Rates of safety incident reporting in MRI in a large academic medical center.

PURPOSE: To describe our multiyear experience in incident reporting related to magnetic resonance imaging (MRI) in a large academic medical center. MATERIALS AND METHODS: This was an Institutional Review Board (IRB)-approved, Health Insurance Portability and Accountability Act (HIPAA)-compliant study. Incident report data were collected during the study period from April 2006 to September 2012. The incident reports filed during the study period were searched for all reports related to MRI. Incident reports were classified with regard to the patient type (inpatient vs. outpatient), primary reason for the incident report, and the severity of patient harm resulting from the incident. RESULTS: A total of 362,090 MRI exams were performed during the study period, resulting in 1290 MRI-related incident reports. The rate of incident reporting was 0.35% (1290/362,090). MRI-related incident reporting was significantly higher in inpatients compared to outpatients (0.74% [369/49,801] vs. 0.29% [921/312,288], P < 0.001). The most common reason for incident reporting was diagnostic test orders (31.5%, 406/1290), followed by adverse drug reactions (19.1%, 247/1290) and medication/IV safety (14.3%, 185/1290). Approximately 39.6% (509/1290) of reports were associated with no patient harm and did not affect the patient, followed by no patient harm but did affect the patient (35.8%, 460/1290), temporary or minor patient harm (23.9%, 307/1290), permanent or major patient harm (0.6%, 8/1290) and patient death (0.2%, 2/1290). CONCLUSION: MRI-related incident reports are relatively infrequent, occur at significantly higher rates in inpatients, and usually do not result in patient harm. Diagnostic test orders, adverse drug reactions, and medication/IV safety were the most frequent safety incidents.

May-Thurner syndrome: diagnosis and management.

For over fifty years, the pathogenesis of May-Thurner syndrome (MTS) has been associated with chronic left common iliac vein compression resulting in the formation of intraluminal, permanent obstructive lesions. However, despite this association, the mechanism by which compression produces these lesions is unknown. Diagnostic accuracy of MTS is critical since it often afflicts young patients requiring endovascular management. This review will focus on the historical, embryological and evolutionary description of MTS and examine its development, diagnosis, clinical management and potential diagnostic errors.

Critical limb ischemia: an update for interventional radiologists.

Critical limb ischemia (CLI) is a growing epidemic with bleak patient outcomes. A variety of treatment modalities have been adopted to address CLI based on comorbidities, life expectancy, and the nature of the arterial disease. With advances in technology and treatment strategies, the clinical outcomes of CLI patients have significantly improved over recent years. However, despite progress, patency rates of both surgical and endovascular interventions, limb-salvage and amputation rates are still dismal. We review the epidemiology, treatment strategies, imaging modalities, and the microcirculation aspect of CLI.

Enhanced hippocampal neurogenesis by intraventricular S100B infusion is associated with improved cognitive recovery after traumatic brain injury.

Evidence of injury-induced neurogenesis in the adult hippocampus suggests that an endogenous repair mechanism exists for cognitive dysfunction following traumatic brain injury (TBI). One factor that may be associated with this restoration is S100B, a neurotrophic/mitogenic protein produced by astrocytes, which has been shown to improve memory function. Therefore, we examined whether an intraventricular S100B infusion enhances neurogenesis within the hippocampus following experimental TBI and whether the biological response can be associated with a measurable cognitive improvement. Following lateral fluid percussion or sham injury in male rats (n = 60), we infused S100B (50 ng/h) or vehicle into the lateral ventricle for 7 days using an osmotic micro-pump. Cell proliferation was assessed by injecting the mitotic marker bromodeoxyuridine (BrdU) on day 2 postinjury. Quantification of BrdU-immunoreactive cells in the dentate gyrus revealed an S100B-enhanced proliferation as assessed on day 5 post-injury (p < 0.05), persisting up to 5 weeks (p < 0.05). Using cell-specific markers, we determined the relative numbers of these progenitor cells that became neurons or glia and found that S100B profoundly increased hippocampal neurogenesis 5 weeks after TBI (p < 0.05). Furthermore, spatial learning ability, as assessed by the Morris water maze on day 30-34 post-injury, revealed an improved cognitive performance after S100B infusion (p < 0.05). Collectively, our findings indicate that an intraventricular S100B infusion induces neurogenesis within the hippocampus, which can be associated with an enhanced cognitive function following experimental TBI. These observations provide compelling evidence for the therapeutic potential of S100B in improving functional recovery following TBI.

Intraventricular infusion of the neurotrophic protein S100B improves cognitive recovery after fluid percussion injury in the rat.

Elevated serum S100B levels have been shown to be a predictor of poor outcome after traumatic brain injury (TBI). Experimental data, on the other hand, demonstrate a neuroprotective and neurotrophic effect of this calcium-binding protein. The purpose of this study was to examine the role of increased S100B levels on functional outcome after TBI. Following lateral fluid percussion or sham injury in male Sprague Dawley rats (n = 56), we infused S100B (50 ng/h) or vehicle into the cerebrospinal fluid of the ipsilateral ventricle for 7 days using an osmotic mini-pump. Assessment of cognitive performance by the Morris water maze on days 30-34 after injury revealed an improved performance of injured animals after S100B infusion (p < 0.05), when compared to vehicle infusion. Blood samples for analysis of clinical markers of brain damage, S100B and neuron specific enolase, taken at 30 min, 3 h, 4 h, 2 days, or 5 days showed a typical peak 3 h after injury (p < 0.01), and higher serum levels correlated significantly with an impaired cognitive recovery (p < 0.01). The correlation of higher serum S100B levels with poor water maze performance may result from injury induced opening of the blood-brain barrier, allowing the passage of S100B into serum. Thus while higher serum levels of S100B seem to reflect the degree of blood-brain barrier opening and severity of injury, a beneficial effect of intraventricular S100B administration on long-term functional recovery after TBI has been demonstrated for the first time. The exact mechanism by which S100B exerts its neuroprotective or neurotrophic influence remains unknown and needs to be elucidated by further investigation.