Updated: Dec 16, 2009
Hip overuse injuries such as tendinitis and bursitis occur commonly in active individuals who participate in running, cycling, and cutting sports such as football, hockey, soccer, etc.[1,2,3,4,5,6,7,8 ]These injuries can occur after an acute injury, such as an adductor strain from soccer, or present as a chronic pain, such as a hamstring tendinopathy from repetitive activities such as running. Training errors, biomechanical issues, and sudden increases in activity levels are also risk factors. In the adolescent age group, traction injuries such as avulsion fracture and apophysitis can occur and cause difficulties with training and performance.[9 ]
The investigation into the cause and treatment of hip overuse injuries can often be frustrating for clinicians and patients alike. Many musculoskeletal injuries can cause referred pain into the hip area, but so can intra-abdominal, gynecologic, urologic, and spinal disorders.[1,3,4,5,6,7,8,10 ]
For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center, Sports Injury Center, and Sprains and Strains Center. Also, see eMedicine's patient education articles Repetitive Motion Injuries and Muscle Strain.
Hip overuse syndrome is a relatively common condition, particularly in people who are physically active.
The hip joint can be imagined as a ball and socket. The ball, called the femoral head, is seated within the acetabulum of the pelvic bone (the socket). Both of these bones are covered by articular cartilage, a lubricating and cushioning layer that helps to prevent damage to the underlying bones. Likewise, the labrum is a cushion of fibrocartilage deep within the socket that helps to aid articulation and provide further cushioning.
The hip joint is subject to strong forces (which can be multiple times the body weight) with all weight-bearing activities, from walking to running, as well as jumping and cutting sports. This is due to the long, lever-arm mechanism of the lower extremity, with the hip joint being the fulcrum. Thus, the hip joint is often the location of degenerative arthritis as people age.
The capsular ligaments of the hip joint, which act like ropes, are formed from thickened portions of the joint capsule, helping to keep the 2 bones together and aid in articulation. These ligaments provide stability and tension to the joint with movement.
Anteriorly, the rectus femoris, iliopsoas, gracilis, and sartorius muscles connect the pelvic bone to the femur and help aid in flexion of the femur, bringing the leg up toward the body. These muscles, along with the rest of the quadriceps muscles, which extend the knee, are the largest and most powerful muscles in the body, responsible for producing large concentric, isometric, and eccentric forces. Because of this, these muscles are subject to traumatic injuries and tears from sudden starts (concentric contraction), stops (eccentric contractions), and direct trauma, as well as overuse injuries from repetitive activities (microtrauma).
Medially, the set of 3 adductor muscles and the pectineus connect the inner aspect of the femur to the front and inferior aspect of the pelvis; contracting these muscles adducts the femur back to midline and across the body (ie, crossing the legs). From the outside, the tensor fasciae latae and biceps femoris (toward the back) aid in abduction, moving the legs outward from the body. Posteriorly, the semitendinous and semimembranous muscles (the hamstrings), the biceps femoris, and the large gluteus maximus extend the leg backward from the body.
The gluteus medius, another posterior muscle of the hip and buttocks, aids in internal rotation and abduction of the thigh. The piriformis, quadratus, and superior and inferior gemelli work in tandem to perform external rotation of the hip.
All of the previously mentioned muscle groups are subject to increased loads in athletic and recreational activity (see Functional Anatomy). Tendons, which attach muscle directly into bone, are structures that are subject to high tensile strength, meaning they must stretch as the muscles shortens, but they do not provide strength. Inflammation of a tendon from injury or repetitive stress is called tendinitis.
Several tendons are cushioned from the underlying bone by a lubricating and cushioning sac called a bursa. The largest bursa in the hip joint is between the iliopsoas muscle and the pelvic brim and is called the iliopsoas bursa. Between the tensor fasciae latae and gluteus medius muscles and the greater trochanter of the femur, a portion of bone that juts out laterally from the proximal femur, lies the greater trochanteric bursa. Any bursa within the body can be inflamed from repetitive stress of the overlying muscles, direct trauma, or a spreading infection.
The tendinous portion of the muscle has poor blood flow, so injury or stress at the attachment of the tendon onto the bone can lead to degeneration of the area. This degeneration is associated with the disorientation of collagen fibers, increased cellularity, and angiofibroblastic degeneration. Pathology examination of these tendons fails to reveal inflammatory cells or increased blood supply to the area. These "scars" within the tendon are difficult to treat because of decreased blood flow into the injured area.
In the pelvic bones of children, adolescents, and young adults, the tendons attach onto a secondary growing portion of bone. This connection between the larger pelvic bone and smaller secondary growth area is called the apophysis, and in this age group it is the weakest link from the musculature to the bone. Consequently, the apophysis can be the direct source of pain from irritation (apophysitis), or it can be broken apart by a strong force on the tendon and pulled away from the larger pelvic bone (avulsion fracture).
Avulsion fractures around the pelvis occur in prepubertal athletes as the result of an actively contracting muscle encountering abrupt resistance such as a misstep, rapid acceleration, or eccentric movements. The treatment of most smaller avulsion fractures is similar to the treatment of strains of the muscle-tendon unit.
Taking an appropriate history from a patient with hip pain is of paramount importance. The first focus should be on the patient’s account of the pain. If the pain was of an acute onset after an injury, the incident should be thoroughly described. Was there a snap or pop? Did it occur during acute acceleration or deceleration? What was the exact motion occurring during the injury (ie, foot planter, how was he/she hit, etc)? Was the athlete able to bear weight after the injury? Could he or she continue playing? These injuries often occur with a pop or snap, with a resultant sudden, severe, well-localized pain and immediate disability.
If the pain has been more long term, a review of the athlete's training methods, distances, and activity level should be explored. Does the pain start during the activity, or only afterward? Is there night pain? Is the pain better the next day or worse? Is the pain occurring earlier in the activity? Do any specific activities or movements increase the pain?
Ask the patient about a previous history of similar problems. Has there been any previous diagnostic testing or treatment?
To rule out more dangerous pathologies, always ask about night sweats, fevers, weight loss, or anorexia. Is there any history of stress fractures, menstrual irregularities, or amenorrhea?
To rule out abdominal sources of the hip pain, ask about nausea, vomiting, diarrhea, changes in stools, or the presence of blood in stools.
To help rule out spinal causes, ask about lower back pain; radiation of pain down the leg into the calf, foot, or toes; and numbness, tingling, or weakness in the leg or foot.
It is important to do a thorough examination of the hip in order to establish any limitations or deficits that the patient may have. Along with a hip examination, an examination of the knee and lumbosacral spine is important to establish if the patient's hip pain is referred pain from these sites. A systematic approach of observation, palpation, checking range of motion (ROM), and strength testing is important.
Observation
Observe the patient from the front, back, and sides. Note any asymmetry, as well as how the patient’s clothing rests on the waist and hips. Then, observe the patient walking to see if one side is favored over the other. These observations can be helpful clues in focusing the examination, as well as in detecting signs of a leg-length discrepancy. Swelling and ecchymosis can be present with more severe strains, but these findings are often absent because the injured structures are deep in the hip.
Palpation
Along with bony palpation (see below), it is important to appreciate the patient's muscle tone as this may be an indicator of muscle strain or guarding against underlying pathology. Acute or chronic injuries lead to tenderness of the muscle and tendon. Spasm after an acute injury is common. Passive stretching and active contraction of the muscle is often difficult but can help to pinpoint the exact anatomic injury.
It is important to establish and palpate the following landmarks:
Special Tests
Rectus Femoris/Quadriceps
The rectus femoris originates at the ASIS (direct head) and AIIS (nondirect head) and crosses the hip and knee joint, making it the only quadriceps muscle to do so. It functions as a hip flexor and knee extender, and it receives innervation from the femoral nerve (L2-L4).
Strains of the rectus, which usually occur in the middle third of the thigh, may result in complete ruptures of the muscle belly, presenting as an acute enlargement of the affected thigh or a pseudotumorous growth. These deformities are out of proportion to their significance, however, because even complete ruptures of the rectus femoris result in little or no functional disability. The site of the strain is often tender to palpation and may be ecchymotic. An obvious defect can be palpated at times.
Chronic proximal rectus femoris or quadriceps pain can occur with apophysitis in the skeletally immature patient. Continued activity will weaken the growth plate, putting this area at risk for an avulsion after an acute stress of the muscle-tendon unit. This injury is accompanied by a pop or snap, with immediate pain and disability.
Iliopsoas Bursitis/Tendinits[6,11,12 ]
The iliopsoas is the primary hip flexor, and it is also an external hip rotator. This muscle is a combination of the psoas major muscle (originating at the lateral surface of the T12-L4 vertebral bodies) and the iliacus muscle (iliac fossa origin) below the inguinal ligament which insert on the lesser trochanter of the femur. The iliopsoas muscle receives its innervations from the femoral nerve and lumbar plexus (L1-L3). The trochanteric bursa lies beneath the muscle and is the largest synovial bursa in humans. This bursa can be from 5-7 cm x 2-4 cm in size and can communicate directly with the hip joint. Pain from the bursa or tendon is usually caused by an overuse injury, acute trauma, or rheumatoid arthritis.
The mechanism of injury for an acute iliopsoas trauma is usually a sudden hyperextension, which is commonly seen in athletes who are involved in rowing, uphill running, track and field, and strength training. This type of injury is usually seen in young adults and is more common in women. Patients present with pain over the anterior thigh with a palpable and/or audible snap. A shortened stride on the affected side may be present, and this is usually due to guarding against hyperextension of the hip.
Chronic anterior hip pain may result from iliopsoas or rectus femoris tendinitis. An audible or palpable snap may be felt with flexion or extension of the hip. As in all tendinitis and tendinosis, this is a result of repetitious weight-bearing activities, such as running and jumping. These conditions will often occur after abrupt changes in levels of activity, such as during preseason training or when an individual is first training for a race. Because tendinosis is a degenerative process, less obvious changes in activity can lead to symptoms in older patients and will have a more insidious onset.
The symptoms of pain and tightness will initially start after an activity but will progress to occur during the workout over time. Eventually, the individuals will stop the workouts because of the pain, and their activities of daily living may be affected.
The patient will complain of anterior hip and groin pain that is worsened with extension of the hip or active flexion of the hip or active extension of the knee against resistance. Getting out of a car or walking up the steps will lead to increased pain.
A palpable mass may also be noted under the inguinal ligament, at which time a consideration of aspiration or a steroid injection may be considered if ultrasound guidance is available.
Gluteus Medius Syndrome and Trochanteric Bursitis[1,8,13,14 ]
The gluteus medius functions as a primary hip abductor. It originates at the external surface of the ilium and inserts onto the posterior lateral surface of the greater trochanter. This muscle is innervated by the superior gluteal nerve (L4-S1).
The greater trochanteric bursa lies directly lateral to the greater trochanter. This lateral growth of the femur abuts the tensor fasciae latae and lateral quadriceps muscles. The bursa provides lubrication and cushioning to allow the muscles to flex and extend over the trochanter without damaging the muscles. It also cushions the tendon before the attachment of the gluteus medius and minimus. Bursitis in this area can be secondary to changes in activity or training, biomechanical problems lower down the leg, or from direct trauma. These conditions lead to increased pressure of the muscles against the bursa and trochanter—with resultant inflammation.
Pain will occur with hip flexion such as walking, climbing stairs, or getting out of a car or a chair. Nocturnal pain while lying on the affected side is common. A snap is occasionally felt or heard in the lateral hip with flexion or extension.
Gluteus medius syndrome involves tenderness to palpation of the gluteus medius muscle, which can be triggered by sudden falls, prolonged weight bearing on one extremity for long periods, activity overuse, or sporting injuries. Most commonly, this situation is observed in middle-aged women who have embarked upon a vigorous walking program or who have started working out at a health club. Patients may present with pain that is transient and worsening over a time period, a Trendelenburg gait, and weakness. These symptoms specifically affect runners, as there is tilting of the pelvis with running. It is important for the clinician to examine the patient for a leg-length discrepancy.
Hip-abduction strengthening should be avoided in the initial stages of gluteus medius syndrome because it only provokes tendinitis. As the acute stage resolves, hip-abductor strengthening is important and is best achieved in the aquatic environment.
It can be difficult to distinguish between trochanteric bursitis and gluteus medius tendinitis due to their proximity at the insertion site. Resistance to abduction or internal rotation of the hip may help distinguish these 2 entities, as trochanteric bursitis will not elicit pain with resisted hip abduction, and gluteus medius tendinitis will present with more posterior tenderness to palpation at the insertion site. Diagnostic ultrasound can be performed to determine if fluid is present in the bursa or to look for echogenic changes that are consistent with tendinopathy. Ultrasound-guided injections into the greater trochanteric bursa will be more effective if fluid and distention of the bursa can be demonstrated.
Groin/Adductor Strain
Adduction of the hip is performed by the gracilis, pectineus, obturator externus, adductor longus, adductor brevis, and adductor magnus muscles. The main origin is along the pubic ramus, and the insertions range from the trochanteric fossa to the tibial tuberosity. The obturator nerve (L2-L4) provides the main innervations for the adductor muscle group.
Adductor or groin strains are commonly seen in ice hockey and soccer players. These injuries are usually the result of strong eccentric contractions and rapid decelerations that occur during these sports activities, and they are often accompanied by a pop, with immediate resultant pain and disability. Often, weight bearing will be difficult, and the athlete may need to use crutches. The adductor longus is most commonly injured, and athletes classically present with pain with the following: (1) palpation of the muscle belly and insertion, (2) passive stretching, and (3) resistance to contraction.
Adductor strains are also common in football, figure skating, and track and field. Athletes at risk are those with decreased adductor strength, lack of off-season conditioning, inadequate warm-up and stretching, and a history of previous strains. Adductor strains are graded from first degree to third degree, ranging from a minimal loss of strength and ROM (first degree) to a complete loss of muscle function (third degree). If these injuries are not properly rehabilitated after the acute stage, they may become chronic, leading to a more frustrating situation for the athlete.
Hamstring[15,16 ]
The hamstrings function as hip extensors and consist of the semitendinosus muscle, semimembranosus muscle, and the biceps femoris. These muscles originate from the ischial tuberosity, with the short head of the biceps femoris coming off the middle third of the femur. They insert onto the medial tibia (semimembranosus and semitendinosus) and lateral fibula (biceps femoris).
Acute hamstring injuries occur with the acceleration associated with sprinting and court or field sports. A snap or pop is felt, and immediate pain will limit further participation. Risk factors for these injuries are similar to other acute injuries mentioned above, such as poor warm-ups, poor flexibility, or decreased strength from previous hamstring strains. Acute hamstring injuries most often occur within the mid belly of the muscle, but myotendinous rupture can occur.
Chronic hamstring pain can result from a poorly rehabilitated acute injury in which the strength was not completely restored. Proximal hamstring tendinitis is less common than chronic muscle-based pain. Apophysitis and acute avulsions from the ischial tuberosity occur in skeletally immature athletes, such as gymnasts and dancers.
| Degenerative Lumbar Disc Disease in the Mature
Athlete | Lumbosacral Radiculopathy |
| Femoral Head Avascular Necrosis | Lumbosacral Spine Sprain/Strain Injuries |
| Femoral Neck Fracture | Lumbosacral Spondylolisthesis |
| Femoral Neck Stress Fracture | Meralgia Paresthetica |
| Femur Injuries and Fractures | Myofascial Pain in Athletes |
| Hamstring Injury | Osteitis Pubis |
| Hip Pointer | Pars Interarticularis Injury |
| Iliopsoas Tendinitis | Piriformis Syndrome |
| Lumbar Disk Problems in the Athlete | Sacroiliac Joint Injury |
| Lumbosacral Disc Injuries | Slipped Capital Femoral Epiphysis |
| Lumbosacral Discogenic Pain Syndrome | Snapping Hip Syndrome |
| Lumbosacral Facet Syndrome | Sports Hernia |
Endometriosis
Gastroenteritis
Inflammatory Bowel Disease
Inguinal Hernia
Ovarian Cysts
Spastic Colon
Ureteral Dysfunction
The initial treatment for all chronic hip overuse injuries is similar, and this can be taught to patients in the office or via formal physical therapy. The initial alleviation of overuse pain is accomplished with relative rest of the painful area. The patient may continue to work out other body parts and attempt to maintain cardiovascular fitness. Pain relief can be improved with oral anti-inflammatory medications, as well as with modalities such as ice, ultrasound treatment, and high-intensity galvanic stimulation. Patients thought to have tendinopathy can use acetaminophen for pain relief because the affected tendon is not inflamed.
To prevent further symptoms, increasing the length of the muscle-tendon unit with stretching and increasing joint flexibility are paramount.[20 ]Active stretching of the injured muscle must be accomplished to improve its length. At the same time, the injured muscle must be strengthened. Eccentric exercises, in which the muscle is lengthened and tightened at the same time (such as with lunges) should be added once full lengthening has returned. Once the proper length of the muscle has been attained and its strength restored, the addition of activity and sport-specific exercises completes the rehabilitation. Increasing the flexibility and strength of the opposing muscle groups is also required.
Because most of these muscles attach to the pelvic ring, attention to stretching and strengthening of all peripelvic tissues is helpful. Increasing the strength of the abductor muscles, such as the gluteus medius, should improve pelvic stability. Manual therapies are also helpful for manipulating the symphysis pubis and SI joints.
Leg-length discrepancies greater than 1 cm should be corrected with shoe lifts to improve balance and pelvic symmetry. Likewise, correction of any pes planus and the use of anti-pronation devices with an over-the-counter or custom orthosis is imperative for active individuals who do weight-bearing exercises or who run and walk regularly.
If the patient's condition is not responding as expected to treatment for the initial diagnosis, a second look at the symptoms and perhaps an additional piece of imaging may be performed to confirm that the diagnosis was appropriate (see Differentials and Other Problems to Be Considered).
Intra-abdominal or pelvic pathology can occasionally cause hip pain. If any gastrointestinal symptoms such as a change in bowel habits; the presence of blood in stool; or the presence of gynecologic symptoms such as bloating, new menstrual irregularities, or dyspareunia are present, a gastrointestinal or genitourinary workup may be necessary.
See Treatment, Acute Phase.
Tendinopathy treatment can often be frustrating for clinicians and patients alike. The degenerative tendon must be lengthened with aggressive and constant stretching. Eccentric exercises have been proven to decrease pain and return patients to a full level of activity in both hamstring and patellar tendinopathy.
The treatment of hip overuse syndrome (traction tendinitis) is never a short-term proposition; thus, treating this condition effectively requires a team approach. Optimally, medical resources are available to include a physical therapist and a fitness trainer who are skilled in laddered, progressive exercise following an individual's injury.
Chronic hip pain often goes undiagnosed, leading to psychologic difficulties from the debilitating nature of the pain itself and the frustration of being unable to return to a sport or exercise in a timely fashion. A psychology consultation may be indicated in such cases.
For patients with hip overuse syndrome, medications are used primarily to decrease pain and inflammation. These agents are best used for short time periods in the acute setting after an injury to prevent further swelling and pain.
Inflammation is part of the normal healing response and may be necessary to allow for complete tissue recovery. Some theories regarding tendinopathy involve the belief that stopping the healing response by halting all inflammation prevents the eventual recovery of tendons by interfering with normal collagen deposition and alignment. By preventing new blood-vessel formation into an injured area, complete healing does not occur.
In patients without known contraindications, nonsteroidal anti-inflammatory medications (NSAIDS) are preferred for short time periods for pain and inflammation control. Providers can decide which NSAIDS are the ones they are most comfortable using.
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well; these may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when anticoagulants are taken (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; patients with peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or a 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 patietns with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when anticoagulants are taken (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; 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.
For relief of mild to moderate pain and inflammation.
Small dosages initially indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase the 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
<12 years: 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 the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when anticoagulants are taken (instruct patients to watch for signs of bleeding); may increase the 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 patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy
Nonacidic NSAID that is rapidly metabolized after absorption to a major active metabolite that inhibits cyclooxygenase enzyme, which in turn inhibits inflammation.
1-2 g PO qd
Not established
Coadministration with aspirin increases the risk of inducing serious NSAID-related side effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; patients with active peptic ulceration, hepatic impairment
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
Elderly patients may require lower doses; caution in the presence of hepatic and renal impairment
COX-2 inhibitors are a class of NSAIDs that have a decreased incidence of adverse GI effects, such as gastritis and ulcers. COX-2 inhibitors may be indicated in patients with a history of gastric ulcers, who require anti-inflammatory medications.
Inhibits primarily COX-2, an isoenzyme that is induced during pain and with inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, the COX-1 isoenzyme not inhibited; therefore, GI toxicity may be decreased. Seek the lowest dose for each patient.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
Coadministration with fluconazole may increase celecoxib plasma concentrations because of inhibition of the celecoxib metabolism; coadministration with rifampin may decrease celecoxib plasma concentrations
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
May cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions predisposing 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
Simple analgesics like acetaminophen may be preferred for conditions in which NSAID use is not advised or in which there is little suspicion of an underlying inflammatory process.
Tramadol hydrochloride is an opioid analgesic that has noradrenergic and serotonergic properties that may contribute to its analgesic activity. Tramadol is used for moderate to severe pain or in cases wherein NSAIDs cannot be taken. The potency of this agent is less than that of traditional opioids, and there is less (but not zero) addiction potential.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, those with upper GI disease, or those taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg 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; known G6PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity is possible in patients with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; many OTC products contain acetaminophen, and combined use with these products may result in cumulative doses of acetaminophen that exceed the recommended maximum dose.
Inhibits ascending pain pathways, altering perception of and response to pain. Also inhibits reuptake of norepinephrine and serotonin.
50-100 mg PO q4-6h; not to exceed 400 mg/d
Not established
Decreases carbamazepine effects significantly; cimetidine increases toxicity, risk of serotonin syndrome with coadministration of antidepressants
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 days; use of SSRIs, TCAs, opioids, acute alcohol intoxication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in patients with liver disease, myxedema, hypothyroidism, hypoadrenalism; pregnancy, breast-feeding women; seizure; development of tolerance or dependency with extended use; swallow extended-release product whole: do not chew, crush, or split
Patients with chronic hip overuse injuries are often frustrated by the lack of progress and delayed return to play. These individuals must be educated from the first day that a prolonged recovery is usual.
Complete painless ROM needs to return before the patient should start significant strengthening exercises. After strengthening is commenced, endurance needs to be attained again. At this point, eccentric and plyometric exercises are started, and eventually, sport-specific drills that include cutting and cross-overs can begin. At any point if significant pain or stiffness returns, the athlete's progress needs to be slowed down and a step backward taken. Team athletic trainers or physical therapists can provide supervision and education to the athlete.
Other than worsening or returning pain, few complications of the overuse injury exist. Educating the athletes will remind them of the long-term nature of these injuries. As we age, our tendons age and degenerate, making recovery from these injuries more difficult.
If the patient's injury is not responding to treatment as quickly as expected, the physician should reconsider the diagnosis (see Differentials and Other Problems to Be Considered). Of paramount importance is reconsidering whether intra-abdominal, intrapelvic, or spinal pathology is responsible for the patient’s symptoms. Further imaging may be necessary to help rule out more worrisome diagnoses.
Downplay the role of stretching, particularly in rapidly growing adolescents or mature weekend warriors because each, in their own way, needs short periods of light cardiovascular workouts, followed by several minutes of stretching of the lumbar, hip, and knee areas.
Most hip overuse syndromes occur not at the beginning of the athletic event, but after considerable time; this mechanism suggests a repetitive-use etiology or eventual microtears that are associated with aging and stiffened tendinous structures. Therefore, ask most patients to continue their warm-up and stretching programs, but athletes should not assume that warm-up and stretching programs, in themselves, are effective. Instead, these patients should attempt to exercise under the threshold that results in repetitive microtears and persistent hip pain. Athletes are well advised to develop programs of cross-training to maintain hip strength and flexibility if the slightest amount of hip tendinitis pain occurs.
Adolescents who present with pain around the hip joint by traction apophysis are expected to recover within a matter of months. Recurrence can be avoided if the intensity and volume of the sports activity is limited modestly until skeletal maturity occurs.
Aggressive athletes in their 20s or 30s may need ongoing physical therapy so that they can ascend the ladder of progressive exercise and return to their sports. Recurrence in this group is high, given the innate desire of these individuals to return to play too quickly. Fortunately, the tendinous structures in this group are pliable, and the chance for repetitive microtearing is lower than that in an older group.
Active athletes older than 40 years have the added burden of a decreasing tendinous pliability and a lower threshold of tendinitis recurrence. Their return to sports must be calculated with great care to slowly ramp up the level and intensity of their activity. A good rule of thumb is to not increase activity more than 10% per week until the patient has progressed back to reasonable exercise levels. In this active group, the reality of abandoning long-distance running or jumping sports may need to be addressed. The treatment team is encouraged to promote the patient's participation in new activities that provoke less hip pain, such as cycling.
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hip tendonitis and bursitis, hip tendinitis and bursitis, trochanteric bursitis, gluteus medius tendonitis, gluteus medius tendinitis, rectus femoris tendonitis, rectus femoris tendinitis, adductor strain, adductor tendonitis, adductor tendinitis, quadriceps tendonitis, quadriceps tendinitis, hamstring tendonitis, hamstring tendinitis, groin injury, groin pull, sports hernia, iliopsoas tendonitis, iliopsoas tendinitis, iliopsoas bursitis, apophysitis, avulsion fracture, tendinopathy
Jeffrey Rosenberg, MD, Director of Primary Care Sports Medicine Fellowship, Assistant Residency Director, Mountainside Hospital and Mountainside Family Practice Associates; Consulting Staff, New Jersey Sports Medicine Institute
Jeffrey Rosenberg, MD is a member of the following medical societies: American Medical Society for Sports Medicine and Society of Teachers of Family Medicine
Disclosure: Nothing to disclose.
Rutvik Patel, DO, Fellow in Sports Medicine, Mountainside Sports Medicine
Rutvik Patel, DO is a member of the following medical societies: American Academy of Family Physicians and American Medical Society for Sports Medicine
Disclosure: Nothing to disclose.
Leslie Milne, MD, Assistant Clinical Instructor, Department of Emergency Medicine, Harvard University School of Medicine
Leslie Milne, MD is a member of the following medical societies: American College of Sports Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
Disclosure: Nothing to disclose.
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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