinjury)? Cartilage damage Reduce load on cartilage (decrease time and/ or magnitude of compressive load). Assess and restore ROM deficits, address postural abnormalities.
Capsule injury * Accessory mobility techniques designed to improve fluid mechanics (grades I and II oscillatory). Exercises to address any muscular deficits and to keep/ restore general levels of fitness. Peripheral nerve injury Damage to nerve will require avoidance of stretch or compression to the nerve. Rehabilitation of the involved muscles.
What are the best interventions for the When to progress reparative phase When to progress to next phase (15-21 days postinjury)? to next phase
Asymptomatic with Vigorous restoration rehabilitation of ROM both activities. physiological (stretching exercises AROM and PROM) as well as accessory motions (joint mobilization). Avoid joint swelling or pain complaints as you begin compression through the joint.
What are the best interventions for the remodeling phase (22-60 days postinjury)?
When to progress to next phase
Swelling remains under Progress weight-bearing Swelling and pain control. exercises slowly, are avoided. rapidly increase exercises such as aquatic activities that keep the joint asymptomatic. Continue to address and eliminate postural abnormalities or alignment issues contributing (orthotic intervention, strengthening, stretching, etc).
Begin gentle stretching Pain and swelling Full accessory mobility ROM and swelling to increase accessory should be monitored should be restored. are normal. mobility using grades and improved. Full physiological III or IV oscillatory mobility as well. techniques or traction. Increase vigor of Continue exercises, exercises, make sure begin to move functional activities through pain-free are included. ROM during exercises.
Stable neurological signs. Improving neurological symptoms
Begin isometric or partial ROM exercises short of pain complaints.
Restoration of some nervous function.
Begin STM, flossing, or sustained tension closer to end-range of nerve mobility.
Restoration of nervous Treatment at end range Asymptomatic function, absence of of motion or near it. after treatment, complaints arising continued from treatment. increase in ROM Other associated and function. symptoms are resolved or resolving.
Adverse neurodynamic tension Flossing or STM at areas Stable neurological of focal hypomobility. signs. Improving neurological symptoms
Continue and maintain integrity of associated areas, avoid loss of muscle function in other areas through a comprehensive program.
AROM, Active range of motion; PROM, passive range of motion; ROM, range of motion; STM, soft tissue mobilization. * Capsular tears should be treated as multidirectional ligament sprains. Capsular hypomobility and inflammation response is addressed here.
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When to progress to next phase
As desired activities. Swelling and pain Note, with extensive are avoided. cartilage damage it may not be possible to return to previous level of function as repetitive and extensive weight bearing should be avoided. Lifestyle modifications may be necessary.
As desired activities.
Restoration of Progress activity while nervous function. avoiding further stretch or damage to nerve, avoid onset of neurodynamic tension.
As desired exercises.
Patient remains asymptomatic and function continues to improve.
Continued resolution of symptoms and improvement of function.
Asymptomatic after treatment, continued increase in ROM and function. CHAPTER 6
ROM testing indicates pain onset after resistance (or with resistance).
What are the best interventions for the maturation phase (60-360 days postinjury)?
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TABLE IV-6-3 Tissue Injury and Intervention Choice (Continued)
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SUMMARY STATEMENT Lower extremity complaints are some of the most prevalent complaints the clinician will see in the clinic. It is critical for the clinician to determine the impact of the involved joint on the rest of the lower extremity. In addition, the postural or kinetic alignment of the lower extremity segments must be addressed with every complaint. Exercises and restoration of full asymptomatic ROM cannot be overemphasized for treatment of lower extremity complaints. The lower extremity complaints are the most fun to treat because the clinician may use imagination in the creation of exercise programs that address the needs of the patients.
REFERENCES
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