Objective: To assess the utility of VNS within our center in reducing the utilization of benzodiazepine rescue medications, status epilepticus, and ER visits. Background: Starting in January 2017, the University of Rochester Epilepsy Center began to place responsive VNS devices (Aspire®, SenTiva®) in pediatric patients primarily with LGS diagnoses, creating a cohort of patients in a dedicated VNS clinic with extensive pre- and post-treatment data, standardized advancement of VNS programming, and uniform assessment of efficacy of the intervention. Design/Methods: Charts of patients with VNS placed at URMC from Jan2017–Aug2019 were reviewed for seizure frequency, medication adjustments, utilization of rescue medications (confirmed with pharmacy information), frequency of ER visits or hospitalizations, adverse events, side effects, and VNS programming and operating parameters. Patient information was compared to their own historical seizure frequency, benzodiazepine usage, etc, in the 3–6 months prior to VNS placement noted in their pre-implantation and immediate post-operative visits. Results: During this period 30 pediatric patients underwent placement of responsive VNS generators (8 were battery replacements). 3 patients (10%) experienced significant adverse events (including failure of the device, infection/sepsis, etc). There was a decrease in utilization of benzodiazepine-based rescue medications with increase in the voltage and decrease in off-time of the VNS in the majority of patients. Frequency of ER visits and seizure related hospitalization was low, and not determined to be significantly different. No specific quality of life (QOL) evaluation was utilized during this treatment period, but patients and families reported improved subjective QOL in the VNS clinic setting after the intervention. Conclusions: Responsive VNS is an effective intervention in the URMC pediatric epilepsy population to reduce exposure to rescue medications and the frequency of seizure cluster and status epilepticus. Duration of treatment at URMC may be too short to show reduction in seizure frequency for patients with the most complex epilepsy syndromes. Disclosure: Dr. Brumfield has nothing to disclose. Dr. Socha has nothing to disclose. Dr. Hughes has nothing to disclose.

Lung volumes, especially functional residual capacity (FRC), are decreased in acute respiratory distress syndrome (ARDS). Positive end-expiratory pressure (PEEP) contributes to increased end-expiratory lung volume (EELV) and to improved oxygenation, but differentiating recruitment of previously nonaerated lung units from distension of previously open lung units remains difficult. This study evaluated simple methods derived from bedside EELV measurements to assess PEEP-induced lung recruitment while monitoring strain. Prospective multicenter study in 30 mechanically ventilated patients with ARDS in five university hospital ICUs. Two PEEP levels were studied, each for 45 min, and EELV (nitrogen washout/washin technique) was measured at both levels, with the difference (Δ) reflecting PEEP-induced lung volume changes. Alveolar recruitment was measured using pressure-volume (PV) curves. High and low recruiters were separated based on median recruitment at high PEEP. Minimum predicted increase in lung volume computed as the product of ΔPEEP by static compliance was subtracted from ΔEELV as an independent estimate of recruitment. Estimated and measured recruitments were compared. Strain induced by PEEP was also calculated from the same measurements. FRC was 31 ± 11% of predicted. Median [25th–75th percentiles] PEEP-induced recruitment was 272 [187–355] mL. Estimated recruitment correlated with recruited volume measured on PV curves (ρ = 0.68), with a slope close to identity. The ΔEELV/FRC ratio differentiated high from low recruiters (110 [76–135] vs. 55 [23–70]%, p = 0.001). Strain increase due to PEEP was larger in high recruiters (p = 0.002). PEEP-induced recruitment and strain can be assessed at the bedside using EELV measurement. We describe two bedside methods for predicting low or high alveolar recruitment during ARDS.

The large surface area for gas exchange makes the respiratory system particularly susceptible to oxidative stress-mediated injury. Both endogenous and exogenous pro-oxidants (e.g. cigarette smoke) trigger activation of leukocytes and host defenses. These mechanisms interact in a "multilevel cycle" responsible for the control of the oxidant/antioxidant homeostasis. Several studies have demonstrated the presence of increased oxidative stress and decreased antioxidants (e.g. reduced glutathione [GSH]) in subjects with chronic obstructive pulmonary disease (COPD), but the contribution of oxidative stress to the pathophysiology of COPD is generally only minimally discussed. The aim of this review was to provide a comprehensive overview of the role of oxidative stress in the pathogenesis of respiratory diseases, particularly COPD, and to examine the available clinical and experimental evidence on the use of the antioxidant N-acetylcysteine (NAC), a precursor of GSH, as an adjunct to standard therapy for the treatment of COPD. The proposed concept of "multilevel cycle" helps understand the relationship between respiratory diseases and oxidative stress, thus clarifying the rationale for using NAC in COPD. Until recently, antioxidant drugs such as NAC have been regarded only as mucolytic agents. Nevertheless, several clinical trials indicate that NAC may reduce the rate of COPD exacerbations and improve small airways function. The most plausible explanation for the beneficial effects observed in patients with COPD treated with NAC lies in the mucolytic and antioxidant effects of this drug. Modulation of bronchial inflammation by NAC may further account for these favorable clinical results.