Updated: Apr 10, 2009
Hamstring injuries are common problems that may result in significant loss of on-field time for many athletes because these injuries tend to heal slowly. Once injury occurs, the patient is at high risk for recurrence without proper rest and rehabilitation.
The hamstring muscles are 3 muscles in the posterior thigh: the semitendinosus, semimembranosus, and biceps femoris. The semitendinosus originates at the ischial tuberosity and inserts at the pes anserine; the semimembranosus originates at the ischial tuberosity and inserts at the posterior medial tibia. The biceps femoris has a long head that originates at the ischial tuberosity and a short head at the posterolateral femur and inserts into the head of the fibula. Both muscles serve as knee flexors and hip extensors. (See image below and Image 1.)
Hamstring strain is a fairly common injury in physically active individuals.
No mortality is associated with hamstring strain; however, morbidity is common, due to pain and reinjury if proper rehabilitation does not occur before the patient returns to preinjury activity levels.
While hamstring injuries can occur in people of any age, incidence increases with age.
Hamstring strain is a noncontact injury and usually occurs with either acute or insidious onset. Strain injuries frequently are seen in athletes who run, jump, and kick. Avulsion injuries are seen in patients who participate in water-skiing, dancing, weight lifting, and ice-skating. The avulsion injury usually follows a burst of speed, and the patient may report a popping or tearing sensation. The most commonly affected muscle area in the hamstring complex is the short head of the biceps femoris,3 possibly because of its innervation.
In addition to pain in the posterior thigh, the physical examination may reveal any of the following signs or symptoms:
Many different causative factors can contribute to hamstring injuries. The most significant causes include the following:
Achilles Tendon Injuries and Tendonitis
Lumbar Degenerative Disk Disease
Lumbosacral Radiculopathy
Trigger points
In a study of 59 Australian footballers who had incurred a hamstring strain, Warren et al found evidence that 2 factors — the amount of time it took a player to walk without pain and whether or not the player had suffered a previous hamstring injury — could be used to help predict the length of time needed for the athletes to return to competition and how likely it was that the injury would again recur.5 According to the study, players who needed more than 1 day to walk without pain were more likely to require more than 3 weeks of convalescence before they could again compete.
Need for surgical intervention is extremely rare after a hamstring injury. Surgery is recommended only in the case of complete rupture of the proximal or distal attachment of the myotendinous complex into the bone.6
The standard choice for medication is nonsteroidal anti-inflammatory drugs (NSAIDs). These medications not only provide analgesia but also can decrease some of the mediators of inflammation. When to administer NSAIDs to achieve the most beneficial effect is debated. One argument is to administer them immediately following injury to avoid side effects that may interfere with muscle remodeling and repair. The other argument is to delay use until 2-4 days after the injury, so they do not interfere with the chemotaxis required for the laying down of new muscle fibers. No consensus has been reached on which approach to timing yields the best outcome.
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
Available in both a regular and delayed-release form.
250-500 mg PO bid
5 mg/kg PO bid
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
Documented hypersensitivity, peptic ulcer disease, recent GI bleeding or perforation, and 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, 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
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
400 mg PO q4-6h, 600 mg q6h, or 800 mg q8h while symptoms persist; not to exceed 3.2 g/d
20-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate; not to exceed 2.4 g/d
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
Documented hypersensitivity, peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or 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 and inflammation. Small doses initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
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
Documented hypersensitivity
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
Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with other NSAIDs, although there is still a risk involved. They should be considered for use in patients with a history of GI bleed or those who have a high risk for a bleed.
Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. Seek lowest dose for each patient.
Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).
Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
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
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in 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 therapy when symptoms or lab results suggest liver dysfunction
Schache AG, Wrigley TV, Baker R, et al. Biomechanical response to hamstring muscle strain injury. Gait Posture. Feb 2009;29(2):332-8. [Medline].
Yu B, Queen RM, Abbey AN, et al. Hamstring muscle kinematics and activation during overground sprinting. J Biomech. Nov 14 2008;41(15):3121-6. [Medline].
Silder A, Heiderscheit BC, Thelen DG, et al. MR observations of long-term musculotendon remodeling following a hamstring strain injury. Skeletal Radiol. Dec 2008;37(12):1101-9. [Medline].
Davis KW. Imaging of the hamstrings. Semin Musculoskelet Radiol. Mar 2008;12(1):28-41. [Medline].
Warren P, Gabbe BJ, Schneider-Kolsky M, et al. Clinical predictors of time to return to competition and of recurrence following hamstring strain in elite Australian footballers. Br J Sports Med. Aug 14 2008;[Medline].
Sallay PI, Ballard G, Hamersly S, et al. Subjective and functional outcomes following surgical repair of complete ruptures of the proximal hamstring complex. Orthopedics. Nov 2008;31(11):[Medline].
Agre JC. Hamstring injuries. Proposed aetiological factors, prevention, and treatment. Sports Med. Jan-Feb 1985;2(1):21-33. [Medline].
Baquie P, Reid G. Management of hamstring pain. Aust Fam Physician. Dec 1999;28(12):1269-70. [Medline].
Brukner P. Hamstring injuries. Aust Fam Physician. Jul 1996;25(7):1109-12. [Medline].
Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. J Am Acad Orthop Surg. Jul-Aug 1998;6(4):237-48. [Medline].
Hartig DE, Henderson JM. Increasing hamstring flexibility decreases lower extremity overuse injuries in military basic trainees. Am J Sports Med. Mar-Apr 1999;27(2):173-6. [Medline].
Hennessey L, Watson AW. Flexibility and posture assessment in relation to hamstring injury. Br J Sports Med. Dec 1993;27(4):243-6. [Medline].
Laskowski E. Concepts in sports medicine. In: Braddom RL, ed. Physical Medicine and Rehabilitation. Philadelphia, Pa: Saunders; 1996:930-1.
Medical Economics Staff. Physician's Desk Reference. 55th ed. Oradell, NJ: Medical Economics Co; 2000:2631-4.
Pomeranz SJ, Heidt RS Jr. MR imaging in the prognostication of hamstring injury. Work in progress. Radiology. Dec 1993;189(3):897-900. [Medline].
Scoggin JF 3rd. Common sports injuries seen by the primary care physician. Part II: Lower extremity. Hawaii Med J. May 1998;57(5):502-5. [Medline].
Speer KP, Lohnes J, Garrett WE Jr. Radiographic imaging of muscle strain injury. Am J Sports Med. Jan-Feb 1993;21(1):89-95; discussion 96. [Medline].
Worrell TW. Factors associated with hamstring injuries. An approach to treatment and preventative measures. Sports Med. May 1994;17(5):338-45. [Medline].
Yamamoto T. Relationship between hamstring strains and leg muscle strength. A follow-up study of collegiate track and field athletes. J Sports Med Phys Fitness. Jun 1993;33(2):194-9. [Medline].
hamstring strain, hamstring, pulled muscle, muscle strain, pulled hamstring, pulled muscles, hamstring injury, strained muscle, strained hamstring, hamstring muscle, hamstring pain, hamstring treatment, torn hamstring, hamstring muscles, hamstring tendon, strained muscles, hamstring injury treatment, hamstring pull
Jeffrey M Heftler, MD, Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT
Jeffrey M Heftler, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Association
Disclosure: Nothing to disclose.
Michael F Saulino, MD, PhD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University, MossRehab
Michael F Saulino, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.