Z Orthop Unfall 2011; 149(2): 231-242
DOI: 10.1055/s-0030-1270984
Refresher Orthopädie und Unfallchirurgie
Rubrikherausgeber: R. Hoffmann, Frankfurt, R. Windhager, Graz
© Georg Thieme Verlag KG Stuttgart · New York

Hüftkopfnekrose – Diagnostik und Differenzialtherapie

Avascular Necrosis of the Hip – Diagnosis and TreatmentW. Drescher1 , T. Pufe2 , R. Smeets3 , R. v. Eisenhart-Rothe4 , M. Jäger5 , M. Tingart1
  • 1Klinik für Orthopädie und Unfallchirurgie – Schwerpunkt Orthopädie, RWTH Universitätsklinikum Aachen
  • 2Institut für Anatomie und Zellbiologie, RWTH Universitätsklinikum Aachen
  • 3Klinik und Poliklinik für Mund-, Kiefer- und Gesichtschirurgie, Universitätsklinikum Eppendorf, Hamburg
  • 4Klinik für Orthopädie und Unfallchirurgie, Klinikum rechts der Isar, Technische Universität München
  • 5Orthopädische Klinik, Universitätsklinikum Essen
Further Information

Publication History

Publication Date:
05 April 2011 (online)

Zusammenfassung

Die Hüftkopfnekrose ist eine ischämische Knochennekrose posttraumatischer oder nicht traumatischer Genese, die im jungen Alter zur sekundären Koxarthrose führen kann. Sie ist heute Indikation für etwa 10 % der Hüftendoprothesenimplantationen. Für die nicht traumatische Hüftkopfnekrose sind neben den führenden Ätiologien Alkohol und Glukokortikoide mittlerweile auch Sichelzellanämie, Taucherkrankheit und Morbus Gaucher identifiziert. Weitere Risikofaktoren sind Chemotherapie bei Tumorerkrankungen, chronisch entzündliche Darmerkrankungen, systemischer Lupus erythematodes und Multiple Sklerose, wobei bei diesen die hochdosierte Kortisongabe von Bedeutung ist. Schwangerschaft stellt einen weiteren Risikofaktor dar, und es verbleibt noch ein Anteil an idiopathischen Hüftkopfnekrosen. Diagnostisch wichtig ist die ARCO-Stadieneinteilung nach der internationalen Association of the Research of Osseous Circulation. Während im Stadium 0 lediglich ein histologischer Nachweis erfolgen kann, zeigen sich im reversiblen Frühstadium 1 bereits kernspintomografische Signaländerungen. Erst im irreversiblen Frühstadium 2 zeigt das Nativröntgenbild gering verminderte Transparenz aufgrund von neuer Knochenauflagerung auf tote Trabekel. Im Stadium 3 erfolgt die subchondrale Fraktur und im Endstadium 4 liegt die sekundäre Koxarthrose vor. Therapeutisch bieten sich im Stadium 1 die Kernanbohrung, Physiotherapie und zunehmend gesichert auch die Bisphosphonattherapie an. Zur extrakorporalen Stoßwellentherapie liegen für die Hüftkopfnekrose nur wenige Daten vor. Noch als experimentelle, aber hoffnungsvolle Therapie im Stadium 1 und 2 ist die autologe Stammzelltransplantation zu werten. Im Stadium 2 und 3 kommen nicht vaskularisierte und gefäßgestielte Knochentransplantate zum Einsatz. Selten ist eine Umstellungsosteotomie des proximalen Femurs indiziert. Noch seltener werden ein Tantalumimplantat aus trabekulärem Metall nach Kernanbohrung implantiert oder Knorpel-Knochen-Zylinder transplantiert. Im Stadium 4 ist die Standardversorgung noch immer die herkömmliche Hüfttotalendoprothese. Die ersten kurz- bis mittelfristigen Erfahrungen mit Oberflächenersatz liegen nun vor. Die in den letzten Jahren entwickelten Kurzschaftendoprothesen könnten eine Hoffnung für diese junge Patientengruppe darstellen.

Abstract

Femoral head necrosis is an ischaemic bone necrosis of traumatic or nontraumatic pathogenesis which can lead to hip joint destruction in young age. It is today the indication for 10 % of all the total hip joint replacements. Known aetiologies of nontraumatic femoral head necrosis are alcoholism, steroids, sickle cell anaemia, caisson, and Gaucher's disease. Further risk factors are chemotherapy, chronic inflammatory bowel disease, systemic lupus erythematosus, and multiple sclerosis, in which also steroids are involved. Gravidity is another risk factor, but still idiopathic pathogenesis is found. In diagnosis, the ARCO-classification of the Association for the Research of Osseous Circulation is essential. While stage 0 can only be found histologically, the reversible early stage 1 shows MR signal changes. In the irreversible early stage 2, first native x-ray changes are seen as lower radiolucency reflects new bone apposition on dead trabeculae. In stage 3, subchondral fracture follows, and in stage 4 secondary arthritis of the hip. Established therapy in stage 1 is core decompression, physiotherapy, and more and more also bisphosphonates. Sufficient data to support extracorporeal shock wave therapy are still lacking. Stem cell therapy seems to be a promising new therapy method in stage 2. In stage 2 and 3 mainly proximal femoral osteotomies and (non)vascularised bone transplantation are performed. In stage 4, depending on size and location of the necrotic zone and pathology of the adjacent bone, resurfacing or short stem hip arthroplasty can be performed. However, conventional THA is still golden standard. The problem and challenge, however, is the often young patient age in femoral head necrosis. Especially chemotherapy-associated osteonecrosis in leukaemia is found in patients in their second decade of life. Therefore, the hip should be preserved as long as possible.

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Priv.-Doz. Dr. med. Wolf Drescher, Oberarzt

Klinik für Orthopädie und Unfallchirurgie
Schwerpunkt Orthopädie
Universitätsklinikum Aachen

Pauwelsstraße 30

52074 Aachen

Email: wdrescher@ukaachen.de

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