Performance and Resilience Analysis of a New York Drinking Water System to Localized and System-Wide Emergencies.

Drinking water utilities are vulnerable to both human-caused and natural disasters that can impact the system infrastructure and the delivery of potable water to consumers. Analyzing system performance and resilience can help utilities identify areas of high risk or concern, understand the impacts on consumers, and evaluate response actions during disasters. In this case study, the Water Network Tool for Resilience (WNTR) was used to investigate the performance and resilience of a drinking water system in New York during increased demands due to firefighting, pipe damage, and loss of the source water emergencies. This case study introduced a new combined performance index (CPI) resilience metric, which served to quantify system resilience as a ratio of system performance during an emergency to normal operations. The results revealed that this drinking water system was able to maintain service to most of the consumers during these emergencies due to high redundancy within the system, and conservation efforts extended water service for an additional 20 h. The analysis in this paper can be used by other drinking water utilities to understand their vulnerabilities and evaluate resilience-improving actions in similar disaster scenarios.

Prevalence of Corneal Astigmatism in an NHS Cataract Surgery Practice in Northern Ireland.

PURPOSE: Post-operative corneal astigmatism following cataract surgery can leave the patient with visual impairment. Correcting it at the time of surgery with a toric intraocular lens (TIOL) can give patients a better final visual outcome. The purpose was to determine the prevalence of corneal astigmatism in a cataract population and assess the demand for TIOL. METHODS: Keratometric data was collected and analyzed for all patients who attended for routine cataract surgery under the care of a single surgeon based in Altnagelvin Area Hospital, Northern Ireland (NI). All patients were included between January 2008 and December 2014. Data was collected retrospectively for this observational study. RESULTS: There were 2080 consecutive eyes of 1788 patients. The mean corneal astigmatism was 1.09 ± 0.83. Corneal astigmatism was 1.50D or less in 1621 eyes (78%). It was more than 2.00 D in 242 eyes (11.6%), more than 2.50 D in 127 eyes (6.1%), more than 3.00D in 68 eyes (3.27%) and more than 3.50 D in 45 eyes (2.16%). CONCLUSION: For routine cataract surgery, 41.3% of eyes had more than 1.00 D of corneal astigmatism and 11.6% had more and 2.00D. Females had more astigmatism than males. This shows the potential demand for the TIOL in this population.

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB-dependent mechanism.

OBJECTIVES: Hypercapnic acidosis protects against ventilation-induced lung injury. We wished to determine whether the beneficial effects of hypercapnic acidosis in reducing stretch-induced injury were mediated via inhibition of nuclear factor-κB, a key transcriptional regulator in inflammation, injury, and repair. DESIGN: Prospective randomized animal study. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: In separate experimental series, the potential for hypercapnic acidosis to attenuate moderate and severe ventilation-induced lung injury was determined. In each series, following induction of anesthesia and tracheostomy, Sprague-Dawley rats were randomized to (normocapnia; FICO2 0.00) or (hypercapnic acidosis; FICO2 0.05), subjected to high stretch ventilation, and the severity of lung injury and indices of activation of the nuclear factor-κB pathway were assessed. Subsequent in vitro experiments examined the potential for hypercapnic acidosis to reduce pulmonary epithelial inflammation and injury induced by cyclic mechanical stretch. The role of the nuclear factor-κB pathway in hypercapnic acidosis-mediated protection from stretch injury was then determined. MEASUREMENTS AND MAIN RESULTS: Hypercapnic acidosis attenuated moderate and severe ventilation-induced lung injury, as evidenced by improved oxygenation, compliance, and reduced histologic injury compared to normocapnic conditions. Hypercapnic acidosis reduced indices of inflammation such as interleukin-6 and bronchoalveolar lavage neutrophil infiltration. Hypercapnic acidosis reduced the decrement of the nuclear factor-κB inhibitor IκBα and reduced the generation of cytokine-induced neutrophil chemoattractant-1. Hypercapnic acidosis reduced cyclic mechanical stretch-induced nuclear factor-κB activation, reduced interleukin-8 production, and decreased epithelial injury and cell death compared to normocapnia. CONCLUSIONS: Hypercapnic acidosis attenuated ventilation-induced lung injury independent of injury severity and decreased mechanical stretch-induced epithelial injury and death, via a nuclear factor-κB-dependent mechanism.

Overexpression of pulmonary extracellular superoxide dismutase attenuates endotoxin-induced acute lung injury.

PURPOSE: Superoxide is produced by activated neutrophils during the inflammatory response to stimuli such as endotoxin, can directly or indirectly injure host cells, and has been implicated in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). We wished to determine the potential for pulmonary overexpression of the extracellular isoform of superoxide dismutase (EC-SOD) to reduce the severity of endotoxin-induced lung injury. METHODS: Animals were randomly allocated to undergo intratracheal instillation of (1) surfactant alone (vehicle); (2) adeno-associated virus (AAV) vectors containing a null transgene (AAV-null); and (3) adeno-associated virus vectors containing the EC-SOD transgene (AAV-EC-SOD) and endotoxin was subsequently administered intratracheally. Two additional groups were randomized to receive (1) vehicle or (2) AAV-EC-SOD, and to undergo sham (vehicle) injury. The severity of the lung injury was assessed in all animals 24 h later. RESULTS: Endotoxin produced a severe lung injury compared to sham injury. The AAV vector encoding EC-SOD increased lung EC-SOD concentrations, and enhanced the antioxidant capacity of the lung. EC-SOD overexpression decreased the severity of endotoxin-induced ALI, reducing the decrement in systemic oxygenation and lung compliance, decreasing lung permeability and decreasing histologic injury. EC-SOD attenuated pulmonary inflammation, decreased bronchoalveolar lavage neutrophil counts, and reduced interleukin-6 and CINC-1 concentrations. The AAV vector itself did not contribute to inflammation or to lung injury. CONCLUSIONS: Pulmonary overexpression of EC-SOD protects the lung against endotoxin-induced ALI.

Differential effects of buffered hypercapnia versus hypercapnic acidosis on shock and lung injury induced by systemic sepsis.

BACKGROUND: Acute hypercapnic acidosis protects against lung injury caused by nonseptic insults and after both pulmonary and systemic sepsis. The authors wished to dissect the contribution of the acidosis versus hypercapnia per se to the effects of hypercapnic acidosis on the hemodynamic profile and severity of lung injury induced by systemic sepsis. METHODS: In the hypercapnic acidosis series, adult male Sprague-Dawley rats were randomized to normocapnia or hypercapnic acidosis-produced by adding 5% carbon dioxide to the inspired gas-and cecal ligation and puncture performed. In the buffered hypercapnia series, animals were first randomized to housing under conditions of environmental normocapnia or hypercapnia-produced by exposure to 8% carbon dioxide-to allow renal buffering. After 96 h, cecal ligation and puncture was performed. In both series, the animals were ventilated for 6 h, and the severity of the lung injury and hemodynamic deterioration were assessed. RESULTS: Both hypercapnic acidosis and buffered hypercapnia attenuated the development and severity of hypotension and reduced lactate accumulation compared to normocapnia. Hypercapnic acidosis reduced lung injury and inflammation, decreased mean (+ or - SD) bronchoalveolar lavage protein concentration (232 + or - 50 versus 279 + or - 27 microg x ml(-1)) and median neutrophil counts (3,370 versus 9,120 cells x ml(-1)), and reduced histologic lung injury. In contrast, buffered hypercapnia did not reduce the severity of systemic sepsis induced lung injury. CONCLUSIONS: Both hypercapnic acidosis and buffered hypercapnia attenuate the hemodynamic consequences of systemic sepsis. In contrast, hypercapnic acidosis, but not buffered hypercapnia, reduced the severity of sepsis-induced lung injury.

A comparison of the Glidescope, Pentax AWS, and Macintosh laryngoscopes when used by novice personnel: a manikin study.

PURPOSE: Direct laryngoscopic tracheal intubation is a potentially lifesaving procedure, but a difficult skill to acquire and maintain. The consequences of poorly performed intubation attempts are potentially severe. The Pentax AWS and the Glidescope are indirect laryngoscopes that may require less skill to use. We therefore hypothesized that AWS and Glidescope would prove superior to the Macintosh laryngoscope when used by novices in the normal and simulated difficult airway. METHODS: In this prospective randomized crossover trial following standardized didactic instruction, medical students with no prior experience of laryngoscopy performed tracheal intubation using each device. Each student was allowed up to three attempts to intubate in a Laerdal Intubation Trainer in two laryngoscopy scenarios and in a Laerdal SimMan manikin in one scenario. The students then performed tracheal intubation of the normal airway a second time to characterize the learning curve for each device. RESULTS: The Pentax AWS provided better intubation conditions than the Glidescope or the Macintosh, resulting in greater success of intubation, particularly in the difficult laryngoscopy scenarios. The Glidescope demonstrated advantages over the Macintosh, particularly in the more difficult scenarios. Both the AWS and the Glidescope decreased the duration of intubation attempts, reduced the number of maneuvers required, and reduced the potential for dental trauma. In direct comparisons, the AWS provided the best intubation conditions. CONCLUSIONS: The Pentax AWS appears to constitute a better alternative to the Macintosh for novice personnel to acquire the skills of tracheal intubation.

Hypercapnic acidosis attenuates shock and lung injury in early and prolonged systemic sepsis.

OBJECTIVE: To investigate whether acute hypercapnic acidosis--induced by adding CO2 to inspired gas--would protect against severe systemic sepsis-induced lung and systemic organ injury resulting from cecal ligation and puncture. Acute hypercapnic acidosis protects against lung injury after both nonseptic and early pneumonia-induced lung injury. In contrast, prolonged hypercapnia worsens pneumonia-induced lung injury. The effects of hypercapnia and acidosis in the setting of systemic sepsis remain to be determined. DESIGN: Prospective randomized animal study. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: In the early systemic sepsis series, post induction of anesthesia and tracheostomy placement, animals were randomized to normocapnia (Fico2 = 0.00, n = 12) or hypercapnic acidosis (Fico2 = 0.05, n = 12). Cecal ligation and puncture were performed and the animals were ventilated for 3 hrs. In the prolonged systemic sepsis series, rats were anesthetized, cecal ligation and puncture were performed, and the animals were allowed to recover. The animals were then randomized to housing under conditions of environmental normocapnia (Fico2 = 0.00, n = 20) or hypercapnia (Fico2 = 0.08, n = 20). After 96 hrs, the animals were reanesthetized, and the severity of lung and hemodynamic injury was assessed. RESULTS: In early systemic sepsis, hypercapnic acidosis attenuated the development and severity of hypotension, and reduced lactate accumulation and the decrement in central venous oxyhemoglobin levels, compared with normocapnia. Hypercapnic acidosis reduced bronchoalveolar lavage neutrophil infiltration, and lung wet/dry weight ratios. In prolonged systemic sepsis, hypercapnic acidosis reduced histologic indices of lung injury. There was no evidence that hypercapnia worsened prolonged systemic sepsis-induced lung injury. Hypercapnic acidosis did not alter lung or systemic bacterial loads in early or prolonged systemic sepsis. CONCLUSION: Hypercapnic acidosis exerts beneficial effects in early and prolonged cecal ligation and puncture-induced polymicrobial systemic sepsis.

Determination Of The Efficacy And Side-effect Profile Of Lower Doses Of Intrathecal Morphine In Patients Undergoing Total Knee Arthroplasty.

BACKGROUND: Intrathecal (IT) morphine provides excellent post-operative analgesia, but causes multiple side effects including nausea and vomiting (PONV), pruritus and respiratory depression, particularly at higher doses. The lowest effective dose of spinal morphine in patients undergoing total knee arthroplasty is not known. METHODS: We evaluated the analgesic efficacy and side effect profile of 100 - 300 µg IT morphine in patients undergoing elective total knee replacement in this prospective, randomized, controlled, double-blind study. Sixty patients over the age of 60 undergoing elective knee arthroplasty were enrolled. Patients were randomized to receive spinal anaesthesia with 15 mg Bupivacaine and IT morphine in three groups: (i) 100 µg; (ii) 200 µg; and (iii) 300 µg. RESULTS: Both 200 µg and 300 µg IT morphine provided comparable levels of postoperative analgesia. However, patients that received 100 µg had greater pain postoperatively, with higher pain scores and a greater requirement for supplemental morphine. There were no differences between groups with regard to PONV, pruritus, sedation, respiratory depression or urinary retention. CONCLUSION: Both 200 µg and 300 µg provided comparable postoperative analgesia, which was superior to that provided by 100 mug IT morphine in patients undergoing total knee arthroplasty. Based on these findings, we recommend that 200 µg IT morphine be used in these patients. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT00695045.