Updated: Mar 31, 2008
Tendonitis is an inflammatory condition characterized by pain at tendinous insertions into bone. The term tendinosis refers to the histopathologic finding of tendon degeneration. The term tendinopathy is a generic term used to describe a common clinical condition affecting the tendons, which causes pain, swelling, or impaired performance. Because of the fact that most pain from tendon conditions is not actually inflammatory in nature, tendinopathy may be a better term than tendonitis.
Common sites of tendinopathy include the following:
For a related CME activity, see CME - Tendinopathy -- From Basic Science to Treatment.
Tendons transmit the forces of muscle to the skeleton. As such, they are subjected to repeated mechanical loads, which are felt to be a major causative factor in the development of tendinopathy. Pathologic findings include tendon inflammation, mucoid degeneration, and fibrinoid necrosis in tendons. Microtearing and proliferation of fibroblasts have also been reported. However, the exact pathogenesis of tendinopathy is unclear.
Chronic tendinopathy can lead to weakening of the tendon and subsequent rupture.
Middle-aged adults are most susceptible to the development of tendinopathy.
Overuse is the most common etiology.
| Abdominal Pain in Elderly Persons | Gout and Pseudogout |
| Ankle Injury, Soft Tissue | Hand Infections |
| Arthritis, Rheumatoid | Knee Injury, Soft Tissue |
| Bursitis | Plantar Fasciitis |
| Carpal Tunnel Syndrome | Psoriasis |
| Compartment Syndrome, Extremity | Reactive Arthritis |
| Deep Venous Thrombosis and
Thrombophlebitis | Rotator Cuff Injuries |
| Gonorrhea | Tenosynovitis |
Osteoarthritis
The goal of treatment is to reduce pain and to return to activity.
Treatments of tendinopathy are listed below.
An ED consultation is rarely necessary for tendonitis.
The goals of pharmacotherapy are to control pain and decrease inflammation.
These agents are used for the relief of mild to moderate pain. Although the effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen usually is the drug of choice (DOC) for initial therapy. Other options include naproxen and indomethacin.
Usually DOC for treatment of mild to moderate pain if no contraindications are present.
Inhibits inflammatory reactions and pain, probably by decreasing activity of the enzyme cyclooxygenase, which results in inhibition of prostaglandin synthesis.
400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 20-40 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate upward; not to exceed 2.4 g/d
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; cross-sensitivity to other NSAIDs may occur; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of enzyme cyclooxygenase, which results in decrease of prostaglandin synthesis.
200-250 mg PO q6-8h or 500 mg PO bid; not to exceed 1.25 g/d; may increase to 1.5 g/d for limited periods
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d
1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and possibly toxicity of NSAIDs; may decrease effects 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
Documented hypersensitivity; GI bleeding or renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
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 persistent leukopenia, granulocytopenia, or thrombocytopenia)
These agents have both anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability. Dosage varies with degree of inflammation and size of affected area.
4-16 mg intralesionally (0.5-1 mL) mixed with equal or double volume of 1% local anesthetic (ie, lidocaine)
<12 years: Not established
>12 years: Administer as in adults
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, PUD, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Use 0.5-1 mL (40 mg/mL) mixed with equal or double volume of 1% local anesthetic (ie, lidocaine). Dosage varies with degree of inflammation and size of affected area.
Tendon sheath inflammation: 4-30 mg intralesionally
Not established
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Documented hypersensitivity; viral, fungal, or tubercular skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hyperglycemia, edema, osteonecrosis, PUD, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Use 0.5-1 mL (25 or 50 mg/mL) mixed with equal or double volume of 1% local anesthetic (ie, lidocaine). Dosage varies with degree of inflammation and size of affected area.
5-12.5 mg intralesionally
Not established
Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia
Documented hypersensitivity; viral, fungal, or tubercular skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis
[Best Evidence] Warden SJ, Kiss ZS, Malara FA, Ooi AB, Cook JL, Crossley KM. Comparative accuracy of magnetic resonance imaging and ultrasonography in confirming clinically diagnosed patellar tendinopathy. Am J Sports Med. Mar 2007;35(3):427-36. [Medline].
Warden SJ, Metcalf BR, Kiss ZS, Cook JL, Purdam CR, Bennell KL, et al. Low-intensity pulsed ultrasound for chronic patellar tendinopathy: a randomized, double-blind, placebo-controlled trial. Rheumatology (Oxford). Apr 2008;47(4):467-71. [Medline].
Adler RS, Finzel KC. The complementary roles of MR imaging and ultrasound of tendons. Radiol Clin North Am. Jul 2005;43(4):771-807, ix. [Medline].
Biundo JJ Jr, Mipro RC Jr, Fahey P. Sports-related and other soft-tissue injuries, tendinitis, bursitis, and occupation-related syndromes. Curr Opin Rheumatol. Mar 1997;9(2):151-4. [Medline].
Biundo JJ, Irwin RW, Umpierre E. Sports and other soft tissue injuries, tendinitis, bursitis, and occupation-related syndromes. Curr Opin Rheumatol. Mar 2001;13(2):146-9. [Medline].
Crawford JO, Laiou E. Conservative treatment of work-related upper limb disorders: a review. Occup Med (Lond). Jan 2007;57(1):4-17. [Medline].
Garrick JG, Webb DR. Sports Injuries: Diagnosis and Management. Philadelphia, Pa: WB Saunders; 1990.
Gold L, Igra H. Levofloxacin-induced tendon rupture: a case report and review of the literature. J Am Board Fam Pract. Sep-Oct 2003;16(5):458-60. [Medline].
Hales TR, Bernard BP. Epidemiology of work-related musculoskeletal disorders. Orthop Clin North Am. Oct 1996;27(4):679-709. [Medline].
Harrell RM. Fluoroquinolone-induced tendinopathy: what do we know?. South Med J. Jun 1999;92(6):622-5. [Medline].
Khaund R, Flynn SH. Iliotibial band syndrome: a common source of knee pain. Am Fam Physician. Apr 15 2005;71(8):1545-50. [Medline].
McLoughlin RF, Raber EL, Vellet AD, et al. Patellar tendinitis: MR imaging features, with suggested pathogenesis and proposed classification. Radiology. Dec 1995;197(3):843-8. [Medline].
Sharma P, Maffulli N. Tendon injury and tendinopathy: healing and repair. J Bone Joint Surg Am. 2005;87-A:187-202. [Medline].
Sorosky B, Press J, Plastaras C, Rittenberg J. The practical management of Achilles tendinopathy. Clin J Sport Med. Jan 2004;14(1):40-4. [Medline].
Tytherleigh-Strong G, Hirahara A, Miniaci A. Rotator cuff disease. Curr Opin Rheumatol. Mar 2001;13(2):135-45. [Medline].
van Tulder M, Malmivaara A, Koes B. Repetitive strain injury. Lancet. May 26 2007;369(9575):1815-22. [Medline].
Wang JH, Iosifidis MI, Fu FH. Biomechanical basis for tendinopathy. Clin Orthop Relat Res. Feb 2006;443:320-32. [Medline].
Wilson JJ, Best TM. Common overuse tendon problems: A review and recommendations for treatment. Am Fam Physician. Sep 1 2005;72(5):811-8. [Medline].
tendonitis, pain at tendinous insertions, lateral epicondylitis, tennis elbow, medial epicondylitis, calcific tendinitis, rotator cuff tendonitis, patellar tendonitis, popliteus tendonitis, iliotibial band syndrome, shinsplints, Achilles tendonitis, supraspinatus tendonitis, bicipital tendonitis, Yergason test, Speed test, Renne test, tendonopathy, tendinopathy, tendinitis
Mark Steele, MD, Associate Dean for Truman Medical Center Programs, Professor, Department of Emergency Medicine, University of Missouri-Kansas City
Mark Steele, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Jeffrey G Norvell, MD, Clinical Assistant Professor of Emergency Medicine, University of Kansas School of Medicine
Jeffrey G Norvell, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard S Krause, MD, Clinical Assistant Professor, Residency Program Director, Department of Emergency Medicine, State University of New York at Buffalo School of Medicine
Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment