1 Diagnostic Ultrasound and Guided Injection

10.1055/b-0038-160896

1 Diagnostic Ultrasound and Guided Injection

Abstract

Given its comparative ease of availability, short scanning time, and ability to dynamically assess tissue and structure interplay, ultrasound is rapidly becoming the investigation of choice for many musculoskeletal conditions. This chapter outlines both the normal and common pathological ultrasound appearance of tendons, joints, bursae, muscles, and nerves as well as the use of ultrasound to ensure accurate needle placement during interventional procedures.

In addition to the diagnostic capabilities of ultrasound in the assessment and management of musculoskeletal conditions and in contrast to magnetic resonance imaging (MRI), ultrasound also has the capacity to be used as an interventional modality enhancing the accuracy of injection techniques.

Eustace (1997) demonstrated that even in the hands of musculoskeletal specialists only a minority of injections for shoulder pain were performed accurately with only 29% of subacromial and 42% of intra-articular injections reaching their intended target. Similar results have been demonstrated in patients with de Quervain’s tenosynovitis (Zhingis 1998). Perhaps, not surprisingly, outcome has been demonstrated to significantly correlate with accuracy of injection with a systematic review and meta-analysis demonstrating that ultrasound-guided shoulder girdle injections are more accurate and more effective than landmark-guided injections (Aly et al 2014). Needle placement into smaller joint spaces is of particular difficulty, a fact in part due to the lack of aspirate from smaller joints, such as the carpometacarpal joint of the thumb, making accurate needle placement in these joints extremely difficult. For this reason injections performed under imaging are becoming more popular (Balint 1997, Ghozlan 2000, Koski 2000, Weidner 2004). Fig. 1‑1 and Fig. 1‑2 demonstrate the accuracy possible with ultrasound-guided injection. In Fig. 1‑1 an injection is given between the flexor tendon sheath and the tendon of flexor pollicis longus at the level of the metacarpophalangeal joint of the thumb. In Fig. 1‑2 a needle is placed immediately deep to the median nerve in the carpal tunnel.

Fig. 1.1 Ultrasound-guided injection of the tendon sheath of flexor pollicis longus at the level of the metacarpophalangeal joint of the thumb (MC). The needle (*yellow arrowhead*) may be seen approaching from the left of the image. The needle rests between the flexor sheath (*yellow curved arrow*) and the tendon itself (*white oval*). In this image the sheath measures approximately 1 mm in depth and demonstrates the accuracy of needle placement possible with ultrasound guidance.

Fig. 1.2 Transverse ultrasound image of the carpal tunnel. The median nerve appears as a low echo oval-shaped foci (*yellow oval*). The tendons of flexor digitorum superficialis (*white oval*) may be seen deep to the median nerve. A needle may be seen immediately between the two (*yellow arrowheads*).

Fig. 1.2 Accurate needle placement is also of importance in more deeply placed structures such as the hip joint in order that both the correct target is injected and that neurovascular structures are avoided. A study by Leopold (2001) assessed the accuracy of needle placement with intra-articular hip injection using only anatomical landmarks as a guide. Using this “blind” approach the needle pierced or contacted the femoral nerve in 27% of anterior injections and was within 5 mm of the femoral nerve in 60% of all anterior attempts. Using a lateral approach the needle was never within 25 mm of any neurovascular structure in any injection; however, only 80% of injections managed to reach the joint cavity. Fig. 1‑3 demonstrates injection of the anterior aspect of the hip joint.

Fig. 1.3 Longitudinal image of the anterior hip joint. A needle (*yellow arrowheads*) may be seen lying up against the anterior joint capsule (*curved arrow*) prior to injection.

1.1 Diagnostic Ultrasound and Musculoskeletal Medicine

1.1.1 Tendons

Ultrasound may be considered the gold-standard investigation for examination of tendons demonstrating detailed internal structure not clearly seen with MRI (Grassi 2000, Joseph 2009). In addition to a high degree of spatialresolution, ultrasound also has the advantage of relatively short scanning time, may be performed as a bedside procedure and, as it takes place in real time, allows the dynamic assessment of tendons and their relationship with surrounding tissue interface.

Tendons are collagenous structures with additional tenocytes, water, and other matrix components. Tendons are normally surrounded by loose connective tissue, the paratenon, which forms an elastic sleeve that allows free movement of the tendon. Where the tendon must travel through a narrow space, or come in contact with a bony area, such as the dorsal compartments of the wrist, this loose connective tissue becomes more specialized into a tenosynovial sheath, helping to reduce friction between the tendon and surrounding structures (Kannus 2000).

In the nonpathological state, normal tendon structure as imaged with ultrasound is characterized by the following key features:

The internal fibrillar architecture is clearly visible in longitudinal scan being produced by parallel fascicles of collagen fibers. Between these echogenic fibers finer hypoechoic lines may be seen in keeping with intratendinous ground substance. With transverse imaging, this architectural arrangement produces the classic appearance of hyperechoic dots, representing collagen fascicles embedded within hypoechoic ground substance. There should be little internal irregularity with the tendon displaying a high degree of homogeneous echogenicity. These appearances may be considered analogous to a “packet of spaghetti.”
The tendon does not appear thickened with clearly delineated and regular margins distinct from surrounding tissues. A fine anechoic periphery may be noted in tendons which have a synovial sheath situated between the tendon and sheath. There should be no thickening of the sheath and no significant fluid or evidence of significant vascularity within the sheath.
The tendon exhibits no internal vascularity or what is commonly termed “neovascularity” when examined under Power Doppler imaging.

Fig. 1‑4 and Fig. 1‑5 demonstrate the normal appearance of the Achilles tendon in both longitudinal and transverse planes. The fibrillar pattern may be clearly seen.

Fig. 1.4 Longitudinal image of the lower third of the Achilles tendon and its insertion onto the posterior aspect of the calcaneum (*yellow arrows*). The normal fibrillar pattern of the tendon is clearly seen. Note anisotropy at the most distal aspect of the insertion (*curved arrow*).

Fig. 1.5 Transverse image of the lower third of the Achilles tendon (*yellow arrows*). The image demonstrates the dot-like appearance of the collagen fascicles seen in cross-section.

Tendon pathology may be considered to encompass a number of distinct entities and should not be thought of as a single process but rather a spectrum of disorders, including lesions within the tenosynovium, the paratenon, the enthesis, and the tendon proper. In many cases lesions may coexist. Table 1‑1 outlines the individual pathological processes which may affect a tendon, either in isolation or in combination with one another.

Table 1.1 Summary overview of tendon pathology
Disorder	Description	Example	Clinical signs^a
Paratenonitis	Disorder of the loose paratenon layer covering the tendon	Achilles paratenonitis	Pain, tenderness, diffuse swelling, crepitus, and warmth
Tenosynovitis	Disorder of the tendon sheath	de Quervain’s tenosynovitis	Pain, tenderness, swelling within the sheath, crepitus, and warmth
Tendinopathy	An intratendinous disorder	Rotator cuff, patellar tendon, common extensor origin	Pain, focal tenderness, palpable swelling
Enthesiopathy	An intratendinous disorder affecting the tendon origin or insertion	Insertional Achilles tendinopathy	Tenderness and swelling at tendon insertion
Tear	Loss of normal tendon integrity leading to a partial or complete rupture	Ruptured supraspinatus, Achilles tendon	Pain and weakness. Possible palpable gap
^aThese clinical signs are variable and patients may present with more than one condition. For example, in chronic cases of de Quervain’s tenosynovitis there may coexist a degree of tendinopathy within the tendon and a tenosynovitis within the tendon sheath.

In regard to tenosynovitis and paratenonitis, these two conditions may be considered to be pathological processes related to the tendon sheath or, when absent, the connective tissue surrounding the tendon. They may be either related to a systemic inflammatory disease or more commonly due to a mechanical overload. In many of the cases the tendon itself is relatively spared and ultrasound demonstrates no evidence of pathology within the tendon.

Characteristics of tendon sheath pathology on ultrasound include widening of the sheath due to an increase in fluid. Although usually anechoic in appearance, this fluid may appear to contain echogenic foci indicative of proteinaceous material or synovial proliferation (Fig. 1‑6 a–c; Fig. 1‑7 ). When assessed with Power Doppler, there may be an increase in blood flow within the synovial lining of the tendon sheath indicative of an active inflammatory process (Fig. 1‑6 c, Fig. 1‑8 ).

Fig. 1.6 **(a)** Longitudinal image of the tendon of tibialis posterior (TP). The tendon itself appears intact and of a good fibrillar pattern. However, there is a marked synovial thickening (*arrowheads*) and fluid (*white stars*) around the tendon within the sheath. These findings are in keeping with a tenosynovitis. **(b)** Transverse image of the tendon of TP. The tendon appears intact. There is, however, marked effusion (*white stars*) and synovial thickening (*arrowheads*) around the tendon. Findings are in keeping with a tenosynovitis. **(c)** This is the same image as in part (b). Power Doppler demonstrates that in addition to synovial thickening and effusion there is an increased vascularity within the synovial thickening.

Fig. 1.7 Longitudinal image of the tendon of tibialis posterior (TP) around the medial malleolus. The tendon itself appears of good echogenicity and fibrillar pattern. There is, however, marked synovial thickening (*yellow arrowheads*) and effusion (*white stars*) within the tendon sheath in keeping with a chronic tenosynovitis.

Fig. 1.8 Transverse image of the first dorsal compartment of the wrist and the tendons of abductor pollicis longus (*curved yellow arrow*) and extensor pollicis brevis (*curved white arrow*). Although there appears to be no effusion or synovial thickening within the sheath, Power Doppler imaging demonstrates a marked synovitis in keeping with a de Quervain’s tenosynovitis.

With regard to both tendinopathy and enthesiopathy these two conditions may be considered intratendinous different only in their geographical location with enthesiopathy being an insertional tendinopathy. As such, tendinopathy has been shown to have either absent or minimal inflammatory cell infiltrate (Ollivierre 1996). Rather, the condition is better considered to be “degenerative” in nature affecting the Achilles tendon (Astrom 1995, Movin 1997), the rotator cuff (Hashimoto 2003), the patellar tendon (Khan 1998), and the common extensor tendon at the elbow (Potter 1995). Macroscopically, the tendon becomes soft and disorganized with tissue looking yellow or brown in appearance, a condition termed mucoid degeneration. In addition, there is a loss of the normally tightly bundled collagen fibers (Khan 1999). Microscopically, there is degeneration and disorganization of collagen with fibrosis (Maffulli 2000) and extensive neovascularization may be present (Khan 1999, Maffulli 2000). Importantly, tendinopathy may not be symptomatic and the degree of pathological change does not necessarily correlate well with clinical symptoms (Maffulli 2003).

Although the term tendinopathy has replaced that of tendonitis, given the degenerative-like change which exists, more recent evidence would suggest that this may be an oversimplification and it is likely that elements of the inflammatory response play a role in the progression or continuation of tendon disrepair. Schubert (2005) demonstrated the presence of macrophages and T and B lymphocytes in chronic Achilles tendinopathy. This has been supported by other studies demonstrating increased levels of macrophage-derived interleukin 1 (IL 1) (Gotoh 1997), cyclo-oxygenase 1(COX-1) (Sullo 2001), COX-2 (Zhang 2010, Khan 2005), IL-6 (Legerlotz 2012), isoforms of transforming growth factor β (TGF-β) (Fenwick 2000), and increased substance P (Gotoh 1998) in chronic tendinopathy.

In particular, substance P has been demonstrated as a proinflammatory mediator (Garrett 1992) and together with calcitonin gene-related peptide (CGRP) these nociceptive mediators have been shown to be significantly expressed in chronic tendinopathy. In addition to being a proinflammatory mediator, substance P has also been shown to exert a proliferative effect on tenocytes initiating an increase in the ratio of type III to type I collagen mRNA contributing to formation of the smaller collagen fibers seen in tendinopathic tendons (Fong 2013). Consequently, although it would seem that the idea of “tendonitis” cannot be supported, there is evidence that tendinopathy, considered an ongoing tendon degenerative process, does contain many elements of an inflammatory-mediated response.

In clinical practice and on ultrasound, it is worth noting that patients may present with either a tenosynovitis or tendinopathy but also not uncommonly a combination of both pathologies (Fig. 1‑9 ).

Fig. 1.9 Transverse image of the tendon of tibialis posterior (TP). There is synovial thickening (*yellow arrowheads*) and effusion (*white star*) in keeping with a tenosynovitis. In addition, there is a loss of the normal oval-shaped tendon which appears of a heterogeneous echogenicity. These findings are in keeping with both a tenosynovitis of the tendon sheath and tendinopathy affecting the tendon itself.

In relation to ultrasound, tendinopathic changes may manifest as one or more of the following findings:

Tendon thickening with heterogeneous echogenicity.
Hypoechoic foci representing intrasubstance tears (defined as linear hypoechoic foci associated with discontinuity of tendon fibers).
Calcifications and enthesophytes at the tendon attachment.
Neovascularization on Power Doppler (Levin 2005, Zanetti 2003) (Fig. 1‑10 , Fig. 1‑11 ).

Although intrasubstance tears may be considered as one of the characteristics of tendinopathy, ultrasound is also capable of assessing more significant tears and complete ruptures which may be the consequence of a chronic tendinopathy, trauma, or often a combination of both (Fig. 1‑12 , Fig. 1‑13 ).