Updated: Aug 6, 2009
A medial calf injury is a musculotendinous disruption of varying degrees in the medial head of the gastrocnemius muscle that results from an acute, forceful push-off with the foot.[1,2,3,4,5,6 ]This injury occurs commonly in sports activities (eg, hill running, jumping, tennis), but it can occur in any activity. A medial calf injury is often seen in the intermittently active athlete, often referred to as the "weekend warrior."
This condition has been termed "tennis leg" because of its prevalence in this particular sport, but medial calf injury can happen in a variety of sports or other activities. One mechanism that occurs is on the back leg during a lunging shot, in which the knee is extended while the foot is dorsiflexed. This action puts maximal tension on the gastrocnemius muscle as the lengthened muscle is contracted at the "push off," resulting in a medial calf injury. (See also the eMedicine article Body Contouring, Calf Augmentation.)
Medial calf injuries occur more commonly in men than in women, and these injuries usually afflict athletes and others in the fourth to sixth decade of life. Medial calf injuries are most commonly seen acutely, but up to 20% of affected patients report a prodrome of calf tightness several days before the injury, thus suggesting a potential chronic predisposition.
The medial head of the gastrocnemius muscle originates from the posterior aspect of the medial femoral condyle, and as it courses distally, the medial head merges with the lateral head of the gastrocnemius. Further distally, the joined heads of the gastrocnemius merge with the soleus muscle-tendon complex to form the Achilles tendon. The main function of the gastrocnemius muscle is to plantar flex the ankle, but it also provides some knee flexion, as well as contributes to the posterior stability of the knee and partially to the motion of the menisci with flexion/extension of the knee. Throughout the belly of the muscle, the medial gastrocnemius has several origins of tendinous formation. Most strains occur at this musculotendinous junction.
The medial calf injury usually occurs when an eccentric force is applied to the gastrocnemius muscle, which usually happens when the knee is extended, the ankle is dorsiflexed, and the gastrocnemius attempts to contract in the already lengthened state.[1,2,3,4,5,6 ]This is the common position of the back leg in a tennis stroke, and it results in the greatest force to the muscle unit; but medial calf injuries can also occur during a typical contraction of ankle plantar flexion, especially if the athlete is pushing or lifting a large weight or force.
Achilles Tendon Rupture
Compartment Syndromes
Baker cyst rupture
Deep venous thrombosis
Plantaris tendon rupture
Acute compartment syndrome after rupture of the medial head of the gastrocnemius
Chronic exertional compartment syndrome (posterior)
Posterior tibial tendon rupture or tendinitis
Popliteal artery entrapment syndrome
Anomalous gastrocnemius muscle rupture
A Baker cyst is a reactive outpouching of the knee joint capsule. The presence of a Baker cyst implies chronic internal knee pathology, often arthritic in nature, but it may also include traumatic meniscal pathology. The cyst is usually painless but often cosmetically unacceptable to the patient. If the Baker cyst ruptures, the leg swells, and the pain is diffuse. This condition can be confused with a ruptured gastrocnemius muscle.
(See also the eMedicine articles Baker Cyst [in the Radiology section], Knee Injury, Soft Tissue [in the Emergency Medicine section], and Cystic Lesions About the Knee and Limping Child [in the Orthopedic Surgery section].)
A femoral or popliteal deep venous thrombosis (DVT) can cause leg swelling, which can result in leg pain. If this condition occurs in the same time frame as an acute leg injury, the 2 conditions can be confused.
(See also the eMedicine articles Deep Venous Thrombosis and Thrombophlebitis [in the Emergency Medicine section] and Deep Venous Thrombosis, Lower Extremity [in the Radiology section].)
The plantaris tendon originates in the popliteal area, and this tendon is also a plantar flexor of the ankle. If the plantaris tendon ruptures, the leg swells, and the resulting tenderness can be in the same area as where a gastrocnemius strain would occur.
Achilles tendon injury can occur with the identical mechanism of a medial gastrocnemius rupture. Because the ensuing fluid and edema may migrate proximally, the 2 conditions may mimic each other. An Achilles tendon rupture results in an inability to plantar flex the foot, and a more distal defect of the tendon is usually palpable. A Thompson test can be used to differentiate the 2 injuries. The test is performed with the patient prone and the knee held in flexion. Then, the gastrocnemius muscle is squeezed. A negative sign results in normal plantar flexion of the foot and ankle. If the flexion is not appreciated, the test is positive and due to a disrupted Achilles tendon. (See also the eMedicine article Achilles Tendon Rupture.)
Acute compartment syndrome of the lower extremity occurs after trauma, with accumulation of blood or fluid in a closed compartment of the leg. The resultant pressure produces pain and swelling, and if the posterior compartment is affected, this could clinically present similarly to a medial gastrocnemius tear.
(See also the eMedicine articles Compartment Syndrome, Lower Extremity [in the Orthopedic Surgery section], Compartment Syndrome [in the Physical Medicine and Rehabilitation section], and Compartment Syndrome, Extremity [in the Emergency Medicine section].)
Chronic compartment syndrome results in affected individuals after a degree of exertion and from vascular compromise with edema in the compartment of the leg. The pain that ensues can mimic that of gastrocnemius muscle strains, but this condition becomes symptom-free after the exertion is completed. (See also the eMedicine article Compartment Syndromes [in the Sports Medicine section].)
The popliteal tendon courses posteriorly on the medial side of the leg. Injuries to this structure can distribute pain in the same regions as a tennis leg injury. (See also the eMedicine articles Pes Planus [in the Orthopedic Surgery section] and Athletic Foot Injuries [in the Sports Medicine section].)
The popliteal artery may be entrapped during its course in the leg. The most common cause is an anomalous gastrocnemius muscle. Typically, popliteal artery entrapment manifests during exertion, and the symptoms of this condition are more consistent with the symptoms of chronic exertional compartment syndrome.
(See also the eMedicine articles Peripheral Arterial Occlusive Disease [in the Vascular Surgery section], Compartment Syndrome, Lower Extremity [in the Orthopedic Surgery section], and Compartment Syndromes [in the Sports Medicine section].)
Initial treatment of a medial calf injury includes relative rest, ice, compression, elevation (RICE), and early weight bearing, as tolerated. The initial treatment should continue for 24-72 hours. Ice therapy is best instituted over a damp elastic wrap, which also provides compression. Preventing the limb from hanging dependently prevents further swelling. The use of crutches with a feathering gait and bilateral heel lifts is indicated if normal gait is compromised. Active foot and ankle ROM can be carried out if there is pain-free ROM.
Pain management should include analgesics as indicated. Caution should be used with nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute injury phase, as these agents can predispose the patient to increased bleeding and hematoma formation in the initial days after an injury. Theoretically, cyclooxygenase-2 (COX-2) inhibitors may provide pain control without the risk of bleeding in acute injuries, which is a concern with traditional NSAIDs.
Ankle/foot bracing should be used to keep the ankle in a position of maximal tolerable dorsiflexion. Studies have shown an increased rate of healing with this intervention.
Ice therapy and active resistance dorsiflexion exercises can be undertaken until the athlete is pain free. Then, light plantar flexion exercises against resistance are initiated. Progression of therapy includes reduction in heel-lift height and gradual introduction of stationary cycling, leg presses, and heel raises. At this stage, ultrasonography, used with or without phonophoresis, and muscle stimulation are also applicable. Massage techniques can help with the removal of interstitial fluid. Apply compression dressing from the metatarsal heads to the gastrocnemius for the first 2 weeks. Partial weight-bearing ambulation should begin as soon as tolerable to maximize the contact of the sole of the foot to the ground, then progress to increased cyclic loading, advanced proprioception and balance training, and eventual full weight-bearing ambulation, with dynamic change of speed and direction as tolerable.
Once the athlete is pain free with full and symmetric ROM and full strength is regained, sports-specific activities can be resumed. Strengthening and stretching of the injured area should continue for several months to overcome the increased risk for reinjury due to the deposition of scar tissue that is involved in the healing process.
Medications are directed at maintaining patient comfort in what can be a very painful injury of the medial head of the gastrocnemius. Clinicians must carefully consider pain therapy in the first 48 hours, as decreased platelet activity may result in increased bleeding and larger hematoma formation—with resultant effects on healing.
The simplest, yet least powerful of the recommended analgesics is acetaminophen. Typical doses of 1000-1300 mg, 3-4 times daily can be used as needed. This agent does not affect platelet function but may not greatly control pain.
To gain better pain control, more potent analgesics can be used, such as NSAIDs or an acetaminophen/narcotic combination. As referred to above (see Medical Issues/Complications in the Treatment, Acute Phase section), NSAIDs may enhance bleeding shortly after the injury has occurred. These agents are also likely to cause symptoms of gastrointestinal (GI) discomfort, and they can result in mucosal injury and even bleeding ulcers. On the other hand, opioid analgesic agents may cause GI side effects but not result in bleeding issues; these medications are generally better at pain control, but opioid analgesics have the possible complication of addiction or abuse.
Opioid medications come in various forms and various dosages. An alternative to the above medications is to use a newer NSAID from the COX-2 inhibitor class. The new COX-2 inhibitor drugs affect inflammation in a more specific manner by not affecting the prostaglandins that can cause the above side effects; these agents have also been shown to provide equianalgesia to the traditional NSAIDs.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet (ie, decrease pulmonary secretions, open the airways), and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants. No benefit as an anti-inflammatory agent. No effect on platelet function.
325-650 mg PO q4-6h or 1000 mg PO tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h
Rifampin can reduce the analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity.
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity is possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products, and combined use with these products may result in cumulative APAP doses that exceed the recommended maximum dose.
First-line agent for moderate to severe pain. Has no anti-inflammatory benefit. With the combination of a narcotic and acetaminophen, pain control is much better than acetaminophen alone.
1-2 tab PO q4-6h prn
Not established
Toxicity increases with CNS depressants or tricyclic antidepressants
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
Caution in patients who are dependent on opiates because this substitution may result in acute opiate-withdrawal symptoms; caution in the presence of severe renal or hepatic dysfunction; narcotic side effects of GI upset, constipation, sedation, and addictive potential are possible.
COX-2 inhibitors promote control of moderate pain and anti-inflammatory effects, especially in patients who have sensitivity to the traditional NSAIDs. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with the traditional NSAIDs. Ongoing analysis of the cost avoidance of GI bleeding will further define the populations that will benefit from the use of COX-2 inhibitors.
Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme during pain and with 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 the lowest dose of celecoxib for each patient.
100 mg PO qd to bid, or 200 mg PO qd
Not established
Coadministration with fluconazole may cause an 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
Category D in 3rd trimester of pregnancy; may cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions that predispose to fluid retention; caution in the presence of severe heart failure and hyponatremia because circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or laboratory results suggest liver dysfunction.
When an athlete will be able to return to play is predicated on the patient being pain free and recovering full ROM. This period can last 1-12 weeks, depending on the degree of tissue damage that was sustained. Strength testing should reveal that more than 90% of the uninjured side accounts for the patient's dominance preference.
The most common complication of a medial calf injury is scar-tissue formation, which results in chronic pain or dysfunction that is caused by a functional shortening of the muscle-tendon unit. This scar tissue can then predispose to frequent reinjury. Another complication is the formation of a DVT as a result of patient inactivity and trauma.
A medial calf injury may not be preventable, but regular physical activity with maintenance of flexibility in the gastrocnemius muscle may help to reduce one's chances of sustaining such an injury.
If the above treatments are followed (see Treatment, Acute Phase, Recovery Phase, and Maintenance Phase), the prognosis for recovery and return to sports after a medial calf injury is excellent.
Instructions for appropriate stretching and warm-up techniques should be provided to the patient for the implementation of maximal prevention of reinjury.
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medial gastrocnemius strain, tennis leg, medial calf strain, medial gastrocnemius muscle injury, gastrocnemius strain
Anthony J Saglimbeni, MD, Staff Physician, Family Practice Residency, President, South Bay Sports and Preventive Medicine Associates; Private Practice; Team Internist, San Francisco Giants; Team Internist, West Valley College; Team Physician, Bellarmine College Prep; Team Physician, Presentation High School
Disclosure: Nothing to disclose.
Janos P Ertl, MD, Assistant Professor, Department of Orthopedic Surgery, Indiana University School of Medicine; Chief of Orthopedic Surgery, Wishard Hospital
Janos P Ertl, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Hungarian Medical Association of America, and Sierra Sacramento Valley Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
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