Kienböck's disease: preventing disease progression in early-stage disease.

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Abstract

[Indexed for MEDLINE] 13. Hand Clin. 2022 Nov;38(4):367-376. doi: 10.1016/j.hcl.2022.03.011. Pathophysiology of Avascular Necrosis. Wells ME(1), Dunn JC(2). Author information: (1)William Beaumont Army Medical Center, El Paso, TX, USA; Texas Tech University Health Sciences Center El Paso, El Paso, TX, USA. Electronic address: Matthew.Eric.Wells@gmail.com. (2)William Beaumont Army Medical Center, El Paso, TX, USA; Texas Tech University Health Sciences Center El Paso, El Paso, TX, USA; Uniformed Services University of the Health Sciences, Bethesda, MD, USA. Avascular necrosis is a complicated, multifactorial disease with potentially devastating consequences. Although the underlying root cause is a lack of appropriate vascular perfusion to affected bone, there are often varying patient-specific, anatomic-specific, and injury-specific predispositions. These factors generally fall into 3 categories: direct vascular disruption, intravascular obliteration, or extravascular compression. The initial stages of disease can be insidiously symptomatic because edematous bone marrow progresses to subchondral collapse and subsequent degenerative arthritis. Although much of the current literature focuses on the femoral head, other common areas of occurrence include the proximal humerus, knee, and the carpus. The low-incidence rate of carpal avascular necrosis poses a challenge in establishing adequately powered, control-based validated treatment options, and therefore, optimal surgical management remains a continued debate among hand surgeons. Appreciation for expectant fracture healing physiology may help guide future investigation into carpal-specific causes of avascular necrosis. Published by Elsevier Inc. DOI: 10.1016/j.hcl.2022.03.011