eMedicine Specialties > Physical Medicine and Rehabilitation > Lower Limb Musculoskeletal Conditions

Hamstring Strain: Treatment & Medication

Author: Jeffrey M Heftler, MD, Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT
Coauthor(s): Michael F Saulino, MD, PhD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University, MossRehab
Contributor Information and Disclosures

Updated: Apr 10, 2009

Treatment

Rehabilitation Program

Physical Therapy

• Acute phase - During the acute phase (1-5 d), most of the treatment is geared toward decreasing the inflammation and maintaining range of motion. As for most strains, PRICE (ie, protection, rest, ice, compression, elevation) is the initial treatment. When the pain has decreased, the therapist may begin painless gentle passive range of motion and active-assistive range of motion. The patient also may benefit from a cane or crutches to aid in ambulation to keep active. Even if a patient with a first-degree injury is feeling better after a few days and wants to return to participating in his or her sport, it is usually recommended that he or she complete a rehabilitation program to avoid chronic injury. Muscle strengthening, balance, and stretching should be emphasized to the patient as a prevention of recurrence.
• Subacute phase - The subacute phase (5 d to 3 wk) is when the inflammation of the injury appears to be lessening. The goal of treatment in this stage is to begin some active range of motion and start strengthening. Aquatic therapy is helpful in encouraging activity with decreased weight bearing. Pain-free submaximal isometric exercises also are encouraged. A transcutaneous electrical nerve stimulation unit may be used to provide some pain relief at this time. Ice is also helpful to decrease pain and inflammation. The patient also should resume cardiovascular training, which may include swimming with a pull buoy between the legs, and upper extremity exercises.
• Remodeling phase³ - The remodeling phase (1-6 wk) is when the patient is able to perform isometric exercises at 100% effort without pain. Prone isotonic hamstring exercises are now added to the transcutaneous electrical nerve stimulation unit and ice. Begin unilaterally with ankle weights, using low weight and a high number of repetitions. Slowly increase the weight as tolerated as long as the patient's pain is not increased afterwards. Importantly, do not increase the weight too rapidly because this could lead to a chronic injury.
  
  Once concentric strengthening is tolerated at a normal level, the patient may begin eccentric strengthening. Because this exercise puts the most strain on the muscle, supervised exercising and slow progression of weight is recommended. In the prone position, the patient performs a unilateral contraction to 90° of knee flexion and then slowly lowers the weight. If the patient experiences pain or stiffness, then decrease the weight to a more tolerable amount. When the affected leg is within 10% of the unaffected leg, then the patient may advance to a more aggressive therapy program. Continued stretching of the hamstring is essential and should occur prior to exercise. Moist heat prior to exercise may provide improved results. A posterior pelvic tilt may help eliminate lumbar compensation.
• Functional stage - The functional stage is 2 weeks to 6 months. At this point, the patient should have a normal gait pattern and can begin fast walking. When the patient can ambulate for 20-30 minutes at a fast speed without pain or stiffness, short periods of jogging can be added to the fast walking. When the patient can perform a 15- to 30-minute jog, then short periods of sprinting may be added to the jog. Eventually, more sport-specific exercises may be added. Have the patient continue with the hamstring strengthening and stretching throughout this stage.
  
  During the later stages of therapy, plyometric exercises may be used to increase speed and power during training. These exercises consist of muscle stretching followed by concentric contraction, allowing for a stronger contraction because of muscle facilitation and decreased inhibition. Low-level exercises may be used initially (eg, jumping rope), followed by higher-level exercises as tolerated (eg, side jumping over a low object, jumping onto and off a box). Because the higher level exercises are associated with a higher rate of injury, they should be performed with supervision.
• Return to play - This can occur anywhere between 3 weeks and 6 months. Isometric strength testing and flexibility testing may be performed prior to returning to play to ensure that no subtle deficits are present that may lead to chronic injury. The clinician must impress upon the patient the importance of stretching and warm-up prior to activities to prevent reinjury. Less than 5 weeks are required before return to play for patients with (1) superficial muscle injury or (2) muscle injury that involves a small cross-section of muscle. In patients whose injury was due to poor biomechanics, care should be taken to correct the underlying cause. The patient should be supervised during stretching and exercise in order to assess poor technique and correct it.

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.

Surgical Intervention

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

Medication

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.

Nonsteroidal anti-inflammatory drugs

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.

Naproxen (Anaprox, Naprelan, Naprosyn)

Available in both a regular and delayed-release form.

Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Ketoprofen (Orudis, Actron)

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.

COX-2 inhibitors

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.

Celecoxib (Celebrex)

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.

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