Person:

Novack, Victor

Background: There is an increase in admission rate for elderly patients to the ICU. Mortality rates are lower when more liberal ICU admission threshold are compared to more restrictive threshold. We sought to describe the temporal trends in elderly admissions and outcomes in a tertiary hospital before and after the addition of an 8-bed medical ICU. Methods: We conducted a retrospective analysis of a comprehensive longitudinal ICU database, from a large tertiary medical center, examining trends in patients’ characteristics, severity of illness, intensity of care and mortality rates over the years 2001–2008. The study population consisted of elderly patients and the primary endpoints were 28 day and one year mortality from ICU admission. Results: Between the years 2001 and 2008, 7,265 elderly patients had 8,916 admissions to ICU. The rate of admission to the ICU increased by 5.6% per year. After an eight bed MICU was added, the severity of disease on ICU admission dropped significantly and crude mortality rates decreased thereafter. Adjusting for severity of disease on presentation, there was a decreased mortality at 28- days but no improvement in one- year survival rates for elderly patient admitted to the ICU over the years of observation. Hospital mortality rates have been unchanged from 2001 through 2008. Conclusion: In a high capacity ICU bed hospital, there was a temporal decrease in severity of disease on ICU admission, more so after the addition of additional medical ICU beds. While crude mortality rates decreased over the study period, adjusted one-year survival in ICU survivors did not change with the addition of ICU beds. These findings suggest that outcome in critically ill elderly patients may not be influenced by ICU admission. Adding additional ICU beds to deal with the increasing age of the population may therefore not be effective.

Background: Administration of onabotulinumtoxinA (BoNT-A) to peripheral tissues outside the calvaria reduces the number of days chronic migraine patients experience headache. Because the headache phase of a migraine attack, especially those preceded by aura, is thought to involve activation of meningeal nociceptors by endogenous stimuli such as changes in intracranial pressure (i.e. mechanical) or chemical irritants that appear in the meninges as a result of a yet-to-be-discovered sequence of molecular/cellular events triggered by the aura, we sought to determine whether extracranial injections of BoNT-A alter the chemosensitivity of meningeal nociceptors to stimulation of their intracranial receptive fields. Material and methods Using electrophysiological techniques, we identified 161 C- and 135 Aδ-meningeal nociceptors in rats and determined their mechanical response threshold and responsiveness to chemical stimulation of their dural receptive fields with TRPV1 and TRPA1 agonists seven days after BoNT-A administration to different extracranial sites. Two paradigms were compared: distribution of 5 U BoNT-A to the lambdoid and sagittal sutures alone, and 1.25 U to the sutures and 3.75 U to the temporalis and trapezius muscles. Results: Seven days after it was administered to tissues outside the calvaria, BoNT-A inhibited responses of C-type meningeal nociceptors to stimulation of their intracranial dural receptive fields with the TRPV1 agonist capsaicin and the TRPA1 agonist mustard oil. BoNT-A inhibition of responses to capsaicin was more effective when the entire dose was injected along the suture lines than when it was injected into muscles and sutures. As in our previous study, BoNT-A had no effect on non-noxious mechanosensitivity of C-fibers or on responsiveness of Aδ-fibers to mechanical and chemical stimulation. Discussion This study demonstrates that extracranial administration of BoNT-A suppresses meningeal nociceptors’ responses to stimulation of their intracranial dural receptive fields with capsaicin and mustard oil. The findings suggest that surface expression of TRPV1 and TRPA1 channels in dural nerve endings of meningeal nociceptors is reduced seven days after extracranial administration of BoNT-A. In the context of chronic migraine, reduced sensitivity to molecules that activate meningeal nociceptors through the TRPV1 and TRPA1 channels can be important for BoNT-A’s ability to act as a prophylactic.