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Bone Flap Necrosis After Decompressive Hemicraniectomy for Malignant Middle Cerebral Artery Infarction
Authors:Christian Ewald  Pedro Duenisch  Jan Walter  Theresa Götz  Otto W. Witte  Rolf Kalff  Albrecht Günther
Affiliation:1. Neurosurgical Department, Jena University Hospital, Friedrich Schiller University Jena, Erlanger Allee 101, 07747, Jena, Germany
2. Biomagnetic Center, Hans-Berger-Department of Neurology and Center for Sepsis Control and Care (CSCC), Jena University Hospital, Friedrich Schiller University Jena, Erlanger Allee 101, 07747, Jena, Germany
3. Hans-Berger-Department of Neurology and Center for Sepsis Control & Care (CSCC), Jena University Hospital, Friedrich Schiller University Jena, Erlanger Allee 101, 07747, Jena, Germany
Abstract:

Background

Autologous bone flap reinsertion follows as a second surgical intervention after decompressive craniectomy in patients with malignant middle cerebral artery (MCA) infarction. In addition to surgery-related short-term complications, aseptic resorption of the reimplanted bone flap is a possible long-term problem which has not yet been sufficiently elucidated in these patients.

Methods

A total of 109 patients who had undergone decompressive hemicraniectomy for malignant MCA infarction in our institution between September 1994 and December 2011 were included in the study. Clinical and radiological findings were retrieved retrospectively. Aseptic bone necrosis was classified into two categories based on computer tomographic features.

Results

A total of 76 patients received their own cryoconserved bone flap (mean age 54.34 ± 10.73 years; 49 males). The overall short-term complication rate was 9.2 %. Bone flap necrosis occurred in 26 patients (22.8 %) with 7 flaps showing signs of surgically relevant type II necrosis after a median time of 14 months (interquartile range [IQR] 4–22).

Conclusions

There is a noticeable complication rate in patients undergoing bone flap reinsertion after hemicraniectomy due to malignant MCA infarction. Aseptic bone necrosis represents a significant complication during long-term follow-up. The pathophysiological mechanisms remain unclear and more efforts should be undertaken to understand and possibly prevent this complication in these patients.
Keywords:
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