Kyphoplasty and vertebroplasty

Percutaneous vertebroplasty is the injection of a vertebral compression fracture (VCF) with bone cement, generally polymethylmethacrylate. Percutaneous kyphoplasty is the placement of balloons into the vertebral body with an inflation/deflation sequence to create a cavity before the cement injection. These procedures are most often performed in a percutaneous fashion on an outpatient (or short stay) basis. The procedure is indicated for painful VCFs due to osteoporosis or malignancy, and painful hemangiomas. The procedure may have efficacy in painful vertebral metastasis and traumatic compression fractures. Much evidence favors the use of this procedure for pain associated with these disorders. The overall risks of the procedure are low, but serious complications (including spinal cord compression) can occur. With good patient selection and careful technique, these complications are avoidable, making the risk-to-benefit ratio highly favorable.     

Geriatrics and physical medicine and rehabilitation: common principles,complementary approaches,and 21st century demographics

The demographic changes occurring in the United States transcend the capabilities of any specific medical specialty to provide optimum care for the elderly. This commentary discusses a statement of principles drafted by representatives of the American Academy of Physical Medicine and Rehabilitation who collaborated with members of 9 other medical and surgical specialties. In this commentary, we argue that geriatrics and physical medicine and rehabilitation (PM&R) share common principles and complementary approaches. We urge physiatrists and other rehabilitation professionals to address the needs of elderly patients and recommend that these principles be incorporated into PM&R practice.     

Effect of a single 30-minute treatment of high voltage pulsed current on edema formation in frog hind limbs.

The purpose of this study was to investigate the effect of a single treatment of high voltage pulsed current (HVPC) on edema formation. Twenty-four frogs were anesthetized, and both hind limbs of each frog were traumatized by impact. Limb volumes were measured by water displacement immediately before and after trauma and at predetermined intervals for 24.0 hours posttrauma. One limb of each frog was randomly selected to receive 30 minutes of continuous, 120-pulse per second, cathodal HVPC at voltages 10% less than motor threshold levels. Data were analyzed by an analysis of variance for repeated measures. Sources of significant differences were determined by paired t tests (probability values determined by Bonferroni adjustment). A single 30-minute application of HVPC significantly curbed edema formation for between 4.0 and 7.5 hours following treatment (ie, volumes of treated limbs were significantly less than those of untreated limbs). These results suggest that regimens currently applied to humans (ie, one treatment per day or three times per week) may be insufficiently aggressive to provide sustained treatment effects.     

Patient profiling can identify patients with adult spinal deformity (ASD) at risk for conversion from nonoperative to surgical treatment: initial steps to reduce ineffective ASD management

Background Context

Non-operative management is a common initial treatment for patients with adult spinal deformity (ASD) despite reported superiority of surgery with regard to outcomes. Ineffective medical care is a large source of resource drain on the health system. Characterization of patients with ASD likely to elect for operative treatment from non-operative management may allow for more efficient patient counseling and cost savings.

Hyperphosphatemia,Phosphoprotein Phosphatases,and Microparticle Release in Vascular Endothelial Cells

Hyperphosphatemia in patients with advanced CKD is thought to be an important contributor to cardiovascular risk, in part because of endothelial cell (EC) dysfunction induced by inorganic phosphate (Pi). Such patients also have an elevated circulating concentration of procoagulant endothelial microparticles (MPs), leading to a prothrombotic state, which may contribute to acute occlusive events. We hypothesized that hyperphosphatemia leads to MP formation from ECs through an elevation of intracellular Pi concentration, which directly inhibits phosphoprotein phosphatases, triggering a global increase in phosphorylation and cytoskeletal changes. In cultured human ECs (EAhy926), incubation with elevated extracellular Pi (2.5 mM) led to a rise in intracellular Pi concentration within 90 minutes. This was mediated by PiT1/slc20a1 Pi transporters and led to global accumulation of tyrosine- and serine/threonine-phosphorylated proteins, a marked increase in cellular Tropomyosin-3, plasma membrane blebbing, and release of 0.1- to 1-μm-diameter MPs. The effect of Pi was independent of oxidative stress or apoptosis. Similarly, global inhibition of phosphoprotein phosphatases with orthovanadate or fluoride yielded a global protein phosphorylation response and rapid release of MPs. The Pi-induced MPs expressed VE-cadherin and superficial phosphatidylserine, and in a thrombin generation assay, they displayed significantly more procoagulant activity than particles derived from cells incubated in medium with a physiologic level of Pi (1 mM). These data show a mechanism of Pi-induced cellular stress and signaling, which may be widely applicable in mammalian cells, and in ECs, it provides a novel pathologic link between hyperphosphatemia, generation of MPs, and thrombotic risk.