Pathology

Tendinopathies can be acute or chronic and can affect athletic and sedentary patients, leading to long periods of sport cessation and interfering with the activities of daily living. ^, Intrinsic (age, gender, body composition, tendon temperature, systemic diseases, muscle strength, flexibility, previous injuries, anatomic variants, genetic predisposition and blood supply) and extrinsic factors (overloading, underloading, training loading error, drugs), alone or in combination, can cause tendinopathy. Pathologic tendons become increasingly painful in response to loading. Clinically, they appear swollen and thickened, and are painful on palpation.

The diagnosis of tendinopathy is based on careful history and detailed clinical examination. High-resolution real-time ultrasonography is frequently used to image tendon disorders and confirm the diagnosis. Ultrasonography is an operator-dependent technique that can influence the image obtained, depending on transducer handling and machine settings. Consequently, the interobserver reliability of ultrasonographic assessment of tendon structures can be problematic, and changes over time may make it difficult to evaluate the progression or the improvement of the tendinopathy.

Ultrasound Imaging Findings

Sonographic features of tendinopathy include abnormal tendon size (thickness), shape (bulging), changes in echogenicity, altered fibrillar appearance, the presence of fluid, sheath thickening, and neovascularization in the tendon or its sheath. Neovessels are associated with abnormal nerves ingrowth, which are thought to contribute to tendinopathic pain. ^, Color Doppler and power Doppler ultrasonography are established methods to detect increased blood flow associated with neovascularization within the tendons. Neovascularization in the absence of pain may not be pathologic, and can just indicate a physiologic response to recent physical activity; however, neovascularization within the tendinopathic area is generally present in patients with chronic painful tendinopathy. ^,

Treatment Options

Conservative treatment of tendinopathy can be disappointing, and 25% to 45% of patients may require surgery. ^, Surgery used to be indicated after a 6-month period of nonoperative management, but is now advocated only as a last resort.

Platelet-rich plasma (PRP) injections have become popular in clinical practice for chronic tendinopathy, as it is hypothesized that a variety of growth factors may promote a healing response in the tissue. However, the results of randomized controlled trials (RCTs) have been mixed, and at present there is insufficient evidence for the effectiveness of PRP for tendinopathy of the main body of the Achilles tendon.

There is no accepted standard regimen for the management of tendinopathies, but the inclusion of progressive tendon loading through heavy load concentric and/or eccentric exercise as part of the management plan is crucial. ^, Loading exerts beneficial effects on tenocyte homeostasis and promotes tendon collagen synthesis, and can result in decreased pain and increased performance. If the clinical symptoms of tendinopathy do not resolve, other nonoperative treatments are available, including extracorporeal shockwave therapy or nitric oxide patches. Injections at the interface between the tendon and peritendinous tissues should also be considered if physiotherapy and shockwave therapy are unsuccessful in reducing pain and facilitate tendon loading.

The rationale behind high-volume image-guided injections (HVIGIs) for the management of tendinopathy is to use a large quantity of fluid to mechanically sever the neovessels and the accompanying nerve ingrowth, either by direct mechanical trauma or through pressure-mediated secondary ischemia. In addition, the local anesthetic used in the HVIGI contributes to reducing nociception by producing a short-term local block of the neonerves, and through longer-term neonerve neurotoxicity. Local anesthetics produce a variable neurotoxic effect. The use of corticosteroids likely counteracts the mechanically induced reaction to the injection of the large volume of fluid; it may also contribute to slowing down the re-formation of adhesions between the tendon and peritendinous tissues. ^,

HVIGI may be more effective than PRP in improving outcomes of chronic tendinopathies in the short term and similar results long term, with numerous studies confirming the value of HVIGI in tendinopathies. ^{, ,} In patients with chronic tendinopathies, HVIGI significantly reduces pain and stiffness, reduces tendon thickness and intratendinous vascularity on ultrasonographic imaging, and improves function at both the short-term follow-up (2 weeks) and up to an average of 30.3 weeks. ^, The success rate of HVIGI in returning patients to the desired level of sport is up to 68%.

Corticosteroids are an adjunct to the high-volume injection (very diluted with 0.25 mL in 50 mL of local anesthetics + saline), and are injected at the interface between the Achilles Tendon and Kager’s fat to minimize the risk of tendon rupture or other adverse events associated with intratendinous injections. Some authors believed that HVIGI without corticosteroids yielded similar effects on pain reduction and functional improvement in comparison to HVIGI with corticosteroids. However, a recent level 1 RCT found HVIGI with corticosteroids had better outcomes in pain reduction, improved function, and reduced tendon thickness. ^,

The clinical diagnosis and management of tendinopathies are not straightforward. Hence, patients should understand that symptoms may recur with either conservative or surgical approaches. Below we describe the technique for the Achilles tendon in detail but see Table 27.1 for general instructions for other areas.

TABLE 27.1

Local Anesthetic and Corticosteroid Dosages, Saline Volumes, Needle Approach and Injection Site, Ultrasound Transducer Placement, and Equipment Needed for the High-Volume Image-Guided Injection (HVIGI) of Different Pathologies.

HVIGI	Local Anesthetic	Corticosteroid Dosage	Saline Volume	Needle Approach and Injection Site (US Imaging Plane)	Equipment
Achilles tendinopathy	Bupivacaine 0.5% 10 mL	Depo-Medrone 0.25 mL (=10 mg)	4 × 10 mL	Medial approach, interface between Achilles tendon and Kager’s fat pad (US transverse plane)	5 × 10 mL Luer Lock syringes Long connecting tube Green needle (21 G × 40 mm)
Patellar tendinopathy	Bupivacaine 0.5% 10 mL	Depo-Medrone 0.25 mL (=10 mg)	3 × 10 mL	Medial or lateral approach, interface between patellar tendon and Hoffa’s fat pad (US transverse plane)	4 × 10 mL Luer Lock syringes Long connecting tube Green needle (21 G × 40 mm)
Shoulder subacromial impingement (rotator cuff tendinopathy, SASD bursitis)	Bupivacaine 0.5% 20–30 mL	Depo-Medrone 40 mg	—	Lateral approach into the SASD bursa (US transverse plane)	2–3 × 10 mL Luer Lock syringes Long connecting tube Green needle (21 G × 40 mm)
Sinus tarsi syndrome	Bupivacaine 0.5% 10 mL	Triamcinolone 40 mg	—	Anterolateral approach perpendicular to skin, deep at the apex of the sinus tarsi.	1 × 10 mL Luer Lock syringe Long connecting tube Green needle (21 G × 40 mm)
Elbow lateral epicondyle tendinopathy (“tennis elbow”)	Bupivacaine 0.5% 10 mL	Depo-Medrone 40 mg	—	Distal approach until needle is in contact with bone, at common extensor tendon enthesis (US longitudinal plane)	3 × 3 mL Luer Lock syringes Long connecting tube Orange needle (25 G × 25 mm)
Plantar fasciopathy	Bupivacaine 0.5% 10 mL	Depo-Medrone 40 mg	—	Medial approach, at plantar fascia insertion onto calcaneus (US transverse plane)	1 × 10 mL Luer Lock syringe Long connecting tube Green needle (21 G × 40 mm)
Greater trochanteric pain syndrome (gluteal tendinopathy)	Bupivacaine 0.5% 20 mL	Depo-Medrone 40 mg	—	Lateral approach until needle is in contact with bone, at lateral facet of greater trochanter	2 × 10 mL Luer Lock syringes Long connecting tube 22 G spinal needle
Small tendons tendinopathy/tenosynovitis (tibialis posterior, finger flexor, etc.)	Bupivacaine 0.5% 10–20 mL	Depo-Medrone 40 mg	—	Transverse or longitudinal approach, interface between tendon and tendon sheath (US TS or LS plane)	1–2 × 10 mL Luer Lock syringe Short connecting tube Orange needle (25 G × 25 mm)
Morton’s neuroma	Bupivacaine 0.5% 10 mL	Depo-Medrone 40 mg	—	Approach from dorsum via intermetatarsal space, directly into the fibrotic capsule of the neuroma (US on plantar aspect, transverse across metatarsal heads)	1 × 10 mL Luer Lock syringe Long connecting tube Green needle (21 G × 40 mm)

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