Postoperative stroke after hemiarthroplasty for femoral neck fracture: a report of 2 cases and review of literature.

INTRODUCTION: Femoral neck fractures in the elderly comprise a significant number of orthopedic surgical cases at a major trauma center. These patients are immediately incapacitated, and surgical fixation can help increase mobility, restore independence, and reduce morbidity and mortality. However, operative treatment carries its own inherent risks including infections, deep vein thromboses, and intraoperative cardiovascular collapse. Cerebrovascular stroke is a relatively uncommon occurrence after hip fractures. METHODS: We present 2 cases with unusual postoperative medical complication after cemented hip hemiarthroplasty for femoral neck fracture that will serve to illustrate an infrequent but very serious complication. RESULTS: Case 1 was a 73-year-old man with a Garden IV femoral neck fracture who underwent a right hip unipolar cemented hemiarthroplasty under general anesthesia. After uneventful surgery, he developed neurological deficits, and a postoperative noncontrast head computed tomography showed a right medial thalamic infarct. Case 2 was an 82-year-old man with a Garden IV femoral neck fracture who underwent a right hip unipolar cemented hemiarthroplasty under general anesthesia. After uneventful surgery, the patient became hemodynamically unstable. A postoperative noncontrast head computed tomography showed a large evolving left middle cerebral artery stroke. CONCLUSIONS: General anesthesia in the setting of decreased cardiac function (decreased ejection fraction and output) carries the risk for ischemic injury to the brain from decreased cerebral perfusion. Risk factors including advanced age, history of coronary artery disease, atherosclerotic disease, and atrial fibrillation increase the risk for perioperative stroke. Furthermore, it is known that during the cementing of implants, microemboli can be released, which must be considered in patients with preoperative heart disease. As a result, consideration of using a noncemented implant or cementing without pressurizing in this clinical scenario should be an important aspect of the preoperative plan in an at-risk patient. Further studies are needed that can elucidate a causal relationship.

mSin3-associated protein, mSds3, is essential for pericentric heterochromatin formation and chromosome segregation in mammalian cells.

The histone code guides many aspects of chromosome biology including the equal distribution of chromosomes during cell division. In the chromatin domains surrounding the centromere, known as pericentric heterochromatin, histone modifications, particularly deacetylation and methylation, appear to be essential for proper chromosome segregation. However, the specific factors and their precise roles in this highly orchestrated process remain under active investigation. Here, we report that germ-line or somatic deletion of mSds3, an essential component of the functional mSin3/HDAC corepressor complex, generates a cell-lethal condition associated with rampant aneuploidy, defective karyokinesis, and consequently, a failure of cytokinesis. mSds3-deficient cells fail to deacetylate and methylate pericentric heterochromatin histones and to recruit essential heterochromatin-associated proteins, resulting in aberrant associations among heterologous chromosomes via centromeric regions and consequent failure to properly segregate chromosomes. Mutant mSds3 molecules that are defective in mSin3 binding fail to rescue the mSds3 null phenotypes. On the basis of these findings, we propose that mSds3 and its associated mSin3/HDAC components play a central role in initiating the cascade of pericentric heterochromatin-specific modifications necessary for the proper distribution of chromosomes during cell division in mammalian cells.