Late Stage Infection in Sleeping Sickness

At the turn of the 19th century, trypanosomes were identified as the causative agent of sleeping sickness and their presence within the cerebrospinal fluid of late stage sleeping sickness patients was described. However, no definitive proof of how the parasites reach the brain has been presented so far. Analyzing electron micrographs prepared from rodent brains more than 20 days after infection, we present here conclusive evidence that the parasites first enter the brain via the choroid plexus from where they penetrate the epithelial cell layer to reach the ventricular system. Adversely, no trypanosomes were observed within the parenchyma outside blood vessels. We also show that brain infection depends on the formation of long slender trypanosomes and that the cerebrospinal fluid as well as the stroma of the choroid plexus is a hostile environment for the survival of trypanosomes, which enter the pial space including the Virchow-Robin space via the subarachnoid space to escape degradation. Our data suggest that trypanosomes do not intend to colonize the brain but reside near or within the glia limitans, from where they can re-populate blood vessels and disrupt the sleep wake cycles

Automatic Notifications Mediated by Anesthesia Information Management Systems Reduce the Frequency of Prolonged Gaps in Blood Pressure Documentation

BACKGROUND: Arterial blood pressure (BP) measurement at least every five minutes is part of the American Society of Anesthesiologists' (ASA) monitoring standard, but prolonged BP gaps in electronic anesthesia records have been noted. We undertook multicenter studies to determine the frequency of cases with at least one interval ≥ 10 minutes between successive BP measurements and then to ascertain if educational feedback via an electronic, near real-time notification system alerting providers to the presence of such gaps would reduce their incidence. METHODS: We evaluated 212,706 electronic anesthesia records from three large academic centers. We determined the fraction of cases with ≥ 10 minute BP monitoring gaps at baseline and did a root cause analysis to determine common causes for these lapses. We then designed and implemented automated systems at two of the hospitals to notify point-of-care providers immediately after such 10-minute gaps occurred and determined the subsequent impact of this feedback on BP gap incidence, compared to baseline. RESULTS: At Hospital A, the notification system reduced the incidence of cases with at least one BP gap (1.48% ± 0.19% SD vs 0.79% ± 0.36% SD, p<0.0001). At Hospital B, the gap incidence was not significantly altered when notification was provided after a 10-min gap had already occurred (2.72% ± 0.60% SD vs. 2.45% ± 0.48% SD, P=0.27), but the incidence was reduced when such notification was provided after 6 minutes without a BP reading (2.72% ± 0.60% SD vs 1.54% ± 0.19% SD, P<0.0001). At Hospital C, where notification was not implemented, the baseline rate of BP gaps was consistent across the preintervention and follow-up periods (7.03% ± 1.27% SD vs. 7.13% ± 0.11% SD, p=0.74). Although monitors disconnected during position change was the most common identifiable cause of BP gaps, reasons for the missing BPs were often not documented. During a week when the electronic charting system was temporarily inoperable, no BP gaps were noted on a convenience sample of 500 paper records from Hospital A (99% upper confidence limit = 0.83%). CONCLUSIONS: BP gaps of ≥ 10 minutes were common in electronic anesthesia records, and their incidence was reduced but not eliminated by near real-time feedback to providers. The ASA standard for every 5 min BP documentation may not be achievable with current practices and technology. Anesthesia information management systems users need to be cognizant of the potential for gaps in BP measurement, take steps to minimize their occurrence, and document an explanation when such failures occur