You are in: eMedicine Specialties > Orthopedic Surgery > FOOT AND ANKLE Plantar FasciitisArticle Last Updated: Oct 1, 2004AUTHOR AND EDITOR INFORMATIONAuthor: Shepard R Hurwitz, MD, Executive Director Designate, American Board of Orthopaedic Surgery Shepard R Hurwitz is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association for the Advancement of Science, American College of Rheumatology, American College of Sports Medicine, American College of Surgeons, American Diabetes Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Association for the Advancement of Automotive Medicine, Eastern Orthopaedic Association, Orthopaedic Research Society, Orthopaedic Trauma Association, and Southern Orthopaedic Association Editors: James K DeOrio, MD, Director of Foot and Ankle Fellowship Program, Assistant Professor of Orthopedic Surgery, Orthopedic Surgery, St. Luke's Hospital, Jacksonville, Florida; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shepard R Hurwitz, MD, Executive Director Designate, American Board of Orthopaedic Surgery; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: heel pain, plantar heel pain, inflamed fascia, foot deformity INTRODUCTIONBackgroundPlantar heel pain is a common problem in adults. The most common cause of heel pain is inflammation to the dense tissue extending from the calcaneus to the metatarsal region, thus the descriptive term plantar fasciitis. Though not all cases of plantar heel pain are due to plantar fasciitis, an inflamed or damaged fascia may contribute to painful conditions caused by nerve injury or soft-tissue inflammation in local muscle and the fat pad. With the Internet and an increasing public awareness of plantar fasciitis comes greater demand for treatment when time and home remedies do not alleviate pain. The nature of upright human activity is repetitive tensile and compressive stress of the fascia that has a cumulative ability to damage or transform the tissue. Longer lifespans and greater recreational expectations of working adults also are contributing to the volume of patients seeking attention for plantar fasciitis. PathophysiologyThe functional role of the plantar fascia still is being defined through basic research. One role is the so-called windlass mechanism, which is a vital connection between the hindfoot and forefoot, important in stance and gait. Cadaver studies indicate that cutting the plantar fascia weakens the medial longitudinal support of the arch and increases tensile force in other ligaments and the posterior tibial tendon. The plantar fascia contributes more mechanical support to the arch than does the spring ligament, plantar ligaments, or intrinsic muscles. Changes within the fascia substance may initiate dysfunction, or the histologic changes may be secondary to a damage or disease process. Current evidence indicates that normal cells and extracellular matrix are not associated with pain. The origin of the plantar fascia on the calcaneus is an area that has fibrocartilage at the site of attachment to bone. This specialized zone of tissue has longitudinal fibers of collagen to resist tension but is metabolically active in the formation of cartilage. Therefore, the healing response may lead to calcified cartilage and eventual bone formation. There is a rich pattern of sensory innervation within the plantar fascia that includes the tissue near the attachment to the calcaneus. This may explain why repair processes beneath the heel are so painful. Plantar fascia pain may be due to long-term damage with incomplete repair leading to an endless cycle of reparative attempts by the local tissue. The chemical mediators of inflammation most likely are the proximate cause of pain, thus the pain-relieving effects of anti-inflammatory medication reported in clinical experience. The actual repair of torn collagen fibers may be impaired by the mechanical demands of the plantar fascia with repetitive high loading in both tension and compression. Another process affecting the fascia from within is myxoid degeneration and replacement of normal matrix with abnormal substances that are mechanically inefficient. Spontaneous rupture of all or part of the fascia may occur in extremely high-load situations, and the natural healing of torn fascia often is complicated by painful scar formation. FrequencyUnited StatesThe prevalence of heel pain, particularly plantar fasciitis, has not been reported, and the incidence cannot be determined at present. No epidemiologic surveys have been taken for this condition. The general consensus from the orthopedic, podiatric, and general medicine literature is that plantar fasciitis is a common condition in adults older than 40 years. Mortality/MorbidityMorbidity associated with plantar fasciitis primarily is the pain of weightbearing activity. Patients who rupture the fascia acquire a characteristic foot deformity that is similar to pes planus: collapse of the longitudinal arch, valgus of the calcaneus, and abduction of the forefoot. The collapsed foot may require custom insole orthotics and accommodative shoes or corrective surgery to realign and fuse the hindfoot. The morbidity of surgery includes the same collapse of the foot due to the intentional disruption of the plantar fascia. Surgical morbidity may add considerable impairment if a calcaneal nerve branch is injured. Work activity and many daily living activities may be limited by the degree of plantar heel pain. Mortality data from this condition are not available, though of itself, plantar fasciitis is not a lethal condition. The notable exception is the rare soft-tissue sarcoma in the foot, as when fibrosarcoma of the plantar fascia is the pathological condition. An estimated 30 such sarcomas of the foot are reported annually in the United States. Due to the delay in diagnosis of most soft-tissue sarcomas of the foot, the 5-year survival rate is less than 10%. RaceDifferences based on race have not been reported, but risk factors have been identified. SexDifferences based on sex have not been reported, but risk factors have been identified. AgeAs mentioned, plantar fasciitis is a common condition in adults who are middle aged and older. This may be the result of decreased elasticity and subsequent tearing or a diminished healing response. CLINICALHistoryClinically diagnosing plantar fasciitis is easier than determining the various possible causes. Patients complain of pain underneath the heel that is most pronounced on first arising in the morning or after a period of nonweightbearing activity. The pain often is described as a searing or tearing of the tissues under the heel and often improves with further activity, only to recur following continued or prolonged weightbearing activity. Delays in symptoms are common. Therefore, when pain occurs the morning following physically stressful activity, the patient and physician may overlook strenuous or prolonged weightbearing as a source of the symptoms. Another characteristic of plantar fasciitis is the location of the pain, which usually is at the origin of the plantar fascia from the medial portion of the posterior calcaneus.
PhysicalDiagnosis of plantar fasciitis is confirmed by focal tenderness near the origin of the plantar fascia that often is aggravated by stretching the fascia. On physical examination, heel pain may be reproduced through simultaneous passive dorsiflexion of the toes and ankle. Occasionally, pain radiates along the plantar fascia toward the toes when a tender area is squeezed, and pain may expand to the lateral side of the foot when pressure is applied on the plantar surface of the calcaneus. Causes
DIFFERENTIALS
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| Drug Name | Ibuprofen (Motrin, Ibuprin) |
|---|---|
| Description | DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. |
| Adult Dose | 400-800 mg PO bid/tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when anticoagulants are taken (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy |
| Drug Name | Sulindac (Clinoril) |
|---|---|
| Description | Decreases activity of cyclooxygenase and, in turn, inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators. |
| Adult Dose | 200 mg PO bid with food |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; hypersensitivity to aspirin, iodides, or other NSAIDS; GI bleeding; renal insufficiency |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely, and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if there is persistent leukopenia, granulocytopenia, or thrombocytopenia; caution in anticoagulation defects or are receiving anticoagulant therapy |
| Drug Name | Rofecoxib (Vioxx) |
|---|---|
| Description | On September 30, 2004, Merck & Co, Inc, announced a voluntary withdrawal of rofecoxib (Vioxx) from the US and worldwide market because of its association with an increased rate of cardiovascular events (including heart attacks and strokes) compared to that of placebo. Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited thus GI toxicity may be decreased. Seek lowest dose of rofecoxib for each patient.The suspension dose, 12.5 mg/5 mL or 25 mg/5 mL, may be substituted for 12.5 or 25 mg tabs, respectively. |
| Adult Dose | 25-50 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with fluconazole may cause increase in rofecoxib plasma concentrations because of inhibition of rofecoxib metabolism; coadministration of rofecoxib with rifampin may decrease rofecoxib plasma concentrations |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; severe heart failure and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs or abnormal liver lab results suggesting liver dysfunction Alert: On September 30, 2004, Merck & Co, Inc, announced a voluntary withdrawal of rofecoxib (Vioxx) from the US and worldwide market because of its association with an increased rate of cardiovascular events (including heart attacks and strokes) compared to that of placebo. A major FDA study of rofecoxib found an apparent 3-fold increase in the risk of sudden cardiac death or heart attack among patients who had taken higher doses of the drug compared to the risk of patients who had not recently received similar medication. The report showed that even patients taking the standard starting dose of 12.5 mg or 25 mg of rofecoxib had a 50% greater chance of heart attack or sudden cardiac death than patients on any dose of celecoxib (Celebrex). The large-scale study was conducted after analyzing the medical records of 1.4 million people insured by Kaiser Permanente in Oakland, Calif, between 1999-2001. Note: The study has inherent limitations in that it is observational, rather than randomized andcontrolled. |
| Drug Name | Celecoxib (Celebrex) |
|---|---|
| Description | Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient. |
| Adult Dose | 100-200 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; severe heart failure and hyponatremia, because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction, or in abnormal liver lab results |
| Drug Name | Meloxicam (Mobic) |
|---|---|
| Description | Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators. |
| Adult Dose | 7.5-15 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; active GI bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia) |
Article Last Updated: Oct 1, 2004