Tarsal navicular stress fractures - Radiologic Decision-Making

Author: Eric E. Coris, John A. Lombardo
Date: Jan 1, 2003

The navicular bone of the foot is a flattened, concave, boat-shaped bone wedged between the head of the talus and the three cuneiforms. Some common variants have an additional facet articulation with the cuboid bone. Medially the navicular tuberosity provides an insertion site for the tibialis posterior tendon (Figure 1). The location and unique impingement during foot strike of the navicular bone predispose it to well-localized stress and remodeling. (1)

During foot strike, the navicular bone becomes impinged with maximal effort between the proximal talus and the distal cuneiforms. Biomechanical analysis of navicular motion during stride reveals that most of this impingement force is focused at the central one third of the navicular bone. (2-4)

This anatomic impingement is even more significant in light of the vascular anatomy of the navicular bone. A microangiopathic study (5) of cadaveric feet showed that while the navicular bone is supplied by both the anterior and posterior tibial arteries, the branches enter at the small "waist" of cortical bone and branch out to supply the medial and lateral thirds. (2) This design leaves the central one third, the area of greatest stress, as an area of relative avascularity (Figure 2).

Tarsal navicular stress fractures were first described in 1958 in a study of racing greyhounds. (6) The fractures were always seen in the right hind foot and were initially termed "broken hock." The counterclockwise racing of the greyhounds on a banked track may have predisposed their uphill foot to increased stress. The lesion was first described in humans in a 1970 study. (7) Even then, the difficulty of locating the lesion on plain radiographs was noted. Because of the vertical nature of the fracture, it was understood that diagnosis "may require special views and laminography for detection." (7)

Studies (8-10) in the 1980s projected a navicular fracture incidence of 0.7 to 2.4 percent of all stress fractures. Recent studies (1,11,12) reveal an incidence of 14 to 35 percent of all stress fractures. A study (11) of elite-level athletes showed that track athletes accounted for 59 percent of all tarsal navicular stress fractures.

Vague symptomatology and elusive radiographic localization typically lead to a delay in diagnosis averaging four months from initial symptom onset. (5,13) Early diagnosis of these lesions and proper management usually yields a favorable outcome (5); however, delayed diagnosis may result in inadequate treatment and either delayed union or nonunion healing of the fracture. (13,14) In a landmark study, (5) the most common treatment of navicular stress fractures was found to be limitation of activity, which had a dismal 26 percent cure rate.

Mechanism of Injury

The anatomic predisposition to localization of stress in the avascular central one third of the navicular bone combined with the repetitive foot strike of weight-bearing exercises that involve antagonistic muscular load are thought to eventually result in bone failure. (15) The premonitory symptoms of navicular "bone strain" are generally undetectable by radiographs and computed tomographic (CT) scans. Until a diagnosis is made, there is increased stress and bony resorption focused at the central one third of the navicular bone. A bone scan performed at this phase will be positive. If stressful activity continues, the resorptive changes continue to progress until a fracture line becomes evident on CT scan and plain radiographs. (1,16)

Several authors have attempted to identify persons who are at increased risk of navicular stress fracture. One study (17) used force-plate analysis and proposed calcaneal pitch angle, talometatarsal angle, and pronation velocity as potential risk factors for navicular stress fractures. Other studies (5,18-20) have shown that the following factors predispose a person to navicular stress fractures: pes cavus, wide-heeled shoes, short first metatarsals, metatarsus adductus, metatarsus hyperostosis, medial narrowing of the talonavicular joint, talar beaking, limited subtalar motion, and limited ankle dorsiflexion. However, no statistically significant risk factors have been demonstrated, and no consensus exists as to persons at risk. As with all overuse injuries, training errors, improper equipment, improper technique, environment, and anatomic variants may all increase the risk for injury.

Clinical Presentation

Commonly occurring in track and field athletes (Table 1), (1,5,7,10,13,17,18,21-23) navicular stress fractures present as vague, aching pain in the dorsal midfoot that may radiate along the medial arch. The pain typically increases with activity such as running and jumping. With continued participation, the pain occurs sooner during activity and lasts longer into post-activity rest periods. (1,5,17,24) Symptoms are rarely bilateral.

Various factors contribute to the common delay in diagnosis of navicular stress fractures. Often, athletes can continue activity until pain increases too much by altering their gait and decreasing use of the forefoot. (18) Pain also resolves rapidly with rest, making it possible for athletes to resume participation after a week of respite from activity.

Physical Examination

Patients who present with navicular stress fractures typically have a normal range of motion and strength to manual muscle testing, and the neurovascular examination is normal. There is no ecchymosis or deformity and usually no swelling. The talonavicular joint can be localized by inverting-everting the forefoot. The nickel-sized area at the central region of the proximal dorsal navicular bone, referred to as the "N" spot, is tender in 81 percent of patients with navicular stress fractures. (5) Patients generally exhibit increased pain with hopping, toe hopping, and standing on their toes in the equinus position. (18)

Radiologic Tests

PLAIN RADIOGRAPHS

When suspicion justifies diagnostic studies, the initial step is typically plain radiographs. Unfortunately, only 33 percent of plain radiographs have sensitivity for navicular stress fractures, (1,25) because the majority of fractures are incomplete. (1) In addition, because bony resorption requires 10 days to three weeks to allow visualization of these fractures on plain radiographs, even complete fractures are often not seen on initial films. (26) However, plain films are useful if positive, and they also assist in ruling out other etiologies. (27)

BONE SCAN

If plain films are negative or inconclusive, triple-phase bone scan is the next recommended diagnostic procedure. Bone scan, unlike plain radiography, is positive at an early stage and is almost 100 percent sensitive for navicular stress fracture. (1) The entire navicular bone demonstrates uptake in all phases in a positive test (24) (Figure 3); delayed-phase images may take up to two years after union to return to normal. (15) The high negative predictive value of bone scanning essentially excludes the diagnosis with a negative test; however, the positive predictive value is lower. A bone scan may be positive with negative follow-up studies (e.g., CT scan, magnetic resonance imaging [MRI]). This phenomenon is thought to represent "bone strain" or subclinical stress reaction, and it inevitably proceeds to actual fracture if physical activity is continued at the same intensity level. (28) Positive bone scans must always be correlated with further imaging (i.e., CT scan) because of lack of specificity, poor demonstration of comminution and displacement, and lack of resolution of the anatomic characteristics of these fractures. (24)

CT SCANNING

CT scanning is the gold standard for optimal evaluation of a fracture once bone scan has demonstrated increased uptake in the navicular bone. (24) Unlike bone scanning, the anatomic resolution of CT scans is excellent. The best images are obtained with 1.5-mm slices using a bone algorithm through the plane of the talonavicular joint. (29) False-negative CT reports, estimated at 7 percent, are typically caused by confusion of an actual fracture with nutrient arteries. (13)

CT scans most commonly demonstrate a partial fracture coursing from the proximal dorsal central one third of the navicular bone and extending toward the distal plantar pole of the bone (1) (Figure 4). Fragmentation is seen in approximately 14 percent of navicular fractures. (13) Sclerosis is typically seen at the proximal articular rim; this finding is believed to represent the normal stress of weight bearing, not early evidence of nonunion. (29)

(22.) O'Connor K, Quirk R, Fricker P, Maguire K. Stress fracture of the tarsal navicular bone treated by bone grafting and internal fixation: three case studies and a literature review. Excel 1990;6:16-22.

(23.) Roper RB, Parks RM, Haas M. Fixation of a tarsal navicular stress fracture. A case report. J Am Podiatr Med Assoc 1986;76:521-4.

(24.) Quirk R. Stress fractures of the navicular. Foot Ankle Int 1998; 19:494-6.

(25.) Alfred RH, Belhobek G, Bergfeld JA. Stress fractures of the tarsal navicular. A case report. Am J Sports Med 1992;20:766-8.

(26.) Anderson EG. Fatigue fractures of the foot. Injury 1990;21:275-9.

(27.) Baquie P, Feller J. Midfoot pain. Aust Fam Physician 2000;29:875-7.

(28.) Matheson GO, Clement DB, McKenzie DC, Taunton JE, Lloyd-Smith DR, Macintyre JG. Scintigraphic uptake of 99mTc at non-painful sites in athletes with stress fractures. The concept of bone strain. Sports Med 1987;4:65-75.

(29.) Kiss ZS, Khan KM, Fuller PJ. Stress fractures of the tarsal navicular bone: CT findings in 55 cases. AJR Am J Roentgenol 1993;160: 111-5.

(30.) Saxena A, Fullem B, Hannaford D. Results of treatment of 22 navicular stress fractures and a new proposed radiographic classification system. J Foot Ankle Surg 2000;39:96-103.

(31.) Lee JK, Yao L. Stress fractures: MR imaging. Radiology 1988;169: 217-20.

(32.) Ariyoshi M, Nagata K, Kubo M, Sonoda K, Yamada Y, Akashi H, et al. MRI monitoring of tarsal navicular stress fracture healing-a case report. Kurume Med J 1998;45:223-5.

Coordinators of this series are Mark Meyer, M.D., University of Kansas School of Medicine, Kansas City, Kan., and Walter Forred, M.D., University of Missouri-Kansas City School of Medicine, Kansas City, Mo.

ERIC E. CORIS, M.D., is currently clinical assistant professor in the Department of Family Medicine at the University of South Florida College of Medicine, Tampa, Fla. He was previously a cliincal assistant professor in the Department of Family Medicine at the Ohio State University College of Medicine, Columbus. Dr. Coris received a medical degree from Ohio State University College of Medicine, after also attending the University of South Florida College of Medicine. He completed a residency in family medicine at St. Vincent's Medical Center, Jacksonville, Fla., and a fellowship in sports medicine at Ohio State University College of Medicine.

JOHN A. LOMBARDO, M.D., is a professor in the Department of Family Medicine at the Ohio State University College of Medicine, medical director for the Ohio State University Sports Medicine Center, and head team physician for the Ohio State University athletic department. Dr. Lombardo received his medical degree from Ohio State University College of Medicine. He completed a residency in family medicine at St. Elizabeth Medical Center, Dayton, Ohio.

Address correspondence to Eric E. Coris, M.D., University of South Florida College of Medicine, Department of Family Medicine, 12901 Bruce B. Downs Blvd., MDC 33, Tampa, FL 33612 (e-mail: ecoris@hsc.usf.edu). Reprints are not available from the authors.

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