Semin Musculoskelet Radiol 2018; 22(S 01): S1-S5
DOI: 10.1055/s-0038-1639519
Scientific Presentations and Posters
Georg Thieme Verlag KG Stuttgart · New York

Detection and Staging of Idiopathic Osteonecrosis of the Scaphoid (Preiser’s Disease)

C. Gietzen
1   Radiologie, Universitätsklinikum Würzburg, Würzburg, Germany
,
J.P. Grunz
1   Radiologie, Universitätsklinikum Würzburg, Würzburg, Germany
,
T. Pillukat
2   Handchirurgie, Herz- und Gefäßklinik Bad Neustadt, Bad Neustadt an der Saale, Germany
,
T. Bley
1   Radiologie, Universitätsklinikum Würzburg, Würzburg, Germany
,
R. Schmitt
1   Radiologie, Universitätsklinikum Würzburg, Würzburg, Germany
3   Radiologie, Herz- und Gefäßklinik Bad Neustadt, Bad Neustadt an der Saale, Germany
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Publikationsverlauf

Publikationsdatum:
26. März 2018 (online)

 

Objective: To detect idiopathic osteonecrosis of the scaphoid (Preiser’s disease) and to stage the disease by using high-resolution computed tomography (CT) and contrast-enhanced magnetic resonance imaging (MRI).

Material and Methods: Imaging findings of 32 patients (18 male, 14 female) were evaluated retrospectively including projection radiography (dorsopalmar, lateral, and Stecher’s views), high-resolution CT (oblique-sagittal and oblique-coronal reformations along the scaphoid axis), and plain and contrast-enhanced MRI (proton-density-weighted fast spin-echo [FSE] fat saturated, T1-weighted FSE, and contrast-enhanced T1-weighted FSE fat saturated). Images were analyzed comprehensively by consensus of two board-qualified radiologists.

Results: Changes in morphology and signal intensity were most extensive at the proximal scaphoid poles as follows: bone marrow edema in 23 patients, hyperenhancement in 12 patients, lack of enhancement in 20 patients, osteosclerosis in 29 patients, bone atrophy (“nipple sign”) in 24 patients, and insufficiency fractures in 15 patients. In the middle scaphoid segment, hyperenhancement and focal osteopenia were seen in 27 patients. Changes of the distal segment were found in seven patients including five patients with completely signal-compromised scaphoids and lacking any contrast enhancement.

Conclusion: Preiser’s disease is characterized by a zonal structure consisting of a proximal necrotic zone, a middle repair zone, and a distal zone of maintained bone viability. The natural course as well as topographic changes in Preiser’s disease can be explained with the nutrient vessels running recurrently within the scaphoid.