FIGURE 5-54 Gouty arthritis of the first MTP joint. A) Extensive erosive changes of the medial aspect of the first MTP joint, primarily involving the head of the metatarsal. Note the extensive tophaceous soft tissue mass involving the medial, more than the lateral, aspect of the joint. B,C) Larger tophus in a different patient, with relatively little erosive change in the first MTP joint.

Involved digits exhibit eccentric and asymmetric joint swelling. Joint space loss is often absent, but there can be asymmetric joint space loss late in the disease process [16,69]. When the joint space is narrowed, the changes may resemble rheumatoid arthritis or erosive osteoarthriltis [16]. Bone mineralization is generally normal, but occasionally there may be mild osteopenia [14]. Although bony proliferation resulting in overhanging edges is typical of gout, osteophytes are not characteristic of gout. Chronic gout often results in an enlarged, irregular first metatarsal head. Malalignment and subluxations are rare in gout, but hallux valgus deformity is observed frequently.

Gout in the mid or hindfoot and ankle can present a confusing picture if there are no changes in the forefoot (Fig. 5-57). The ankle joint is rarely afflicted with gout, but posterior calcaneal erosions are common (Fig. 5-58). Retrocalcaneal bursitis is associated with soft tissue swelling, Achilles tendon thickening, and erosions of the posterior tendon secondary to tophi. In addition, the Achilles tendon can undergo fusiform or nodular enlargement and may eventually rupture [67]. TMT joint erosions may be marked. The monosodium urate crystals can inflict an intense inflammatory reaction, resulting in enhancement of tendon sheaths, ligaments, muscles, and bone marrow [14,16,56,84].

Though radiographs are most often used to follow patients with chronic gout, ultrasound, and CT and MR imaging are also more commonly used today [6,10,18,25,46,56,75,95]. Ultrasound is readily available, is less expensive, and in experienced hands can provide useful information regarding joint and synovial changes as well as demonstrate tophi in the soft tissues. Gouty tophi are typically nodular with heterogeneous hyperechoic appearance on ultrasound images [18,25]. In addition, ultrasound is very useful for joint aspiration to identify the typical crystals associated with gout [75].

In our practice, CT is not commonly used to evaluate and follow patients with gout. However, osseous erosions and bone and soft tissue tophi can be easily identified on CT images (Fig. 5-59). Interosseous lesions containing calcification are clearly demonstrated on CT images. Gerster et al. [28] demonstrated that tophi with Hounsfield units greater than or equal to 160 may be diagnostic for gout.

MR imaging reflects the changes caused by the proliferative synovitis (Fig. 5-60). Tophi are almost universally isointense to muscle on T1-weighted imaging, but they can have variable T2-weighted characteristics depending on the degree of calcification (Fig. 5-61) [6,10,56,95]. The T2-weighted signal is most commonly heterogeneously low to intermediate, but it can range from homogeneously increased to near-homogeneously decreased [95]. Contrast enhancement is variable, but peripheral enhancement is more commonly identified (Fig. 5-61) [10]. Although it is unusual to have tophi without prior episodes of gouty arthritis, soft tissue inflammation or masses without articular disease can be a diagnostic dilemma; tophi could be mistaken for neoplasm. Tophaceous gout should be considered when there is a heterogeneous low-to-intermediate signal mass associated with adjacent osseous erosive changes in the right clinical setting [6,10,56,95].

Changes are often nonspecific with MR imaging [6]. Therefore, comparison with radiographs is essential to clarify the disease process (Fig. 5-62).

Management of patients with gout is most often conservative with anti-inflammatory medications including steroids for acute joint inflammation. Systemic or intra-articular steroids are also effective. Injection and joint aspiration can be accomplished with fluoroscopic or ultrasound guidance [75]. Maintenance therapy with colchicine was once the standard, but it is now reserved for patients that cannot tolerate anti-inflammatory medications. Recent reports demonstrate that etoricoxib and indomethacin are equally effective for management of gouty arthropathy [23].

Calcium Pyrophosphate Dihydrate Deposition Disease (CPPD)

Chondrocalcinosis is due to deposition intra-articular deposition of calcium compounds. The most common form is CPPD, though calcium apatite, dicalcium phosphate dehydrate, and calcium oxalate may also cause choncrocalcinosis [16]. Deposition of calcium pyrophosphate dehydrate crystals in the joint can illicit an inflammatory response resulting in synovitis and arthropathy [9,10].

Clinically, the condition increases with age with a 5% incidence in patients over 70 years of age and increasing to 50% by 90 years of age [16]. CPPD is associated with other disorders including hyperparathyroidism (15%), hemochromatosis (41%), and hereditary spherocytosis [16].

A large percentage of patients with radiographic evidence of chondrocalcinosis or CPPD are asymptomatic. Calcium pyrophosphate dehydrate crystals are commonly present in joints in patients without symptoms, but subclinical inflammation is likely due to elevated cell counts and polymorphonuclear cells in the synovial fluid [77]. When symptoms occur, the CPPD can mimic gout, rheumatoid arthritis, osteoarthritis, neuropathic, and other arthropathies. Over the years, largely through the work of McCarty and colleagues, CPPD has been classified into five clinical patterns [16,65,74,77].

Asymptomatic (lanthanic)


Pseudo-osteoarthritis


Pseudogout syndrome


Pseudorheumatoid arthritis


Pseudoneuropathic arthritis

The most common form is lanthanic or the asymptomatic group. These patients have radiographic evidence of chondrocalcinosis, but the involved joint is asymptomatic [16,65,74]. The pseudo-osteoarthritis group has clinical symptoms and radiographic features similar to osteoarthritis, with chondrocalcinosis present in the symptomatic joint. Symptoms may be chronic, with intermittent acute episodes. This form typically involves the knee, hand, and wrist [16,74].

The pseudo-osteoarthritis form demonstrates radiographic features similar to osteoarthritis with superimposed choncrocalcinosis (Fig. 5-63) [16,65,74]. This pattern is one of the most common accounting for 50% of patients with CPPD. The knee, hand, and wrist are most commonly affected in patients with pseudo-osteoarthritis [16,65].

The pseudogout form is a disorder that results from the excessive buildup or impaired degradation of pyrophosphate, leading to crystal deposition, synovitis, and arthritis. It usually manifests in the sixth and seventh decades by chondrocalcinosis and associated secondary osteoarthritis [71,74]. The frequency of calcium pyrophosphate dihydrate deposition is 1 in 1000 and increases with age [71]. This disorder can occur sporadically or in association with such metabolic disorders as hemochromatosis, phosphate and magnesium imbalances, hyperparathyroidism, and hypothyroidism. The weakly birefringent, variably shaped crystals can be recovered from synovial fluid, even in uninflamed joints, and intracellularly [77]. Calcification (Fig. 5-64) of cartilage, ligaments, and tendons is also common, particularly in the Achilles tendon. Pseuodogout can present with sclerosis, osteophytosis, cartilage loss, and subchondral cysts, similar to osteoarthritis. However, it differs from osteoarthritis in that it involves unusual joints, involves unusual sites within the affected joint, and exhibits prominent subchondral cysts, bone destruction, and variable osteophyte formation [33]. The arthropathy most commonly affects the tarsal and MTP joints, and the MTP joints may demonstrate capsular calcification.

The pseudorheumatoid arthritis form presents with symptoms similar to rheumatoid arthritis with morning stiffness and symmetrical distribution. The pseudoneuropathic group resembles changes of neuropathic arthropathy. In both instances the presence of chondrocalcinosis is a differentiating feature. Also, in the latter, there is no neurologic deficit [16,62,65,77].

Chondrocalcinosis in the foot and ankle may be subtle and difficult to detect on radiographs. CT is quite sensitive for detection of the subtle calcification (Fig. 5-63).

Hydroxyapatite Deposition Disease (HADD)

Calcium hydroxyapatite deposition commonly occurs in the tendons and bursae, but may also involve bone. The most common locations include the shoulder (69% of cases), followed by the hip, elbow, wrist, and knee in order of decreasing frequency (Fig. 5-65) [15,26,32]. In the foot, the region of the great toe and the flexor hallucis longus and brevis tendons are most commonly involved [32,97]. The hydroxyapatite may be seen as clumps, purple in color using Wright stain [16].

Hydroxyapatite deposition disease is most common in patients 20 to 70 years of age [16,32]. Patients with calcium hydroxyapatite deposition may be asymptomatic and are more often sedentary workers. In one large series of over 6000 sendentary workers calcifications were noted in 2.7% [32]. The clinical phases have been divided into three phases. The silent phase when calcifications are contained within the tendon, the mechanical phase where the calcifications enlarge and may extend beyond the tendon and the adhesive periarthritis phase with pain and limitation of motion [32]. These phases are most commonly seen in the shoulder.

Images’ features are characteristic on radiographs in most cases (Fig. 5-65). Initially the calcifications may appear smoggy or cloud-like. In the later phases, the calcifications may appear more dense and organized. The shoulder is most commonly involved. Bilateral shoulder involvement occurs in up to 50% of cases [16,32]. Bone erosions are not commonly seen on radiographs. Intra-articular involvement has also been described, and it is not unusual to have calcium pyrophosphate crystals mixed with hydroxyapatite crystals [32,74].

MR images may demonstrate areas of low signal intensity corresponding to the calcifications demonstrated on radiographs. Comparison with radiographs is essential for accurate interpretation of the signal changes noted on MR. Areas of low signal intensity may be confused with tendon thickening on both T1- and T2-weighted sequences. Bone erosions and marrow edema may also be evident. Flemming et al. [27], noted cortical erosions in 76% and marrow edema in 36% of patients with HADD. When marrow edema is present without erosions the image features may be confused with infection, trauma, or neoplasm [15]. Other considerations include renal failure, tumoral calcinosis, gout, and CPPD [60].

Management can be difficult as the etiology is not completely understood [55]. In our practice, it is not unusual to aspirate the calcium, especially if it has as cloud-like radiographic appearance, and inject anesthetic and steroids. This can be accomplished with ultrasound or fluoroscopic guidance [75].

Hemochromatosis

Hemochromatosis is a chronic disease in which iron is excessively deposited in various tissues, resulting in parenchymal fibrosis, damage, and dysfunction. Hemochromatosis may be primary, which is a rare inherited disorder or secondary. Secondary hemochromatosis may follow cirrhosis, multiple transfusions, or excessive iron intake. In recent years, juvenile and neonatal forms have also been described [14,69]. Arthropathy occurs in 24% to 50% of patients with this disorder [14]. This disorder is more common in men and typically presents after 40 years of age [69].

Approximately half of the patients with hemochromatosis have arthritis similar to degenerative arthritis or CPPD [38]. The arthritis consists of osteopenia, subchondral cysts, bony eburnation, prominent chondrocalcinosis, beak-like osteophtytes, and loss of joint space [14,69]. Cystic lesions are subchondral and can become quite large. Sclerosis is due to subchondral trabecular thickening beneath eroded cartilage surfaces. The joint space narrowing is typically uniform [14]. Foot and ankle involvement occurs occasionally and does not differ in appearance from involvement elsewhere in the body (Fig. 5-66).

COLLAGEN VASCULAR DISEASE

There are multiple connective tissue disorders including scleroderma, systemic lupus erythematosus, dermatomyositis, and mixed connective tissue diseases [14,69]. The upper extremities are more commonly involved, particularly the hands and wrists. This section focuses on systemic lupus erythematosus.

Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a deforming, nonerosive (Jaccoud-like) arthropathy that can involve the foot and ankle. Articular involvement occurs in 75% to 90% of patients [14]. The articular deformities of lupus arthropathy are due to capsular and ligamentous laxity, contracture, and muscle imbalance as a result of intra-articular and periarticular inflammation and eventual fibrosis [69]. The arthropathy often is evident early in the disease, although it is more common and severe in patients with chronic disease. Typical findings include soft tissue swelling, regional osteoporosis, hallux valgus deformity (Fig. 5-67), subluxation of the MTP joints (Fig. 5-67), and widening of the forefoot [69]. Joint space narrowing, rare hook erosions of the metatarsal heads, subchondral cysts of the metatarsal heads, and osteonecrosis of the small bones of the foot can also be observed. Systemically or locally injected steroids can lead to tendon weakening and rupture, most commonly involving the Achilles tendon. Soft tissue calcifications can be diffuse, linear, streaky, or nodular in the subcutaneous and deeper soft tissues, plaque-like periarticular, or arterial. Patients with SLE are more prone to avascular necrosis, osteomyelitis, and septic arthritis of the ankle resulting from steroid use [69].

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