ABSTRACT
This case report describes the successful fixation of a periprosthetic patellar fracture in an 89-year-old female patient after total knee arthroplasty (TKA) and cemented retropatellar component. Fixation was performed by use of a fixed-angle plate combined with cerclage, under preservation of the firmly fixed retropatellar prosthetic component. No complications were observed postoperatively. Radiologic controls confirmed bone healing. A range of movement of the knee joint of 0/5/110° was achieved by the last clinical examination 5 years postoperatively. The patient was free of pain and had an age-appropriate mobility. The use of fixed-angle plates in the treatment of type II periprosthetic patellar fractures according to Ortiguera and Berry can provide stable fixation while preserving the retropatellar prosthetic component. Additional augmentation by cerclage, tapes or traction screws is recommended in cases of poor bone stock or severe osteoporosis.
Subject(s)
Femoral Fractures , Knee Injuries , Periprosthetic Fractures , Aged, 80 and over , Bone Plates/adverse effects , Female , Femoral Fractures/etiology , Fracture Fixation, Internal/adverse effects , Humans , Knee Injuries/complications , Patella/diagnostic imaging , Periprosthetic Fractures/diagnostic imagingABSTRACT
Following prolonged exposure to hypoxic conditions, for example, due to ascent to high altitude, stroke, or traumatic brain injury, cerebral edema can develop. The exact nature and genesis of hypoxia-induced edema in healthy individuals remain unresolved. We examined the effects of prolonged, normobaric hypoxia, induced by 16 h of exposure to simulated high altitude, on healthy brains using proton, dynamic contrast enhanced, and sodium MRI. This dual approach allowed us to directly measure key factors in the development of hypoxia-induced brain edema: (1) Sodium signals as a surrogate of the distribution of electrolytes within the cerebral tissue and (2) Ktrans as a marker of blood-brain-barrier integrity. The measurements point toward an accumulation of sodium ions in extra- but not in intracellular space in combination with an intact endothelium. Both findings in combination are indicative of ionic extracellular edema, a subtype of cerebral edema that was only recently specified as an intermittent, yet distinct stage between cytotoxic and vasogenic edemas. In sum, here a combination of imaging techniques demonstrates the development of ionic edemas following prolonged normobaric hypoxia in agreement with cascadic models of edema formation.
