Evaluation and Management of Foot Pain
Evaluation and Management of Foot Pain
Authors: Timothy Rupp, MD, FACEP, Methodist Health System and Children's Medical Center of Dallas, TX, University of Texas Southwestern Medical Center, Dallas; and Robert Hancock, DO, Chief Resident, Division of Emergency Medicine, University of Texas Southwestern, Dallas.
Peer Reviewers: Carl Menckhoff, MD, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Medical College of Georgia, Augusta; and Stephen Geller, DPM, FACFAS, Director, Podiatric Medical Education, Maricopa Medical Center, Phoenix, AZ.
This article originally appeared in the January 22, 2007 issue of Emergency Medicine Reports.
The primary care physician is often asked to deal with foot pain. This issue covers many of the common chronic and acute conditions that plague patients and provides differential diagnoses and therapeutic approaches. A good referral list to an interested podiatrist or orthopedic surgeon specializing in foot and ankle conditions is always welcome.
—The Editor
Anatomy of the Foot
Skeletal Structures: Bones, Joints, Ligaments, and Tendons. The foot is divided into three anatomic regions: the forefoot, made up of the fourteen phalanges and the five metatarsals; the midfoot, made up of the navicular, the cuboid, and the three cuneiforms (the medial, the middle, and the lateral); and the hindfoot, made up the talus and calcaneus. There are two large sesamoid bones located adjacent to the first metatarsophalangeal (MTP) joint, one located medially and the other laterally, both of which are embedded within the flexor hallucis brevis tendon. Another sesamoid bone is located beneath the fifth MTP joint, although not consistently.1
The joint between the forefoot and the midfoot, the tarsometatarsal joint, is called Lisfranc's joint. The joint between the midfoot and the hindfoot is called the transverse tarsal joint, or the Chopart joint, and consists of the talo-navicular and the calcaneo-cuboid joints. The subtalar joint refers to the articulation of the talus with the calcaneus and the navicular.
The transverse ligaments join the second, third, fourth, and fifth metatarsal bases. Lisfranc's ligament joins the medial cuneiform and the base of the second metatarsal. The second metatarsal is recessed into a mortise formed by the cuneiform bones and is the primary structure stabilizing the tarsometatarsal joint complex of the foot.3 The calcaneonavicular (spring) ligament holds the talus and the arches in place.2
The Achilles tendon extends from the distal aspect of the gastrocnemius muscle and attaches to the calcaneus, plantar-flexing the foot at the ankle and lifting the heel at the end of the step. The tibialis anterior tendon inserts onto the medial cuneiform and the base of the first metatarsal and inverts the foot and dorsiflexes the ankle. The tibialis posterior tendon passes beneath the flexor retinaculum on the medial side of the ankle and inserts on the navicular tuberocity and cuneiform bone, preventing pronation from occurring while running. The tendons of the flexor hallucis longus and flexor digitorum longus also pass underneath the flexor retinaculum. The flexor hallucis longus inserts on the distal phalanx of the great toe, flexing the great toe, elevating the arch, and assisting in plantar flexion of the ankle. The flexor digitorum longus tendon inserts onto the distal phalanges of the lateral four digits and flexes the distal phalanges. The peroneus longus tendon runs behind the lateral malleolus and inserts at the lateral margin of the medial cuneiform and the proximal end of the first metatarsal and aids in plantar flexion, ankle flexion, and foot abduction.2,3 The peroneus brevis tendon runs behind the lateral malleolus and inserts on the base of the fifth metatarsal, flexing the ankle and everting the foot. Both structures run through the peroneal tunnel.
Neurovascular Structures. The anterior tibial and the posterior tibial arteries are branches of the popliteal artery and provide the blood supply to the foot. The anterior tibial artery creates the dorsalis pedis pulse palpable on the dorsum of the foot. The posterior tibial artery passes behind the medial malleolus, creating the posterior tibial pulse palpable there, and then divides into the medial and lateral plantar arteries. The plantar arch is formed by the anastomosis of the lateral plantar artery and the dorsalis pedis.2 The largest branch of the posterior tibial artery, the peroneal artery, arises high in the leg and courses downward in the posterior compartment, lateral to and deeper than the posterior tibial artery. It branches through the interosseous membrane to supply blood to the muscles in the anterior compartment and branches into a nutrient artery to the fibula. After sending off an anterior perforating artery, the peroneal artery ends as the lateral calcaneal artery.4
Innervation of the foot is variable. The superficial peroneal nerve supplies the peroneal muscles and provides sensation to the dorsum of the foot. The deep peroneal nerve supplies the tibialis anterior, the extensor digitorum longus, and the extensor hallucis longus muscles and provides sensation to the first web space. The saphenous nerve provides sensation to the medial leg, the ankle, and the hindfoot. The posterior tibial nerve innervates the flexor digitorum longus, the posterior tibialis, the gastrocnemius, and the soleus muscles, and provides sensation to the posterior calf. Branches of the tibial nerve include the medial and lateral plantar nerves, which supply the medial and lateral plantar surfaces, and the medial calcaneal nerve, which provides sensation to the medial and plantar heel. The sural nerve is formed by branches of the tibial and common peroneal nerves, and supplies sensation to the lateral foot.5
Differential Diagnosis and Approach to the Acutely Painful Foot
Disorders of the Great Toe. Acute pain affecting the great toe may result from onychocryptosis, paronychia, arthropathy of the first metatarsophalangeal joint, hyperextension sprain of the first metatarsal joint, or acute fracture. Chronic pain affecting the great toe may result from hallux valgus deformity, neuropathy, sesamoiditis, or sesamoid stress fracture, although acute exacerbations of these painful conditions may prompt a visit to a health care provider for evaluation and management.
Disorders of the Second through Fourth Toes. Acute pain affecting the second through fourth toes may result from acute fracture, dermatophyte infections of the web spaces of the toes, and interdigital nerve entrapment. Chronic pain affecting the toes may result from nerve entrapment proximal to the toes from conditions like tarsal tunnel or occasionally result from plantar fasciitis.
Disorders of the Forefoot. Acute pain affecting the forefoot may result from acute fractures and dislocations of the meta-tarsals. Chronic pain affecting the forefoot region may be the result of tarsal tunnel, plantar fasciitis, and stress fractures involving the metatarsals, and acutely painful exacerbations of these conditions may prompt evaluation.
Disorders of the Midfoot. Painful conditions affecting the midfoot include pain from acute fracture and dislocation. The midfoot is perhaps the most stable structure in the foot complex, and as such, it is prone to more chronically painful conditions such as plantar fasciitis, tarsal tunnel syndrome, and stress fractures.
Disorders of the Hindfoot. Acute pain affecting the hindfoot may be the result of acute fracture, apophysitis, and plantar fasciitis. Although apophysitis and fasciitis may be chronic conditions, acute exacerbations may prompt emergency department evaluation and management.
Disorders of the Arch and the Plantar Surface of the Foot. Acute pain of the arch and plantar surface of the foot may be the result of a superficial dermatophyte infection, plantar fasciitis, or tarsal tunnel. Chronic disorders affecting the arch and the plantar aspect of the foot, like neuropathy secondary to diabetes mellitus, can result in acute exacerbations of neuropathic pain, pain secondary to osteomyelitis, or painful skin ulceration.
Evaluation of the Foot
A problem-focused history and physical assessment usually is sufficient to make the diagnosis. The mechanism of injury alone often will narrow the differential diagnosis, and a thorough history often will help in the diagnosis of other non-traumatic causes of foot pain. As with any patient, the most important information can be gathered using the PQRST mnemonic (Provocation, Quality, Radiation, Severity, and Temporal factors).
The physical exam should begin in areas away from the affected area and slowly move toward the most affected area. It is important to expose the patient's entire leg to evaluate for other injuries. The entire foot and ankle should be palpated for tenderness. This is especially important with fractures that are difficult to evaluate with plain radiographs, particularly stress fractures. As with any extremity injury, a neurovascular exam also should be performed. Inability to bear weight often is a sign of significant injury.
The arches of the foot should be evaluated in both the weight-bearing and non-weight bearing positions. The medial longitudinal arch is expected to have an apex of 1 centimeter when the patient is weight-bearing. A low arch, or pes planus, may be congenital or associated with trauma, posterior tibial tendon dysfunction, rheumatoid arthritis, or contraction of the Achilles tendon. A high arch, or pes cavus, may be idiopathic or associated with congenital or acquired neurologic disease.5
The skin of the foot should be examined for evidence suggesting infectious disease, immunological or circulatory problems, and abnormal loading or weight-bearing.
A detailed discussion of gait biomechanics is beyond the scope of this article. Antalgic gait, however, or gait in which the stance phase is shorter on the affected side, can be encountered in any condition that causes pain in the lower extremity. Antalgic gait results in a shorter stride length on the uninvolved side and an overall decrease in walking velocity.5
Plain radiographs of the foot typically consist of AP, lateral, and oblique views. The forefoot and midfoot are best evaluated with the AP view. The hindfoot is best evaluated with the lateral view. Unfortunately, many significant injuries to the hindfoot and midfoot often are missed on plain radiographs. Computerized tomography (CT) should be performed when the clinician has a high index of suspicion despite normal plain films. Magnetic resonance imaging (MRI) and bone scans are optimal for diagnosing stress fractures, but these may not be readily available.
The Ottawa Ankle and Foot Rules are validated clinical decision rules designed to help clinicians save time and money by avoiding unnecessary radiographs of the midfoot and ankle.6 They may not be appropriate for children, pregnant women, injuries over 10 days old, or diabetics. Patients who are unable to bear weight for at least four steps immediately following the injury or those who demonstrate tenderness over the posterior aspect of the medial or lateral malleoli, over the navicular, or over the base of the fifth metatarsal should have radiographs performed. The Ottawa rules have a high sensitivity in adult patients (0.3% false negative rate) and a 100% sensitivity rate in pediatric patients, although the specificity is around 30-40%.7
Dermatologic Disorders
Tinea Pedis. Tinea pedis usually presents with macerated tissue in the web spaces between the toes, most commonly between the third and fourth toes, and between the fourth and fifth toes, but it also may present in a moccasin-type distribution with dry scaling and erythema. When complicated by secondary bacterial infection, pruritis, and malodor, it is referred to as dermatophytosis complex or athlete's foot.8 Skin scrapings demonstrating hyphae or fungal cultures of the affected area may be used to confirm the diagnosis. Treatment usually includes topical antifungal preparations, and care should be taken to minimize spread and to prevent recurrence.5,9
Onychocryptosis. Onychocryptosis, or ingrown toenail, often is caused by improperly fitting footwear, improper trimming of toenails, trauma, or infection. Ingrown toenails occur as a result of the corner of the toenail digging into the surrounding skin, causing pain, redness, and in some cases, infection. Treatment includes both local and systemic care, complete or partial removal of the affected nail, and, in select populations, matricectomy with silver nitrate, phenol, or carbon dioxide laser to reduce the rate of recurrence by preventing nail regrowth.5,10
Paronychia. Paronychia is an infection of the periungual soft tissue and appears most commonly in association with an ingrown toenail, but other dermatologic conditions such as psoriasis and tinea pedis can cause separation of the proximal nail fold and can predispose to infection. Treatment of acute paronychia is considered a nail emergency both because of pain but also because pressure on the nail matrix can retard proper nail growth. If the abscess is collected under the proximal nail fold or around the base of the nail ("runaround"), avulsion of the proximal third of the nail plate allows drainage of the pus. If the collection is in the lateral nail fold, partial avulsion of a lateral strip of nail plate may be performed, although elevation of the lateral nail fold usually is adequate to permit drainage of pus. Systemic antibiotics may be prescribed if there is surrounding infection.11,12
Onychomycosis. Onychomycosis is a nail infection caused by yeast, mold, or fungi that occurs preferentially in traumatized nails. Commonly encountered in athletes, onychomycosis occurs in 30% of patients who have dermatophyte infections of other body sites, most often tinea pedis. The oral antifungal terbinafine is the agent of choice for the management of onychomycosis caused by dermatophyte infections.8 Onychomycosis caused by yeasts or molds other than the dermatophytes may require broader spectrum agents such as itraconazole for management.
Metabolic Conditions
Diabetic Foot Infections. Diabetic neuropathy is one of the most common long-term complications of type 1 and type 2 diabetes mellitus. Foot ulceration is considered a precursor condition for the development of gangrene and subsequent limb loss. Neuropathy increases the risk of amputation 1.7-fold; 12-fold if there is a deformity associated with neuropathy; and 36-fold if there is a history of previous ulceration. There are 85,000 amputations annually in the United States, one every 10 minutes, and diabetic neuropathy is considered to be the major contributor in 87% of cases.13,14
Infection is diagnosed clinically based upon the presence of pus or at least two of the following physical signs: redness, warmth, swelling, induration, pain, and tenderness to palpation. Aerobic gram-positive cocci, namely Staphylococcus aureus, are the most commonly identified organisms, although individuals with chronic infections or those who recently have been treated with antibiotics are predisposed to infection with gram-negative rods. It is recommended that wounds be cultured prior to the initiation of antibiotic therapy to ensure appropriate coverage, and it is advocated that tissue specimen be obtained for biopsy via curettage or direct aspiration, rather than wound swab.14
Antibiotic therapy is recommended, in addition to cleansing, debridement, and off-loading of pressure, for the successful management of diabetic foot infections. No single drug or combination of drugs appears to be more effective than another. It is recommended that initial therapy be rather broad in spectrum and be based on the severity of infection. Appropriate choices include ofloxacin, piperacillin-tazobactam, levofloxacin plus clindamycin, and vancomycin, although the newer agent linezolid has demonstrated equivalent or superior results to vancomycin when managing complicated skin and soft-tissue infections, even those infections due to methicillin-resistant Staphylococcus aureus.15,16 Fluoroquinolone antibiotics, however, have been associated with increased development of methicillin resistance in both S. aureus and in gram-negative bacilli, such as Pseudomonas aeruginosa.17
Hospitalize a patient with a diabetic foot infection if any of the following criteria are met: systemic toxicity, metabolic instability, rapidly progressive or deep tissue infection, the presence of substantial necrosis or gangrene, evidence suggestive of ischemia, inadequate home support, the inability to care for oneself, or the requirement of urgent diagnostic or therapeutic interventions. Surgery is recommended for foot infections that result in the formation of abscess, infections complicated by extensive bone or joint involvement, the presence of crepitus, substantial necrosis of gangrene, or necrotizing fasciitis. The goal of surgery is the removal of devitalized tissue, the revascularization of the affected area, and the reconstruction of soft-tissue defects or mechanical misalignments.14
Osteomyelitis. Osteomyelitis is the spread of infection to the bone and is one of the most difficult aspects of the management of diabetic foot infections. The diagnosis should be considered if the patient demonstrates: deep or extensive ulceration, especially that which is chronic or overlies a bony prominence; an ulcer that does not heal after at least six weeks of appropriate therapy and off-loading; bone that is visible or that can be palpated with a probe; a swollen foot with a history of ulceration; a red, swollen toe; an unexplained elevated white blood cell count or another inflammatory marker; or radiographic evidence suggestive of bone destruction beneath an ulcer.14 The management of osteomyelitis includes at least four to six weeks of antibiotic therapy. Although the role of amputation is controversial, surgery traditionally has been advocated for the management of osteomyelitis in addition to antibiotic therapy. Bony changes on x-ray may not be seen for 10-21 days. When bone loss is seen on x-ray, there is significant destruction of bone. Patients with osteomyelitis generally require admission, antibiotics, and consultation with orthopedics. MRI or bone scan can be helpful when x-rays are negative. Amputation remains an adjunct therapy in the management of osteomyelitis that must be considered.
Gout. Gout arthropathy, characterized by the deposition of monosodium urate crystals as a result of extracellular urate supersaturation, in most cases affects the joints of the distal lower extremity. The first metatarsophalangeal joint is the most common joint involved in initial attacks of gout arthropathy, although as the course of the disorder progresses, the knee joints, shoulder joints, hip joints, and even the spine and sacroiliac joints may become involved.
Primary gout is the result of underexcretion or overproduction of uric acid, resulting in the precipitation of monosodium urate crystals; secondary gout is the result of disorders or therapies that lead to hyperuricemia. Gout is estimated to affect 8.4 per 1,000 individuals based on self-reporting, but may be as high as twice that number.18 The risk factors for the development of gout arthropathy include male sex, middle age, obesity, hypertension, alcohol consumption, and the use of certain medications—corticosteroids, diuretics, and cytotoxic drugs like cyclosporine.
The diagnosis of gout arthropathy is made by observing the presence of needle-shaped, negatively birefringent monosodium urate crystals on joint aspiration using polarizing light microscopy. The differential diagnosis of gout arthropathy includes pseudogout, the deposition of calcium pyrophosphate crystals in the synovium, and can be distinguished from true gout by observing positively birefringent, rhomboid-shaped crystals using polarizing light microscopy.
The management of acute gout arthropathy includes the administration of analgesics, nonsteroidal anti-inflammatory agents (NSAIDs), cyclooxygenase-2 inhibitors, corticosteroids, the uricosuric agents, and colchicine. The NSAID indomethacin has long been considered the anti-inflammatory agent of choice for the management of acute gout arthropathy, although ibuprofen and naproxen sodium also have been advocated.19 Uricosuric agents like probenecid increase the renal clearance of uric acid by inhibiting the renal tubular absorption or uric acid, resulting in reduced urate crystal formation and reduced uric acid level in blood. Colchicine blocks microtubule formation within the leukocytes and prevents migration of the leukocytes to the site of urate crystal deposition. Colchicine causes adverse GI effects, particularly diarrhea and vomiting, in 80% of patients; and complications such as granulocytopenia, disseminated intravascular coagulopathy, renal failure, hepatocellular toxicity, seizures, and shock, have been associated with the use of colchicines.20
Prevention of future exacerbations of gout arthropathy can be achieved with dietary modification, management of underlying medical conditions predisposing the patient to hyperuricemia, and the administration of the xanthine oxidase inhibitor, allopurinol, which interferes with the conversion of hypoxanthine and xanthine to uric acid. Patients should avoid alcohol because it elevates levels of uric acid and therefore can precipitate attacks of gout. Because of the association of gout with atherosclerosis, a low-cholesterol, low-fat diet is advised. While such a diet may help uric acid levels, such advice should be given primarily to help prevent atherosclerosis.20
Peripheral Nerve Conditions
Entrapment syndromes of peripheral nerves of the foot are characterized by pain, paresthesia, and weakness distal to the region of entrapment. Risk factors for the development of entrapment neuropathies include occupations that require crouching, squatting, or kneeling; sitting or tilting back in chairs for prolonged periods of time; improper fitting shoes with poor arch support; and chronic overuse or repetitive movements.
The tarsal tunnel lies beneath the flexor retinaculum on the medial side of the ankle, and tarsal tunnel syndrome refers to the entrapment neuropathy that affects the posterior tibial nerve. Tarsal tunnel syndrome often is caused by a fracture or dislocation involving the talus, calcaneus, or medial malleolus, compressing the nerve within the flexor retinaculum. Patients with tarsal tunnel syndrome present with a complaint of burning pain, aching pain, numbness, and tingling involving the plantar aspect of the foot, the distal foot, the toes, and occasionally the heel, with the pain often being worse at night. A physical examination may reproduce symptoms when the nerve is tapped at the flexor retinaculum inferiorly and posteriorly to the medial malleolus (Tinel's test) or when the maximal eversion and dorsiflexion of the ankle results in compression of the posterior tibial nerve and reproduces the symptoms (the dorsiflexion-eversion test).21,22
Management of tarsal tunnel syndrome includes rest, cessation of repetitive activity predisposing the patient to symptoms, ensuring proper fit of shoes and the use of arch supports, and the administration of analgesics and NSAIDs. It is recommended that patients with suspected tarsal tunnel syndrome be referred to a podiatrist or orthopedist for further evaluation and management. Casting may be necessary for cases of tarsal tunnel syndrome refractive to conservative therapy.
Compression of the common peroneal nerve may result from injury during contact sports, compression from crossing legs, or wearing tight boots or a cast. The result of compression of the nerve is motor and sensory nerve loss, often resulting in partial or complete foot drop. The differential diagnosis of foot drop includes mononeuritis, sciatica, and heavy metal poisoning.21 Management includes identification of possible underlying etiology when possible and referral to podiatry or orthopedics for splinting, physical therapy, and surgical evaluation.
Interdigital entrapment neuropathy may occur as the result of excessive mobility of the fourth metatarsal, impingement of the plantar nerves between the flattened metatarsal heads, or compression of the nerve as it is angulated over the transverse tarsal ligament.21 The entrapment most often occurs between the third and fourth toes on the plantar surface of the foot, although any interdigital space may be involved. Chronic compression of the nerve can result in neuroma formation (the Morton neuroma). Patients present with hyperesthesia of the toes, numbness, tingling, aching, and burning of the distal forefoot. Patients complain that walking on hard surfaces and wearing high-heeled shoes exacerbates the pain, which more often is unilateral in nature. Physical examination suggestive of interdigital entrapment neuropathy includes reproduction of symptoms when direct pressure is applied to the plantar aspects of the third and fourth metatarsophalangeal joints while the metatarsal heads are squeezed together. Conservative therapy is the management of choice and includes rest, wide-toed shoes, and referral to podiatry or orthopedics for orthotic evaluation, corticosteroid injection, or surgical removal of the neuroma.21
Acute and Chronic Painful Conditions of the Foot
Hallux Valgus. Hallux valgus deformity, or bunion, is defined as the lateral deviation of the hallux on the first metatarsal primarily in the transverse plane, although the deformity often involves rotation of the toe in the frontal plane causing the nail to pronate. The angle created by the bisection of the long axis of the hallux and the long axis of the first metatarsal is the hallux abductus angle, and research suggests that an angle of greater than 20 degrees is abnormal.23
The pathophysiology of the hallux valgus deformity is unclear, although increased pressure on the head of the first metatarsal results in its medial-dorsal displacement. Disorders associated with hallux valgus include connective tissue disease, gout, MS and other neurologic disease, trauma, and congenital deformities.
The hallux valgus deformity results in a number of potentially debilitating complications that include: inflammation of the medial bursa protecting the first metatarsophalangeal joint; degeneration of the plantar surface of the metatarsal head; entrapment of the medial cutaneous nerve; hammertoe deformity of the second toe; central metatarsalgia resulting from shifting of weight from the unstable first digit to the central digits; cartilage degeneration; and synovitis.23
Radiographic evaluation confirms the diagnosis made by clinical inspection and assists in assessment of the severity of the deformity and the damage to the articular surface of the first metatarsophalangeal joint.
Management includes modification of footwear, orthotics, night splinting, bunion pads, and NSAIDs. Surgical management, including soft-tissue mobilization, arthrodesis, arthroplasty, osteotomy, or bunionectomy, may be indicated for more severe cases that do not respond to conservative management.
Plantar fasciitis. Plantar fasciitis is a common cause of heel pain, affecting up to 10% of the U.S. population and accounting for nearly 600,000 outpatient visits annually.24 The plantar fascia, or plantar aponeurosis, is a multilayered fibrous band comprised of a central longitudinal portion flanked by medial and lateral portions. It attaches to the three main weight-bearing points of the foot, the calcaneus and the first and fifth metatarsal heads, to form the longitudinal arch of the foot. Although the term fasciitis connotes an inflammatory process, current literature suggests the pathophysiology of plantar fasciitis is more likely related to a degenerative process rather than an inflammatory one.25 Pathophysiologic findings from biopsy suggest that plantar fasciitis is the result of chronic overload on the plantar fascia.26
Plantar fasciitis is encountered in individuals who take part in sporting events that require repetitive jumping or prolonged standing, such as marching, distance running, ballet, and other types of dance. There is an association between both obesity and flat feet and the development of plantar fasciitis. Case studies also have revealed that limited ankle dorsiflexion results in repetitive longitudinal stress placed on the plantar aponeurosis and may be a risk factor for the development of plantar fasciitis.26
A history of plantar fasciitis is suggested by inferior heel pain on weight-bearing, described as throbbing, searing, or piercing, often experienced during the first few steps taken in the morning and improving after further ambulation. Walking barefoot, on toes, or up stairs may exacerbate the symptoms.25 The physical examination reveals local point tenderness best elicited by passive dorsiflexion of the toes and palpation of the fascia from the heel to the forefoot.27 Radiographic evaluation is recommended only for patients who have not responded to conservative management.24,25
Management of plantar fasciitis begins with conservative care including rest, ice, NSAIDs, night splints, and stretching exercises. Simple exercises that stretch the plantar surface (manually dorsiflexing the toes) or taping of the instep (Low Dye taping) may be helpful.28 Shock wave therapy, iontophoresis, and corticosteroid injections along the plantar aponeurosis may be required for severe fasciitis not responsive to conservative therapy. Surgical management involving release of the plantar fascia may be appropriate for the most severe cases resistant to conservative medical therapy.
Sesamoiditis. Sesamoiditis is manifested by pain beneath the head of the first metatarsal with weight-bearing and commonly is encountered in individuals performing repetitive pushing-off or jumping maneuvers, such as those involved in long distance running, tennis, racquetball, football, soccer, and volleyball. Athletic footwear with little insole padding also may predispose to the development of sesamoiditis and sesamoid stress fractures. Pain is present on dorsiflexion of the great toe and evidenced by restricted movement of the first metatarsophalangeal joint.1,3
Radiographic evaluation is recommended to rule out fractures. Stress radiographs and axial loading are helpful, and radiographic evaluation of the contralateral foot is advocated. Partite sesamoid bones are a normal variant and may be confused with sesamoid fractures. Partite sesamoid bones are smooth-bordered whereas sesamoid fractures typically have irregular edges.1 A bone scan may be required, although it is a nonspecific study as both sesamoiditis and stress fractures may display diffuse uptake in the region of the first metatarsophalangeal joint.
Treatment of sesamoiditis and sesamoid stress fractures consists of rest, wearing athletic shoes with well-cushioned soles, and orthotic devices. Anti-inflammatory drugs have been used to treat the pain associated with sesamoiditis and sesamoid stress fractures, though some authors have questioned their efficacy, citing premature return to activity and the potential for delayed bone healing.29,30 Surgical excision of sesamoid bones is a last option for those who fail conservative therapy.
Apophysitis. The apophysis is a growth plate that does not contribute to the linear growth of the bone. The calcaneal apophysis is the anatomical insertion of the Achilles tendon to the calcaneus. Calcaneal apophysitis, or Sever's disease, typically affects children ages 8-12 years and affects boys three times more commonly than girls, particularly those who take part in soccer, basketball, track and field, and gymnastics.31 Children with Sever's disease account for 8% of all overuse injuries in the pediatric and adolescent population.32
Risk factors for the development of calcaneal apophysitis include: increased metabolic activity at the growth plate during episodes of rapid growth; footwear that provides inadequate heel cushioning; footwear with cleats that may center the force of impact on the heel; and overuse in sports that involve jumping or running.31
Physical examination reveals tenderness to palpation on the calcaneus at the insertion of the Achilles tendon; there may also be decreased flexibility of the gastrocnemius-soleus complex and weakness on dorsiflexion of the ankle. Radiographic evaluation is not necessary to make the diagnosis of calcaneal apophysitis, although radiographs may reveal fragmentation and sclerosis of the calcaneal apophysis and may exclude other pathologic processes.
Management of calcaneal apophysitis is conservative, including rest, NSAIDs, stretching exercises, and orthotic use.
Turf Toe. Hyperextension sprain of the first metatarsophalangeal joint, or turf toe, commonly occurs as a result of forced hyperextension of the great toe and subluxation and damage to the joint capsule. The risk factors for the development of turf toe include loosely fitting or overly flexible athletic footwear or excessive running and direction-changing, particularly on hard artificial surfaces. Symptoms include pain and decreased range of motion at the first metatarsophalangeal joint and difficulty when running or changing directions.3
The findings on physical examination that suggest turf toe include redness, swelling, tenderness, and stiffness of the first metatarsophalangeal joint. Pain usually is greatest with end-range dorsiflexion of the foot. The collateral ligaments are stable, but there may be laxity with anterior-posterior translation at the first metatarsophalangeal joint. Radiographic evaluation assists in ruling out other potential diagnoses, such as avulsion fractures and sesamoid fractures. If radiographs are inconclusive, and the patient has failed a course of conservative therapy, magnetic resonance imaging is recommended.32
Conservative management is recommended if the diagnosis is suspected based upon examination. More severe sprains of the first metatarsophalangeal joint may be debilitating, particularly for competitive athletes, and may warrant immobilization and non-weight bearing. Surgery rarely is required.
Stress Fractures. Stress fractures are the result of bone breakage after being subjected to repetitive tensile or compressive forces that individually would be insufficient to cause the bone to fracture. Pain is exacerbated by impact loading and is ameliorated with rest.
Any abrupt change in the duration, intensity, or frequency in physical activity without adequate periods of rest, change in athletic footwear, or change in playing surface may predispose to pathologic changes in bone resulting from an imbalance in bone resorption and formation. Stress fractures occur due to the accumulation of microtrauma from repetitive loading, followed by fatigue failure that leads to the initiation of a crack in the bone. Repetitive loading on the injured bone propagates fracturing of the bone.33
Of all sports-related injuries, it is estimated that 5-10% involve stress fractures, and may be as high as 20% in some sports like running.34 The incidence is increasing because: increasing numbers of people are participating in sports; there is increasing awareness and suspicion of stress fractures; and there have been changes in the nature and type of sporting activities (i.e., rollerblading).
Stress fractures of the tibia, fibula, and metatarsals are the stress fractures most commonly encountered; stress fractures of the navicular demonstrate variable occurrence; and stress fractures of the femur, first metatarsal sesamoid, and pelvis occur least often.35 Stress fractures of the second, third, and fourth metatarsals account for 90% of metatarsal stress fractures. Stress fractures of the fifth metatarsal are relatively uncommon, although they are associated with a high rate of delayed healing and nonunion.36 Because of increased awareness of stress fractures, the incidence of navicular stress fractures has increased based upon data from recent studies.37
The combination of amenorrhea, disordered eating, and osteoporosis (or the female athlete triad) may put women at greater risk for the development of stress fractures.38 Lower bone mineral density, dietary deficiencies in calcium, and consumption of carbonated beverages, particularly cola beverages, may put individuals at risk for the development of stress fractures.38
Initially radiographs may not reveal a stress fracture. The positive findings of periosteal elevation, cortical thickening, sclerosis, or visible fracture line are specific for stress fractures, but the sensitivity of plain radiographs is poor with only 50% of stress fractures seen on plain radiographs. Periosteal and endosteal callus formation typically is seen within 2 weeks of injury, while callus formation reaches its maximum at 6 weeks.3
The criterion standard for the diagnosis of stress fractures is a technetium bone scan, which may be positive as early as 48-72 hours following clinical signs of injury. MRI has been found to be just as sensitive and more specific, but rarely is indicated emergently.3
Management of stress fractures begins with activity reduction for 4-8 weeks. High-impact activity can be resumed gradually thereafter. Casting and crutch-walking is indicated for stress fractures that cause the patient severe pain, and for stress fractures of the navicular.37 NSAIDs have been recommended for acute pain associated with stress fractures, although some authors have cited animal studies that demonstrated impaired bone healing when taking NSAIDs.36 The concern about masking painful symptoms, prompting return to activity and, thus, potentially exacerbating a stress fracture, also has been cited as a deterrent to the use of NSAIDs in the management of stress fractures. Stress fractures of the fifth metatarsal shaft may require prolonged immobilization and surgical fixation to prevent delayed healing and nonunion. Some authors recommend early surgical repair of stress fractures of the navicular to minimize time lost from participation in practice and competition.37
Dislocations and Fractures
Calcaneus Fracture. The calcaneus is the largest of the tarsal bones and the one most commonly fractured, accounting for approximately 60% of all foot fractures and 2% of all fractures.39 Fractures of the calcaneus require a tremendous amount of force, and the mechanism of action that most commonly results in calcaneal fracture is a fall from height, although they also can result from motor vehicle collisions and twisting of the foot with axial loading. Calcaneal fractures, moreover, are associated with injuries of the long bones of the leg and injuries of the vertebrae, as the force of injury is transmitted up from the foot and ankle through the leg to the trunk.
Fractures that involve the calcaneus are divided into those that involve the subtalar joint (intraarticular) and those that do not involve the subtalar joint (extraarticular). Intraarticular fractures are the most common type of calcaneus fracture and account for 75% of all fractures of the calcaneus. Extraarticular fractures of the calcaneus are divided further into those involving the anterior and posterior processes of the bone. Anterior process fractures are more common than posterior process fractures. Anterior process fractures are subdivided further into avulsion and compression fractures, with avulsion fractures being the more common of the two.39
Compression fractures of the calcaneus can be very subtle, and these fractures often are missed on radiographs. When the mechanism of injury or physical exam is highly suggestive of calcaneus fracture, the lateral radiograph should be evaluated by measuring Bohler's angle or the critical angle of Gissane.
Bohler's angle is formed by two lines: one line is formed from the posterior tuberosity of the calcaneus to the apex of the posterior facet; the other line is formed from the posterior facet to the apex of the anterior process. Bohler's angle normally measures between 20 and 40 degrees; Bohler's angle less than 20 degrees is highly suggestive of a compression fracture of the calcaneus.40 The critical angle of Gissane is the angle formed by two strong cortical struts that extend laterally and form an obtuse angle directly inferior to the lateral process of the talus. A normal angle of Gissane measures between 100 and 130 degrees, with a more acute angle being indicative of a compression fracture of the calcaneus.41 A recent study suggests that these angle measurements are of limited use in the emergency department diagnosis of calcaneal fractures. Of emergency department physicians studied, 97.9% were able to make an accurate diagnosis of calcaneus fracture without the benefit of measuring either angle on lateral radiograph.41
Physical examination reveals soft-tissue swelling of the heel and tenderness to palpation. The suggestion of a calcaneus fracture should prompt the clinician to evaluate for associated injuries of the long bones of the leg and the lumbar vertebrae. Calcaneal fractures almost universally require operative repair, although repair often is delayed to allow for resolution of marked soft-tissue swelling.39
Talus Fracture. The talus is the second most commonly fractured tarsal bone.40 The talus distributes the weight of the body during stance and during movement. The tibiotalar joint allows for flexion and extension of the foot at the ankle, and the talocalcaneal joint permits eversion and inversion of the foot.
The blood supply of the talus is precarious, and injury predisposes the talus to avascular necrosis. The talus has both an extraosseous and an intraosseous blood supply.42 The extra-osseous blood supply consists of blood from the anterior tibial, posterior tibial, and peroneal arteries. The talar canal artery is a branch of the deltoid artery that arises from the posterior tibial artery. The intraosseous circulation arises mainly from the anterior tibial and deltoid arteries and creates an anastomosis along the talar dome.
Talar neck fractures carry a high degree of morbidity as a result of avascular necrosis and subtalar necrosis. Talar neck fractures account for 50% of talar fractures and are responsible for 90% of cases of talar avascular necrosis.42 Talar neck fractures occur most often as the result of high-energy injuries that cause hyperdorsiflexion of the foot, such as motor vehicle collisions in which the driver brakes forcefully upon impact. Identification of talar fractures often is done using plain radiographs, although smaller, more subtle talar fractures may be missed on initial radiographic evaluation. Large talar fractures require emergent orthopedic or podiatric consultation, and surgical management usually is required to prevent avascular necrosis or subtalar necrosis.42
Midfoot Fractures. The midfoot is the region of the foot least predisposed to injury because of the inherent stability of the midfoot structures. The navicular is the most commonly fractured bone of the midfoot; cuboid and cuneiform fractures are extremely uncommon.2 Because of its unique morphology and the fact that the navicular serves as the cornerstone of the talonavicular joint, identification of navicular fractures is essential for maintaining congruity of the midfoot. Surgical management often is required to prevent avascular necrosis and nonunion injuries.43 Fractures of the navicular are divided into dorsal avulsion, tuberosity, and body fractures. Dorsal avulsion fractures are the most common type of fracture and account for 47% of navicular fractures.2 Non-displaced fractures most often require casting, although navicular fractures that are displaced greater then 1 mm require open reduction and internal fixation to reduce the risk of avascular necrosis.
Lisfranc's Injury. Injury through the tarsometatarsal joint, or the Lisfranc's fracture-dislocation, is named after Jacques Lisfranc, a field surgeon in Napoleon's army who observed injuries through the tarsometatarsal joint in soldiers whose boots became caught in the stirrup when they fell from horseback. Axial loading on the fixed and plantar-flexed foot is the typical mechanism of injury, as observed in football and rugby players, although tarsometatarsal fracture-dislocations have been observed in windsurfers and snowboarders.3
Recall from earlier discussion of the anatomy of the foot that the second metatarsal rests in a mortise created by the cuneiforms, and that the Lisfranc's ligament attaches the second metatarsal base to the middle cuneiform. This structure serves as the keystone of both the midfoot and the arch. Although fracture of the base of the second metatarsal is pathognomonic for a Lisfranc's injury, the term Lisfranc's injury serves to define a heterogeneous assortment of injuries to the base of the second metatarsal, including fracture, fracture-dislocation, and ligament sprain.2
Disruption of the Lisfranc's ligament can result in mild undetectable subluxations of the metatarsal base to obvious fractures and dislocations. Because of the heterogeneity of presentations, it is understandable that a number of Lisfranc's injuries go undiagnosed during the initial visit to the emergency department.2 Radiographic evidence of a Lisfranc's injury is suggested by any of the following abnormalities: a discontinuity in a line formed from the medial border of the fourth metatarsal and the medial border of the cuboid on oblique view; a discontinuity in a line formed from the lateral border of the third metatarsal base and the lateral cuneiform; a discontinuity in a line formed from the medial border of the second metatarsal base and the medial border of the middle cuneiform; or malalignment between the first metatarsal medially and laterally with the medial cuneiform on anteroposterior radiograph.2 Weight-bearing radiographs can be helpful if initial x-rays are normal.
Because of the importance of the Lisfranc's joint, nearly all Lisfranc's injuries except for simple sprains are aggressively treated with open reduction/internal fixation or percutaneous pinning.
Metatarsal Fractures. Metatarsal fractures are relatively common acute and chronic injuries, particularly in high performance and recreational athletes. Other at-risk populations include elderly women with osteoporosis, decreased physical activity, or benzodiazepine use; and diabetics, especially those who have had diabetes for more than 25 years or those who are more active.44
Acute metatarsal fractures occur as a result of direct injury, such as a crush injury from a heavy object, or indirect injury, such as a twisting injury with the forefoot in a fixed position. Avulsion fractures occur most commonly to the bases of the first and fifth metatarsals. Stress fractures of the second and third metatarsal shafts account for the majority of metatarsal stress fractures.45
Plain radiographic evaluation usually is sufficient to make the diagnosis of metatarsal shaft fracture, although as discussed earlier, initial radiographs may be normal for stress fractures. Weight-bearing radiographs may be required when assessing stability of metatarsal shaft fractures, particularly when evaluating first metatarsal shaft fractures. Fractures of the lesser metatarsals are treated depending on the degree of displacement and angulation: isolated fractures with minimal or no displacement may be treated with a walker boot, hard-soled shoe, or a walking cast with progressive weight-bearing; fractures resulting in angulation greater than 10 degrees and/or displacement of 3-4 mm or greater are treated by open or closed reduction.45
Jones and Dancer's Fractures. Fractures of the proximal fifth metatarsal may pose an important diagnostic challenge for the health care provider. Three separate fracture zones are identified.45 Zone 1 is the most proximal fracture zone and includes the metatarsocuboid articulation, the insertion of the peroneus brevis tendon, and the lateral plantar aponeurosis. Fractures of this zone are most often avulsion-type fractures that occur as a result of inversion (Dancer's or pseudo-Jones fractures). Zone 2 represents the metaphyseal-diaphyseal junction, a site of the true Jones fracture. Fractures at this zone occur as a result of a large adduction force applied to the forefoot when the ankle is plantar-flexed. Zone 3 includes the proximal 1.5 centimeters of the diaphysis, and the majority of injuries to this region are believed to be the result of a stress or fatigue mechanism.45
Distinguishing between the types of fifth metatarsal fractures is important because a difference in millimeters can lead to a different prognosis and management strategy.46 A fracture of the proximal diaphysis, therefore, is more likely to disrupt the blood supply to the diaphysis, inhibiting fracture healing and increasing the risk of nonunion and avascular necrosis.44
Management of fifth metatarsal fractures differs based upon anatomic location of the fracture. Non-displaced avulsion fractures are treated conservatively with a walker boot, hard-soled shoe, or short-leg walking cast. Distraction or displacement to an avulsion fracture greater than 2 mm usually requires open reduction. Acute non-displaced Jones fractures and diaphyseal stress fractures are treated with short-leg casting for 6-8 weeks, although high incidence of delayed union and nonunion have led many clinicians to consider more aggressive operative management of these fractures.45
Fractured Toe. Toe fractures are most often the result of axial loading (stubbing a toe), abduction injury (night-walker fracture), or crush injury from a falling object. Less often, hyperextension or hyperflexion can result in a spiral fracture or an avulsion fracture.47 Plain radiographic evaluation usually is sufficient to diagnose toe fractures.
Management of toe fractures classically has been buddy taping the fractured digit to the adjacent digit, although such therapy has fallen out of favor. Splinting the injured toe to the adjacent toe permits the fractured toe to move with its adjacent toe and does not eliminate movement. The use of a post-operative hard-soled shoe eliminates dorsiflexion of the metatarsophalangeal joint and rests the fractured toe more effectively than buddy taping. Occasionally, short-leg cast is indicated. Toe fractures should be evaluated for potential nail bed injuries and subungual hematomas. Nail removal and nail bed laceration repair remain controversial.47
The management of more complicated toe fractures differs depending on the digit involved. Because of the first toe's crucial role in balance and toe-off phase of gait, fractures with dislocations, displaced intraarticular fractures, and unstable displaced fractures should be referred to an orthopedist or podiatrist for evaluation and management. Lesser toe fractures should be referred for orthopedic or podiatric evaluation and management if they are displaced intraarticular fractures, irreducible fractures, open fractures of the nondistal phalanges, or fractures that do not maintain acceptable position with immobilization.47
References
1. Gravlee JR, Hatch RL. Sesamoid Fractures of the Foot. Up To Date. Available at: http://www.utdol.com. Accessed September 26, 2006.
2. Hals GD, Logan M, Cory J. Management of acute foot and ankle disorders in the emergency department: Part II—Fractures of the foot. Emerg Med Rep 2003;24:277-292.
3. Rupp TJ. Athletic foot injuries. Emedicine.com. Available at: http://www.emedicine.com. Accessed September 26, 2006.
4. Duke Orthopedics. Peroneal artery. Available at: http://www.wheelessonline.com/ortho/peroneal_artery. Accessed December 29, 2006.
5. Young CC, Niefeldt MW, Morris GA, et al. Clinical examination of the foot and ankle. Prim Care Clin Office Pract 2005;32:105-132.
6. Stiell IG, Greenburg GH, McKnight RD, et al. Decision rules for the use of radiography in acute ankle injuries. JAMA 1993;269:1127-1132.
7. Ebell MH. Evaluating the patient with an ankle or foot injury. Am Fam Phys 2004;70:1535-1536.
8. Cordoro KM, Ganz JE. Training room management of medical conditions: Sports dermatology. Clin Sports Med 2005;24:565-598.
9. Johnson R. Herpes gladiatorum and other skin diseases. Clin Sports Med 2004;23:473-484.
10. DeLauro NM, DeLauro TM. Onychocryptosis. Clin Podiatr Med Surg 2004;21:617-630.
11. Holzberg M. Common nail disorders. Dermatol Clin 2006;24: 349-354.
12. Richert B. Basic nail surgery. Dermatol Clin 2006;24:313-322;.
13. Vinik AI, Mehrabyan A. Diabetic neuropathies. Med Clin North Am 2004;88:947-999, xi.
14. Hellekson K. IDSA releases guidelines on the diagnosis and treatment of diabetic foot infections. Am Fam Phys 2005;71:1429-1433.
15. Sharpe JN, Shively EH, Polk HC, Jr. Clinical and economic outcomes or oral linezolid versus intravenous vancomycin in the treatment of MRSA-complicated, lower extremity skin and soft-tissue infections caused by methicillin-resistant Staphylococcus aureus. Am J Surg 2005;189:425-428.
16. Weigelt J, Itani K, Stevens D, et al. Linezolid versus vancomycin in treatment of complicated skin and soft tissue infections. Antimicrobial Agents and Chemotherapy 2005;49:2260-2266.
17. Paterson DL. "Collateral damage" from cephalosporin or quinolone antibiotic therapy. Clin Infect Dis 2004;38 Suppl 4: S341-S345.
18. Becker MA. Clinical manifestations and diagnosis of gout. Up To Date; Available at http://www.utdol.com. Accessed September 26, 2006.
19. Kaplan J. Gout and Pseudogout. eMedicine.com; Available at: http://www.emedicine.com. Accessed October 9, 2006.
20. Francis M, Ranatunga SM. Gout. eMedicine.com. Available at http://www.emedicine.com. Accessed December 29, 2006.
21. Shoen RP. Nerve entrapment syndromes of the leg and foot. Up To Date; Available at http://www.utdol.com. Accessed September 26, 2006.
22. Glazer JL, Hosey RG. Soft-tissue injuries of the lower extremity. Prim Care Clin Office Pract 2004;31:1005-1024.
23. Ferrari J. Hallux valgus deformity (bunion). Up To Date. Available at http://www.utdol.com. Accessed September 26, 2006.
24. Cole C, Seto C, Gazewood J. Plantar fasciitis: Evidence-based review of diagnosis and therapy. Am Fam Phys 2005;72:2237-2242, 2247-2248.
25. Aldridge T. Diagnosing heel pain in adults. Am Fam Phys 2004;70:332-338.
26. Williams SK, Barge M. Heel pain-plantar fasciitis and Achilles enthesopathy. Clin Sports Med 2004;23:123-144.
27. Sheon RP. Plantar fasciitis and other causes of heel and sole pain. Up To Date. Available at http://www.utdol.com. Accessed September 26, 2006.
28. Digiovanni BF, Nawoczenski DA, Malay DP, et al. Plantar-fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis: A prospective clinical trial with two year followup. J Bone Joint Surg Am 2006;88:1775-1778.
29. Stovitz SD, Arendt EA. NSAIDs should not be used in treatment of stress fractures. Am Fam Phys 2004;70:1452, 1454.
30. Wheeler P, Batt ME. Do non-steroidal anti-inflammatory drugs adversely affect stress fracture healing? A short review. Br J Sports Med 2005;39:65-69.
31. Chorley J, Powers CR. Clinical features and management of heel and foot pain in the young athlete. Up To Date. Available at http://www.utdol.com. Accessed September 26, 2006.
32. Pommering TL, Kluchurosky L, Hall SL. Ankle and foot injuries in pediatric and adult athletes. Prim Care Clin Office Pract 2005;32:133-161.
33. Pepper M, Akuthota V, McCarty EC. The pathophysiology of stress fractures. Clin Sports Med 2006;25:1-16, vii.
34. Boden BP, Osbahr DC. High-risk stress fractures: Evaluation and treatment. J Am Acad Orthop Surg 2000;8:344-353.
35. Snyder RA, Koester MC, Dunn WR. Epidemiology of stress fractures. Clin Sports Med 2006;25:37-52, viii.
36. Clugston JR, Hatch RL. Stress fractures of the metatarsal shaft. Up To Date. Available at http://www.utdol.com. Accessed September 26, 2006.
37. Jones MH, Amendola AS. Navicular stress fractures. Clin Sports Med 2006;25:151-8, x-xi.
38. Killie H, Domino FJ, Shaia HJ. Overview of stress fractures. Up To Date. Available at http://www.utdol.com. Accessed September 26, 2006.
39. Germann CA, Perron AD, Miller MD, et al. Orthopedic pitfalls in the ED: Calcaneal fractures. Am J Emerg Med 2004;22:607-611.
40. Perron AD, Brady WJ. Evaluation and management of the high-risk orthopedic emergency. Emerg Med Clin North Am 2003;21:159-204.
41. Knight JR, Gross EA, Bradley GH, et al. Bohler's angle and the critical angle of Gissane are of limited use in diagnosing calcaneus fractures in the ED. Am J Emerg Med 2006;24:423-427.
42. Adelaar RS, Madrian JR. Avascular necrosis of the talus. Orthop Clin North Am 2004;35:383-395, xi.
43. DiGiovanni CW. Fractures of the navicular. Foot Ankle Clin 2004;9:25-63.
44. Hatch RL, Clugston JR. Fractures of the metatarsal shaft. Up To Date. Available at: http://www.utdol.com. Accessed September 26, 2006.
45. Fetzer GB, Wright RW. Metatarsal shaft fractures and fractures of the proximal fifth metatarsal. Clin Sports Med 2006;25:139-150, x.
46. Alsobrook J, Hatch RL. Fractures of the proximal fifth metatarsal. Up To Date. Available at: http://www.utdol.com. Accessed September 26, 2006.
47. Gravlee JR, Hatch RL. Toe fractures. Up To Date. Available at: http://www.utdol.com. Accessed September 26, 2006.
The primary care physician is often asked to deal with foot pain. This issue covers many of the common chronic and acute conditions that plague patients and provides differential diagnoses and therapeutic approaches.Subscribe Now for Access
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