Key points

Introduction

Tendinopathy is an important cause of musculoskeletal pain and disability. Although traditionally thought to be an inflammatory condition and described as tendonitis, subsequent data showed it to be primarily a degenerative problem, more appropriately labeled tendinosis. Tendinosis occurs with multiple microtrauma, leading to degeneration of tenocytes and the extracellular matrix, which fail to mature or remodel into normal tendon. This process has been described as angiofibroblastic hyperplasia, consisting of fibroblasts, vascular hyperplasia, and disorganized collagen. Risk factors for the development of tendinopathy include ballistic performance, repeated or high-force eccentric contractions, an adjacent convex surface or apex of a concavity, muscles that cross 2 joints, scant vascular supply, and repetitive tension.

Although inflammatory cells are generally not seen within the tendon substance in tendinopathy, inflammatory mediators have been found in the tendon’s surrounding milieu, suggesting that tendinopathy is not solely degenerative. This condition has been described as neurogenic inflammation, consisting of inflammatory mediators that induce matrix metalloproteinase production, leading to degradation of the extracellular matrix of the tendon and promoting neoangiogenesis. These abnormal neovessels are associated with neonerves, theorized to contribute to the pain of tendinopathy.

Tendinopathy has historically been treated with a wide range of interventions, including rest; cryotherapy; therapeutic ultrasound (US); stretching; strengthening, including eccentric-biased strengthening; taping; bracing; oral and topical analgesics and nonsteroidal antiinflammatory drugs (NSAIDs); extracorporeal shock-wave therapy; topical vasodilators; and corticosteroid injections. Few of these treatments have been shown to be effective, and corticosteroid injections, once a mainstay of tendinopathy treatment, have been found to be harmful to tendons. Consequently, clinicians have sought safer and more effective interventions for the treatment of this condition.

With the emergence of diagnostic musculoskeletal US, clinicians are better able to evaluate tendinopathy at the point of care while using an easily portable, safe, cost-effective, and high-resolution imaging modality. US is able to characterize tendon disorders in detail by assessing the tendon’s fibrillar architecture; identifying tears, enthesophytes, cortical irregularity, and intrasubstance calcifications; and quantifying hyperemia. With the use of US, the specific location of a disorder within a tendon can be more accurately and completely delineated. As the diagnostic capability of musculoskeletal US has improved, clinicians have also developed more advanced interventional procedures facilitated by US guidance, with procedural mechanisms corresponding with the improved understanding of tendon disorders outlined earlier. These procedures include percutaneous needle tenotomy (PNT), percutaneous ultrasonic tenotomy (PUT), high-volume injection (HVI), percutaneous needle scraping (PNS), and orthobiologic interventions. This article reviews common percutaneous US-guided procedures for the treatment of tendinopathy using chiefly some form of mechanical debridement or similar intervention to stimulate regeneration. For a discussion of orthobiologic substances, such as platelet-rich plasma and mesenchymal stem cells, see Malanga G, Abdelshahed D, Jayaram P: Orthobiologic Interventions Utilizing Ultrasound Guidance , in this issue.

Introduction

Tendinopathy is an important cause of musculoskeletal pain and disability. Although traditionally thought to be an inflammatory condition and described as tendonitis, subsequent data showed it to be primarily a degenerative problem, more appropriately labeled tendinosis. Tendinosis occurs with multiple microtrauma, leading to degeneration of tenocytes and the extracellular matrix, which fail to mature or remodel into normal tendon. This process has been described as angiofibroblastic hyperplasia, consisting of fibroblasts, vascular hyperplasia, and disorganized collagen. Risk factors for the development of tendinopathy include ballistic performance, repeated or high-force eccentric contractions, an adjacent convex surface or apex of a concavity, muscles that cross 2 joints, scant vascular supply, and repetitive tension.

Although inflammatory cells are generally not seen within the tendon substance in tendinopathy, inflammatory mediators have been found in the tendon’s surrounding milieu, suggesting that tendinopathy is not solely degenerative. This condition has been described as neurogenic inflammation, consisting of inflammatory mediators that induce matrix metalloproteinase production, leading to degradation of the extracellular matrix of the tendon and promoting neoangiogenesis. These abnormal neovessels are associated with neonerves, theorized to contribute to the pain of tendinopathy.

Tendinopathy has historically been treated with a wide range of interventions, including rest; cryotherapy; therapeutic ultrasound (US); stretching; strengthening, including eccentric-biased strengthening; taping; bracing; oral and topical analgesics and nonsteroidal antiinflammatory drugs (NSAIDs); extracorporeal shock-wave therapy; topical vasodilators; and corticosteroid injections. Few of these treatments have been shown to be effective, and corticosteroid injections, once a mainstay of tendinopathy treatment, have been found to be harmful to tendons. Consequently, clinicians have sought safer and more effective interventions for the treatment of this condition.

With the emergence of diagnostic musculoskeletal US, clinicians are better able to evaluate tendinopathy at the point of care while using an easily portable, safe, cost-effective, and high-resolution imaging modality. US is able to characterize tendon disorders in detail by assessing the tendon’s fibrillar architecture; identifying tears, enthesophytes, cortical irregularity, and intrasubstance calcifications; and quantifying hyperemia. With the use of US, the specific location of a disorder within a tendon can be more accurately and completely delineated. As the diagnostic capability of musculoskeletal US has improved, clinicians have also developed more advanced interventional procedures facilitated by US guidance, with procedural mechanisms corresponding with the improved understanding of tendon disorders outlined earlier. These procedures include percutaneous needle tenotomy (PNT), percutaneous ultrasonic tenotomy (PUT), high-volume injection (HVI), percutaneous needle scraping (PNS), and orthobiologic interventions. This article reviews common percutaneous US-guided procedures for the treatment of tendinopathy using chiefly some form of mechanical debridement or similar intervention to stimulate regeneration. For a discussion of orthobiologic substances, such as platelet-rich plasma and mesenchymal stem cells, see Malanga G, Abdelshahed D, Jayaram P: Orthobiologic Interventions Utilizing Ultrasound Guidance , in this issue.

Percutaneous needle tenotomy

US-guided PNT has been used as an independent treatment strategy as well as being combined with orthobiologic products. PNT involves repeatedly passing a needle through a tendon with the goal of disrupting the chronic degenerative process, including scar tissue, and encouraging localized bleeding and fibroblast proliferation, which can lead to growth factor release, collagen formation, and ultimately healing.

There is minimal research on the outcomes of US-guided PNT alone. Some of the first published studies that described PNT also involved the injection of local anesthetic and corticosteroid. In 2006, McShane and colleagues reported the results of 55 US-guided elbow common extensor tendon PNTs followed by infiltration of a mixture of corticosteroid and bupivacaine. Following this procedure, 80% of participants reported excellent or good outcomes, with no adverse events among any of the subjects, at an average follow-up of 28 months. In 2008, McShane and colleagues published a similar study of PNT for elbow common extensor tendinosis, but corticosteroid injection was not used in conjunction with the procedure. Of the 52 patients who participated in the study, 92% reported excellent or good outcomes at an average follow-up of 22 months, suggesting that omitting corticosteroid from the procedure improved clinical outcomes.

These findings were similar to a study published by Zhu and colleagues, which also reported 87% excellent or good outcomes after a US-guided elbow common extensor tendon PNT plus corticosteroid and local anesthetic injection, although some patients were treated with this intervention multiple times at intervals of 1 to 2 weeks. Note that, since these studies were published, newer evidence has been published suggesting that injecting corticosteroid directly into a tendon may be harmful and thus should generally be avoided.

In 2010, Housner and colleagues reported similar results with US-guided patellar tendon PNT. Of 47 subjects who underwent the procedure, 72% returned to activity with no or only minimal pain, 81% reported excellent or good satisfaction scores, and only 1 tendon ruptured, at 6 weeks postprocedure. Housner and colleagues also reported the prospective outcomes of US-guided PNT performed on 5 patellar tendons, 4 Achilles tendons, 1 proximal gluteus medius tendon, 1 proximal iliotibial band, 1 proximal hamstring tendon, 1 elbow common extensor tendon, and 1 proximal rectus femoris tendon. In all of these patients, visual analog scale (VAS) scores were significantly lower at the 4-week and 12-week follow-up periods and there were no reported complications. Similarly, Jacobson and colleagues published their retrospective results following US-guided PNT on 11 gluteus medius tendons, 2 gluteus minimus tendons, 8 hamstring tendons, and 1 tensor fascia lata tendon. Of these patients, 45% reported marked improvement, 37% reported some improvement, 9% reported no change, and 9% reported worsening symptoms. There is also 1 published case report of clinical and sonographic improvement after US-guided PNT of the supraspinatus tendon.

Some investigations have used US-guided PNT as the control group in studies comparing this intervention with PNT plus the addition of an orthobiologic product. Krey and colleagues identified 2 studies involving US-guided PNT in a systematic literature review. The first, conducted by Rha and colleagues, showed significant subjective clinical improvements at 6 months following US-guided PNT of the supraspinatus tendon. In this study, PNT alone was compared with PNT plus platelet-rich plasma injections. Similarly, Stenhouse and colleagues compared US-guided common extensor tendon PNT alone versus PNT plus autologous conditioned plasma injections. Following PNT alone, subjective symptom scales significantly improved at both 2 and 6 months postprocedure. Of note, in both of these studies, PNT was performed twice, at 1 month apart. Mishra and colleagues subsequently published a randomized controlled trial comparing PNT alone versus PNT with platelet-rich plasma injection for the treatment of elbow common extensor tendinopathy in 230 patients. In the PNT alone group, pain scores improved 56% versus baseline and treatment success was 68% at 24 weeks postprocedure.

In summary, there has only been 1 prospective study of the outcomes of US-guided PNT as the sole intervention for tendinopathy. However, all of the present PNT literature consistently notes improvement in symptoms and reports rare complications. Larger, randomized controlled trials are needed. Further prospective research is also needed to determine whether PNT should be repeated when a patient experiences suboptimal results or partial improvement and if so, when this is indicated. In addition, future investigations should address whether patients with partial-thickness tears fare better or worse than those with tendinopathy alone when treated with PNT.

Sample procedure: percutaneous needle tenotomy of the elbow common extensor tendon

The patient is placed in a supine position with the elbow flexed to 60° and the pronated forearm resting comfortably on the patient’s abdomen. The proximal end of a high-frequency (>10 MHz) linear-array US transducer is then placed over the palpable bony prominence of the lateral epicondyle ( Fig. 1 ). With the acoustic landmarks of the lateral epicondyle and the radial head visible, a long-axis view of the common extensor tendon is obtained ( Fig. 2 ). The area of tendinopathy is identified sonographically, typically characterized by tendon thickening; loss of normal fibrillar echotexture; hypoechogenicity; hyperemia, as visualized with color or power Doppler imaging; and possibly partial-thickness tears, represented by anechoic tendon defects that may be more conspicuous with transducer compression. The authors generally do not recommend that full-thickness tendon tears are treated with PNT, based on the available literature and proposed mechanism of action.

Patient, clinician, transducer, and needle positioning for performance of a US-guided percutaneous needle tenotomy of the elbow common extensor tendon. Sterile transducer cover not shown. Left, distal; right, proximal.

US image of elbow common extensor tendinopathy shown long axis to the transducer. Note thickening, hypoechogenicity, and loss of normal fibrillar echotexture of the tendon. Arrowheads indicate superficial and deep borders of the common extensor tendon. Bottom, deep; left, proximal; right, distal; top, superficial. LE, lateral epicondyle.

The procedural site and surrounding area is then prepared and draped in a sterile fashion, and the transducer is covered using a sterile transducer cover kit. Then, a 25-gauge needle is used under direct sonographic guidance to anesthetize the skin, subcutaneous tissue, and tendon with a rapid-onset local anesthetic, such as lidocaine. This needle is removed. Thereafter, under direct sonographic visualization, using a distal-to-proximal, needle-in-plane approach, a 19-gauge needle is inserted into the same entry site as the prior needle, and the tip is guided into the area of tendinopathy ( Fig. 3 ). The US transducer and needle are parallel to the fibers of the tendon in this view. With continuous sonographic visualization, the needle tip is then repeatedly passed through the tendinopathic area until the tendon has been adequately fenestrated. Adequate fenestration is subjective but is often appreciated by markedly less resistance perceived when the needle traverses the tendon. Care must be taken to not pass the needle deeper than approximately 50% of the total footprint of the lateral epicondyle in order to avoid inadvertent piercing of the radial collateral ligament, which lies deep to the common extensor tendon.

US image of percutaneous needle tenotomy of the elbow common extensor tendon, with both tendon and needle shown long axis to the transducer. Arrowheads indicate the needle. Bottom, deep; left, proximal; right, distal; top, superficial. LE, lateral epicondyle.

It is recommended that additional local anesthetic, such as lidocaine or ropivacaine, is kept in a syringe attached to the tenotomy needle throughout the procedure, so that additional local anesthetic may be administered if the patient experiences discomfort. However, although patient comfort should be respected, local anesthetic use should otherwise be judicious, because all local anesthetics may be toxic to tenocytes. Among these, bupivacaine may be the most toxic to tenocytes and its use during tendon procedures is generally not recommended by the authors.

The transducer should be periodically rotated 90° during the procedure to obtain a short-axis view of the common extensor tendon to ensure that the entire area of tendinopathy is being treated. In the long-axis view, the needle can also be used to abrade the cortex of the lateral epicondyle and any enthesophytes, potentially stimulating additional tendon healing. Intrasubstance tendon calcifications may also be disrupted by the needle. Following the procedure, the needle is removed from the skin, pressure is applied to the area to achieve adequate hemostasis, and a sterile adhesive dressing is placed over the procedural site.

There are many variables to this procedure, such as the size of the needle used for the tenotomy and the number of passes with the needle. Needles ranging from 16 to 22 gauge have been described in the literature. The number of needle passes may vary based on numerous factors, such as patient characteristics, severity and size of the tendinopathic area, presence or absence of tears, operator experience and comfort level, and needle gauge used. The number of needle passes ranges from 20 to 40 when it has been specifically noted in the available PNT literature, although the authors have frequently found that up to double this number may be necessary to achieve adequate fenestration and a satisfactory clinical outcome.

In addition, there is considerable variability in postprocedural care, such as the avoidance of antiinflammatory medications, the use of bracing, rehabilitation protocols, and return-to-activity guidelines. In general, the authors recommend that the patient remain in a sling for 2 days postprocedure, avoid repeated gripping or heavy lifting activities by the treated limb for 2 weeks postprocedure, perform only active range-of-motion exercises for the first 2 weeks postprocedure with no strengthening or stretching during this 2-week period, and engages in a rehabilitation program and return-to-activity schedule similar to that published by Finnoff and colleagues, culminating in a return to full activities at approximately 8 to 12 weeks postprocedure. In addition, the authors recommend avoidance of NSAIDs for 1 week before the procedure and for 2 weeks following it, at minimum, to avoid suppression of the beneficial and normal inflammatory phase of tendon healing induced by the procedure.