eMedicine Specialties > Sports Medicine > Hip

Piriformis Syndrome

Shishir Shah, DO, Consulting Staff, Comprehensive Woundcare, Banner Baywood Hospital
Thomas W Wang, MD, Consulting Staff, Department of Occupational Medicine, Kaiser-Permanente

Updated: Apr 28, 2009

Introduction

Background

Low back pain (LBP), is ubiquitous. An estimated 30-45% of persons aged 18-55 years have some form of back pain in their lifetime. LBP most commonly involves one of the following conditions: sciatic nerve entrapment, herniated nucleus pulposus, direct trauma, muscle spasm due to chronic or overuse injury, or piriformis syndrome.

Piriformis syndrome is characterized by pain and instability. The location of the pain is often imprecise, but it is often present in the hip, coccyx, buttock, groin, or distal part of the leg. The history and physical findings are key elements in differentiating the more common forms of LBP and piriformis syndrome. The literature and general knowledge on piriformis syndrome is limited, compared with that of sciatica or disc herniation. However, the common findings associated with piriformis syndrome are agreed upon.

Yeoman first described piriformis syndrome in 1928 as periarthritis of the anterior sacroiliac joint. The history of this condition stems from one of many causes of lower back and leg pain. Many patients who underwent unsuccessful surgery in the lumbosacral region were later found to have piriformis syndrome.

For excellent patient education resources, visit eMedicine's Osteoporosis and Bone Health Center and Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education article Back Pain.

Frequency

United States

The female-to-male incidence ratio of piriformis syndrome is 6:1. In one study at a regional hospital, 45 of 750 patients with LBP were found to have piriformis syndrome. Another author estimated that the incidence of piriformis syndrome in patients with sciatica is 6%.

Functional Anatomy

The function of the piriformis muscle is to externally rotate and abduct the thigh. The sacral plexus is closely associated with the anterior surface of the piriformis muscle. The lumbosacral trunk and the ventral rami of the first 3 sacral nerves form the sacral plexus. The sciatic nerve passes inferior to the piriformis muscle.

The sciatic nerve exits the pelvis via 4 routes: (1) The nerve passes anteriorly to the piriformis between the rims of the greater sciatic foramen. (2) The peroneal portion of the sciatic nerve passes through the piriformis; the tibial portion passes anterior to the piriformis muscle. (3) The peroneal branch of the sciatic nerve loops above and posterior to the piriformis muscle, whereas the tibial branch passes anterior to the piriformis muscle. (4) The undivided sciatic nerve penetrates the piriformis muscle.

Dysfunction of the piriformis muscle can cause signs and symptoms of pain in the sciatic nerve distribution, that is, in the gluteal area, posterior thigh, posterior leg, and lateral aspect of the foot.

Sport-Specific Biomechanics

Gait mechanics help in demonstrating the physiologic features of piriformis hypertrophy. When a person takes a step forward, the extremity moves from external rotation to internal rotation, and the piriformis muscle lengthens. This stretching is followed by reflex contraction. A second contraction in the initially stretched piriformis muscle occurs when the opposite foot swings forward. This gait pattern leads to hypertrophy, and the dual contraction is further exacerbated by the stretching of the piriformis muscle on the side of a shortened leg.

More commonly, piriformis syndrome is secondary to inflammation due to gluteal trauma or spasm. The effect of this inflammatory process on the sciatic nerve is chemical rather than mechanical. Several theories suggest that the following are key factors in the muscle hyperfunction or spasm that leads to an interstitial myofibrositis: extravasation of blood; release of serotonin from platelets; and prostaglandin E, serotonin, bradykinin, and histamine release.

Although no general consensus about the etiology and pathophysiology of piriformis syndrome exists, many physicians and physical therapists attribute this syndrome to a specific mechanism involving the sciatic nerve. For example, Benson and Schutzer attributed the syndrome to blunt trauma to the buttocks that results in hematoma formation and subsequent scarring between the sciatic nerve and the short external rotators.¹ Entrapment of the sciatic nerve at the sciatic trunk (where it leaves the pelvis and crosses the greater sciatic notch) is an infrequent cause. This entrapment can also occur as a result of an enlarged hypertrophic piriformis, an inflamed piriformis muscle, tumors, cysts, and pseudoaneurysms.

Clinical

History

Patients with piriformis syndrome have the following symptomatic history:

• Chronic pain in the buttocks
  • This pain may radiate to the lower leg and worsens with walking or squatting.
  • This pain may imitate LBP.
• Pain with bowel movements
• Pain in the labia majora in women; pain in the scrotum in men
• Dyspareunia in women
• Pain when getting up from bed
• Pain exacerbated by hip adduction and internal rotation
• Intolerance to sitting

Physical

Piriformis syndrome is a diagnosis of exclusion.

• At physical examination, the most important factor that differentiates sciatic pain from piriformis syndrome is the absence of neurologic deficit in piriformis syndrome.
• Herniation or disc compression results in intraneural derangement of the nerve root structure, whereas piriformis syndrome causes a qualitative epineural irritation.
• In piriformis syndrome, the only true-positive sign is tenderness over the gluteal region.
  • The pain can be reproduced with maximum elongation of the piriformis muscle in flexion, adduction, and internal rotation of the hip.
  • Weakness can be observed with resisted external rotation and abduction of the hip.
• Several authors describe the use of the following signs in diagnosing piriformis syndrome:
  • Lasegue sign: Pain is present in the vicinity of the greater sciatic notch during extension of the knee with the hip flexed to 90 º, tenderness to palpation of the greater sciatic notch is noted.
  • Pace sign: Pain and weakness are present on resisted abduction-external rotation of the thigh.
  • Freiberg sign: Pain occurs with passive internal rotation of the extended thigh when the patient is supine.
• Robinson, who first described the syndrome, stated that piriformis syndrome had 6 cardinal features:
  • Positive Lasegue sign
  • Sausage-shaped mass over the piriformis muscle
  • Gluteal atrophy in chronic cases
  • Trauma to the region
  • Pain in the sacroiliac joint region, gluteal muscles, or greater sciatic notch
  • Pain exacerbated by lifting and relieved by traction on the affected extremity
• Beatty reproduced the pain of piriformis syndrome in the following way² :
  • The patient lies with the painful side up and the involved leg flexed.
  • The knee of the affected side rests on the table. Pain in the buttocks is reproduced when the patient lifts the leg and knee slightly above the table.
• Other authors conclude that pain can be reproduced in the lateral pelvic wall by means of rectal or pelvic examination.

Causes

• Trauma to the buttocks or gluteal region is the most common cause of piriformis syndrome.
• Skiers, truck drivers, tennis players, and long-distance bikers are at high risk.
• In Morton foot, the prominent head of the second metatarsal causes foot instability and a reactive contraction of the external rotators of the hip during gait.
• Spinal stenosis can lead to bilateral piriformis tenderness.
• Anatomic variations of the divisions of the sciatic nerve above, below, and through the belly of the piriformis muscle may be causative factors.

Differential Diagnoses

Other Problems to Be Considered

• Bursitis or weaver's bottom (ie, ischiogluteal bursitis)
• Gout
• Pelvic mass, tumor, or endometriosis (in women)
• Referred pain to the buttock caused by pronator forces of the foot
• Sciatica caused by compression secondary to a fibrotic band, hematoma, or aneurysm of the inferior or superior gluteal artery
• Spinal stenosis

Workup

Imaging Studies

• Computed tomography (CT) scanning
  • CT scans may demonstrate a large mass anterior to the piriformis muscle.
  • More importantly, CT scans can be used to identify spinal stenosis or arthritic changes.
• Magnetic resonance imaging (MRI)
  • MRI findings can rule out other causes of back pain, such as a herniated disc, spinal tumor, or abscess.
  • The piriformis muscle also can appear enlarged on T1- or T2-weighted images.
• Electromyography (EMG)
  • EMG can also be performed to determine neurologic or muscular changes.
  • In piriformis syndrome, EMG findings in the gluteus minimus, gluteus medius, and tensor fasciae latae muscles are normal.
  • In piriformis syndrome, abnormal patterns are found in the gluteus maximus and piriformis muscles.
  • In the case of a herniated disc, all muscles that are posteriorly and anteriorly innervated should be affected.
  • With a herniated disc, a significant delay in the Hoffman reflex, or H-reflex (motor nerve fiber response after activation of afferent sensory spindle fibers), in the affected limbs is often present during EMG.

Procedures

• Diagnostic injection of the piriformis syndrome trigger point is performed as follows:
  • Localize the pain at the sciatic notch, transvaginally or transrectally.
  • Draw 5-7 mL of 2.5% lidocaine or bupivacaine into a 10-mL syringe with a 27-gauge needle.
  • Prepare a sterile field and apply Betadine over the trigger-point area.
  • Inject the anesthetic after aspirating to confirm that the needle is not in a vascular bundle.
  • Remove the needle, and apply pressure to the area to ensure hemostasis.
  • Allow the patient to ambulate and to abduct and externally rotate the affected leg.
  • If the pain subsides, the likely cause of the pain is piriformis syndrome.
  • This procedure is both therapeutic and diagnostic.

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Occupational Therapy

Professions that involve prolonged sitting can worsen symptoms of piriformis syndrome, and patients should avoid sitting for long periods. Patients should be instructed to stand and walk every 20 minutes. Patients should make frequent stops when driving to stand and stretch.

Surgical Intervention

Most intraoperative findings include adhesions around the piriformis muscle and anatomic variations of the divisions of the sciatic nerve above, below, and through the belly of the piriformis muscle.

Consultations

• Physical therapists are helpful in instructing the patient about the various maneuvers for stretching and pain relief.

• Referral to an orthopedic surgeon is indicated when the diagnosis is not clear or when conservative therapy fails and a surgical evaluation is needed.

• Referral to a neurologist and/or neurosurgeon is indicated for EMG studies and for an evaluation of associated disc herniation and spinal stenosis.

• An osteopathic physician can perform manipulation techniques, along with primary conservative medical intervention.³

• A gynecologist can also assist in differentiating causes of dyspareunia and pelvic pain in women with suspected piriformis syndrome. A gynecologist can assist in identifying trigger points for local injections in female patients via the vaginal route.

Other Treatment

• The most widely recognized treatment is local injection. Local anesthetics (eg, lidocaine, bupivacaine) can be injected in trigger points. The painful piriformis muscle can be identified by palpating the buttocks or by palpating transrectally in males and transvaginally in females. A spinal needle or 25-gauge, 1.5-inch needle is directly aimed at the examining finger. The location is usually through the sciatic notch and inferior to the bony margin; the most common trigger point is 1 inch lateral and caudal to the midpoint of the lateral border of the sacrum. An intramuscular (IM) dose of 50-100 mg can be injected.
• Manual manipulation can also be applied (see Physical Therapy above). A common method, mobilization of the spine, is often used by osteopathic physicians (those with a DO degree).³ The patient is placed in a lateral recumbent position on the unaffected side. The physician faces the patient and rotates the patient’s upper body away by laterally pulling on the lower arm. Then the physician places his or her cephalad hand most superiorly on the paravertebral muscles.The patient’s top leg is brought over the edge of the table. The physician places her caudal hand over the patient's hip in the line of the lowered leg. Force is applied in the direction of the lowered leg but perpendicular to the muscle fibers. When tension is reduced, a thrust (high-velocity low-amplitude [HVLA]) technique can be applied.
• NSAIDs and opiates can also be administered to patients with piriformis syndrome. However, to the author’s knowledge, no study has been performed to assess the treatment of piriformis pain with intravenous (IV) or oral medications. Physician discretion is recommended in using medications such as those used to treat LBP.

Recovery Phase

Rehabilitation Program

Physical Therapy

In the recovery phase, the patient may begin gradual strengthening activities for the piriformis and gluteal muscles. Therapeutic modalities may be continued through this phase to enhance the benefits of rehabilitation. As the patient becomes asymptomatic, he or she may initiate light sport-specific activities and functional training. Addressing posture and faulty pelvic mechanics is important when resuming activity. Some athletes may need to change their footwear or undergo an orthotic consultation to correct their pelvic alignment and avoid further stress on the piriformis muscle.

Other Treatment (Injection, manipulation, etc.)

See Other Treatment for the acute phase.

Maintenance Phase

Rehabilitation Program

Physical Therapy

During the maintenance phase of rehabilitation, the patient should continue performing a home exercise program for increasing flexibility and strength. Athletes may gradually increase their training volume as tolerated. Runners should be cautious when resuming speed training and hill running, doing so in a gradual fashion with proper warm-up and cool-down periods. Compliance to a daily stretching program is crucial to avoid recurrence of this syndrome. Return to play is dependent on many factors (eg, severity of condition, how soon treatment was initiated, level of patient compliance to program).

Surgical Intervention

See Surgical Intervention for the acute phase.

Consultations

See Consultations for the acute phase.

Other Treatment

See Other Treatment for the acute phase.

Medication

NSAIDs are mentioned not in this section because of the lack of any documented or studied effectiveness in piriformis syndrome. However, physicians may use any number of these agents, on the basis of their experience in managing LBP or neuropathies.

Naja et al investigated whether clonidine-bupivacaine nerve-stimulator guided injections are effective in achieving long-lasting pain relief in piriformis syndrome compared with bupivacaine guided injection.⁴ Significantly lower pain scores and analgesic consumption were observed with bupivacaine-clonidine compared with bupivacaine-saline. Additionally, pain at 6 months was significantly greater in the bupivacaine-saline group (78%) compared with the bupivacaine-clonidine group (8%).⁴

Anesthetics

The drugs of choice for local injection in painful piriformis syndrome include the anesthetic agents lidocaine and/or bupivacaine. Both are in the family of amide anesthetics. Use is based on the desired duration of action. Doses, as described below, are intramuscularly (IM) administered by identifying the trigger point. Be sure to aspirate first to avoid injecting the medication into a blood vessel.

Lidocaine HCL (Xylocaine, Dilocaine, Anestacon)

Amide anesthetic that stabilizes neuronal membrane by inhibiting ionic fluxes. Absorbed completely with parenteral administration. Metabolized by the liver. Unchanged metabolites are excreted by the kidneys. Half-life is typically 1.5-2 h. Lidocaine crosses blood-brain and placental barriers by passive diffusion. Indicated for regional and local anesthesia.

Dosing

Adult

<7 mg/kg IM; should not exceed 4.5 mg/kg when used with epinephrine

Regional anesthesia: typically <100 mg IM

Pediatric

<3 years: Not established

>3 years: <3 mg/kg IM; typically, <50 mg IM

Interactions

Coadministration with cimetidine or beta-blockers increases toxicity; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase the effects of succinylcholine

Contraindications

Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes and Wolf-Parkinson-White syndromes; avoid in severe sinoatrial, AV, or intraventricular block if artificial pacemaker not in place

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Oxygen and resuscitative equipment should be available for immediate use; carefully administer solutions containing epinephrine in areas of end arteries (eg, digits, genitalia, nose); perform cardiovascular and respiratory monitoring; caution in patients with liver disease and impaired cardiovascular function; can trigger familial malignant hyperthermia; IM use may increase in creatinine phosphokinase levels (CPK) (can compromise use of CPK as sole marker for myocardial infarction)

Bupivacaine Hydrochloride (Sensorcaine, Marcaine)

Amide anesthetic that blocks conduction of nerve impulses by inhibiting ionic fluxes. Absorbed completely with parenteral administration and metabolized by the liver. Unchanged metabolites are excreted by the kidneys. Half-life is typically 3-4 h and peak levels are achieved in 30-40 min. Bupivacaine crosses blood-brain and placental barriers by passive diffusion. Indicated for regional and local anesthesia.

Dosing

Adult

<400 mg IM

Regional anesthesia: <100 mg IM

Pediatric

<12 years: Not established

>12 years: <50 mg IM

Interactions

Bupivacaine solutions containing epinephrine may interact with MAOIs or tricyclic antidepressants and cause severe, prolonged hypertension; phenothiazines and butyrophenones may reduce the effect of epinephrine solutions; vasopressor drugs and ergot oxytocic drugs may cause persistent hypertension or cerebral vascular accidents when used with lidocaine.

Contraindications

Documented hypersensitivity; septicemia; spinal deformities; severe hypertension; existing neurologic disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Oxygen and resuscitative equipment should be available for immediate use; in solutions containing epinephrine, carefully administer in areas of end arteries (eg, digits, genitalia, nose); perform cardiovascular and respiratory monitoring; caution in patients with liver disease and impaired cardiovascular function; can trigger familial malignant hyperthermia; IM use may increase CPK levels (can compromise use of CPK as sole marker for myocardial infarction)

Follow-up

Return to Play

Athletes with piriformis syndrome may return to play when they demonstrate full pain-free range of motion and strength of the affected side and can perform their sport-specific activities without discomfort. Patients must adhere to the aforementioned stretching exercises and perform a liberal warm-up before the activity. The duration for return to play varies with each individual and the type of treatment rendered. The longer an athlete ignores the problem before seeking treatment, the longer his or her rehabilitation will take.

Prevention

Recurrence of pain in the piriformis muscle can be prevented by continuing the stretching exercises and by avoiding risk factors.

Prognosis

Most patients with piriformis syndrome progress well after a local trigger-point injection. Recurrences are uncommon after 6 weeks of therapy. After surgery, patients treated with piriformis release return to their activities in an average of 2-3 months.

Education

Patients with piriformis syndrome should modify their activity habits. For example, patients are recommended to adhere to the following: avoid prolonged sitting, perform the suggested stretching exercises 2 or 3 times a day and before participating in a sports activity, and avoid direct trauma to the gluteal region.

Patient education should be an ongoing process throughout the course of rehabilitation. Physical therapists and occupational therapists are valuable members of the team for teaching the patient strategies used to recover from this syndrome and also to prevent recurrences. Patients should be informed of the importance of their routine compliance with an individualized home exercise program.

Miscellaneous

Medicolegal Pitfalls

• The authors' review did not reveal any medicolegal issues related to piriformis syndrome.
• As with the management in any back pain, other causes must be excluded before piriformis syndrome can be diagnosed.
• In particular, the physician must be highly sensitive to the possibility of acute cord syndromes, fractures, neurologic deficits, and vascular compromise.

References

1. Benson ER, Schutzer SF. Posttraumatic piriformis syndrome: diagnosis and results of operative treatment. J Bone Joint Surg Am. Jul 1999;81(7):941-9. [Medline].

2. Beatty RA. The piriformis muscle syndrome: a simple diagnostic maneuver. Neurosurgery. Mar 1994;34(3):512-4; discussion 514. [Medline].

3. Boyajian-O'Neill LA, McClain RL, Coleman MK, Thomas PP. Diagnosis and management of piriformis syndrome: an osteopathic approach. J Am Osteopath Assoc. Nov 2008;108(11):657-64. [Medline]. [Full Text].

4. [Best Evidence] Naja Z, Al-Tannir M, El-Rajab M, et al. The effectiveness of clonidine-bupivacaine repeated nerve stimulator-guided injection in piriformis syndrome. Clin J Pain. Mar-Apr 2009;25(3):199-205. [Medline].

5. Filler AG. Piriformis and related entrapment syndromes: diagnosis & management. Neurosurg Clin N Am. Oct 2008;19(4):609-22, vii. [Medline].

6. Greenman PE. Piriformis syndrome. Principles in Manual Medicine. 2^nd ed. Baltimore, Md: Lippincott Williams & Wilkins; 1996:467-74.

7. Jankiewicz JJ, Hennrikus WL, Houkom JA. The appearance of the piriformis muscle syndrome in computed tomography and magnetic resonance imaging. A case report and review of the literature. Clin Orthop Relat Res. Jan 1991;262:205-9. [Medline].

8. Julsrud ME. Piriformis syndrome. J Am Podiatr Med Assoc. Mar 1989;79(3):128-31. [Medline].

9. Physicians' Desk Reference [book on CD-ROM]. Montvale, NJ: Thompson Medical Economics; 1999. Medical Economics.

10. Merlo IM, Poloni TE, Alfonsi E, Messina AL, Ceroni M. Sciatic pain in a young sportsman. Lancet. Mar 22 1997;349(9055):846. [Medline].

11. Naja Z, Al-Tannir M, El-Rajab M, et al. The effectiveness of clonidine-bupivacaine repeated nerve stimulator-guided injection in piriformis syndrome. Clin J Pain. Mar-Apr 2009;25(3):199-205. [Medline].

12. Ozaki S, Hamabe T, Muro T. Piriformis syndrome resulting from an anomalous relationship between the sciatic nerve and piriformis muscle. Orthopedics. Aug 1999;22(8):771-2. [Medline].

13. Pace JB, Nagle D. Piriformis syndrome. West J Med. 1976;24:435-9.

14. Papadopoulos SM, McGillicuddy JE, Albers JW. Unusual cause of 'piriformis muscle syndrome'. Arch Neurol. Oct 1990;47(10):1144-6. [Medline].

15. Parziale JR, Hudgins TH, Fishman LM. The piriformis syndrome. Am J Orthop. Dec 1996;25(12):819-23. [Medline].

16. Pecina HI, Boric I, Smoljanovic T, Duvancic D, Pecina M. Surgical evaluation of magnetic resonance imaging findings in piriformis muscle syndrome. Skeletal Radiol. Nov 2008;37(11):1019-23. [Medline].

17. Silver JK, Leadbetter WB. Piriformis syndrome: assessment of current practice and literature review. Orthopedics. Oct 1998;21(10):1133-5. [Medline].

18. Steiner C, Staubs C, Ganon M, Buhlinger C. Piriformis syndrome: pathogenesis, diagnosis, and treatment. J Am Osteopath Assoc. Apr 1987;87(4):318-23. [Medline].

19. Tibor LM, Sekiya JK. Differential diagnosis of pain around the hip joint. Arthroscopy. Dec 2008;24(12):1407-21. [Medline].

Keywords

piriformis syndrome, hip pocket neuropathy, sciatic neuritis, wallet neuritis, lower back pain, low back pain, LBP, periarthritis of the anterior sacroiliac joint, piriformis muscle, piriformis hypertrophy, sciatic nerve entrapment, herniated nucleus pulposus, muscle spasm due to chronic or overuse injury, sciatica, Morton foot, spinal stenosis, nerve entrapment syndromes

Contributor Information and Disclosures

Author

Shishir Shah, DO, Consulting Staff, Comprehensive Woundcare, Banner Baywood Hospital
Shishir Shah, DO is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Osteopathic Association
Disclosure: Nothing to disclose.

Coauthor(s)

Thomas W Wang, MD, Consulting Staff, Department of Occupational Medicine, Kaiser-Permanente
Thomas W Wang, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Medical Editor

Joseph P Garry, MD, FACSM, FAAFP,, Director of Sports Medicine and Sports Medicine Fellowship, Associate Professor of Family Medicine and Exercise and Sport Science, Department of Family Medicine, East Carolina University Brody School of Medicine
Joseph P Garry, MD, FACSM, FAAFP, is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Heart Association, American Medical Society for Sports Medicine, and North American Primary Care Research Group
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

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.

Chief Editor

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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