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Zusammenfassung Hintergrund Im Rahmen der Cochlea-Implantation (CI) zählen Serom- und Hämatombildung, Wundinfektion oder Schwindel zu den seltenen, aber typischen postoperativen Komplikationen. Emphyseme werden dagegen selten beobachtet. Sie können sowohl in der postoperativen Heilungsphase als auch Jahre später auftreten. Ein Therapiealgorithmus existiert bisher nicht. Methodik Wir berichten von 3 Patient*innen mit subkutanem Emphysem im Bereich des Signalprozessors aus dem eigenen Patientenkollektiv. In einem unsystematischen Review werden anschließend alle Studien mit Beschreibungen von Emphysemen nach CI hinsichtlich möglicher Risikofaktoren und therapeutischer Optionen untersucht. Ergebnisse Bei den vorgestellten Patient*innen entwickelte sich 2–11 Monate postoperativ ein subkutanes Emphysem nach heftigem Schnäuzen bzw. im Rahmen einer cPAP-Therapie. In der Literatur finden sich weitere 35 Fälle von Emphysemen nach CI. Luftinsufflation über die Tube ist die häufigste Ursache. Erkrankungen der Nase und Nasennebenhöhlen, Tubenfunktionsstörungen und obstruktives Schlafapnoesyndrom sind potenzielle Risikofaktoren. Druckverband, Punktion und Paukendrainage gelten als gängige Behandlungsmethoden. In therapieresistenten Fällen oder bei ausgedehnten Emphysemen kann eine operative Revision sinnvoll sein. Schlussfolgerung Die meisten Emphysembildungen sind durch konservative Maßnahmen beherrschbar. Punktionen sollten wegen möglicher Infektionen vermieden werden. Der prophylaktische Einsatz von Antibiotika scheint entbehrlich. Die operative Revision sollte bei Pneumozephalus mit Verdacht auf Leckage im Bereich der Dura erwogen werden. Die Abdeckung der Mastoidektomie mit einem Knochendeckel kann bei Risikokonstellation eine sinnvolle Maßnahme zur Prophylaxe postoperativer Emphyseme darstellen.

In the evolution of technology through the years, antennas are use in varying wireless systems have been in demand. Antennas play a great role in transmitting and receiving signals. As its application is heavily used in many days to day activities, it is important to create a cost-efficient and quick way to analyze its performance, characteristics, and relationship to different variables. As many radiation pattern acquisition devices are expensive, this simulation proposes a quick, reliable, and cost-friendly way to simulate 2D patterns in the E-plane and H-plane of a bowtie dipole antenna with an adaptive finite impulse response (FIR) filter. Through this study, the software MATLAB will be utilized to successfully simulate the radiation patterns of antennas with varying lengths. With the use of MATLAB toolboxes, the researchers aim to be able to compare different antenna lengths and determine the relationship and effect of it in the obtained 2D radiation pattern. If this method is successful various antenna applications may be implemented in the future with the use of 2D radiation pattern results.

John Busby,1 David Price,2– 4 Riyad Al-Lehebi,5 Sinthia Bosnic-Anticevich,6– 8 Job FM van Boven,9 Benjamin Emmanuel,10 J Mark FitzGerald,11 Mina Gaga,12 Susanne Hansen,13,14 Mark Hew,15,16 Takashi Iwanaga,17 Désirée Larenas Linnemann,18 Bassam Mahboub,19,20 Patrick Mitchell,21 Daniela Morrone,22 Jonathan Pham,15,23 Celeste Porsbjerg,14 Nicolas Roche,24,25 Eileen Wang,26,27 Neva Eleangovan,2,3 Liam G Heaney28 1Centre for Public Health, Queen’s University Belfast, Belfast, Northern Ireland; 2Optimum Patient Care, Cambridge, UK; 3Observational and Pragmatic Research Institute, Singapore, Singapore; 4Centre of Academic Primary Care, Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK; 5Department of Pulmonology, King Fahad Medical City, Riyadh, Saudi Arabia; 6Sydney Pharmacy School, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia; 7Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia; 8Central Sydney Local Area Health District, Sydney, Australia; 9Department of Clinical Pharmacy & Pharmacology, Groningen Research Institute for Asthma and COPD (GRIAC), University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 10BioPharmaceuticals Medical, AstraZeneca, Gaithersburg, MD, USA; 11Department of Medicine, The University of British Columbia, Vancouver, Canada; 12 7th Respiratory Medicine Department and Asthma Centre, Athens Chest Hospital, Athens, Greece; 13Center for Clinical Research and Prevention, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark; 14Respiratory Research Unit, Bispebjerg University Hospital, Copenhagen, Denmark; 15Allergy, Asthma & Clinical Immunology Service, Alfred Health, Melbourne, Australia; 16Public Health and Preventive Medicine, Monash University, Melbourne, Australia; 17Center for General Medical Education and Clinical Training, Kindai University Hospital, Osakasayama, Japan; 18Directora Centro de Excelencia en Asma y Alergia, Hospital Médica Sur, Ciudad de México, Mexico; 19College of Medicine, University of Sharjah, Sharjah, United Arab Emirates; 20Rashid Hospital, Dubai Health Authority, Dubai, United Arab Emirates; 21Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada; 22Personalized Medicine, Asthma and Allergy, Humanitas Clinical and Research Center, IRCCS, Rozzano, Italy; 23Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population & Global Health, The University of Melbourne, Melbourne, Australia; 24Respiratory Medicine, Cochin Hospital, APHP.Centre, Paris, France; 25University of Paris, Cochin Institute (UMR1016), Paris, France; 26Division of Allergy & Clinical Immunology, Department of Medicine, National Jewish Health, Denver, CO, USA; 27Division of Allergy & Clinical Immunology, Department of Internal Medicine, University of Colorado School of Medicine, Aurora, CO, USA; 28Wellcome-Wolfson Centre for Experimental Medicine, Queen’s University Belfast, Belfast, Northern IrelandCorrespondence: David PriceCentre of Academic Primary Care, Division of Applied Health Sciences, University of Aberdeen, Polwarth Building, Foresterhill, Aberdeen, AB25 2ZD, UKTel +65 6962 3627Email dprice@opri.sgIntroduction: Asthma morbidity and health-care utilization are known to exhibit a steep socioeconomic gradient. Further investigation into the modulators of this effect is required to identify potentially modifiable factors.Methods: We identified a cohort of patients with asthma from the Optimum Patient Care Research Database (OPCRD). We compared demographics, clinical variables, and health-care utilization by quintile of the UK 2011 Indices of Multiple Deprivation based on the location of the patients’ general practice. Multivariable analyses were conducted using generalized linear models adjusting for year, age, and sex. We conducted subgroup analyses and interaction tests to investigate the impact of deprivation by age, sex, ethnicity, and treatment step.Results: Our analysis included 127,040 patients with asthma. Patients from the most deprived socio-economic status (SES) quintile were more likely to report uncontrolled disease (OR: 1.54, 95% CI: 1.16, 2.05) and to have an exacerbation during follow-up (OR: 1.27, 95% CI: 1.13, 1.42) than the least deprived quintile. They had higher blood eosinophils (ratio: 1.03; 95% CI: 1.00, 1.06) and decreased peak flow (ratio: 0.95, 95% CI: 0.94, 0.97) when compared to those in the least deprived quintile. The effect of deprivation on asthma control was greater among those aged over 75 years (OR = 1.81, 95% CI: 1.20, 2.73) compared to those aged less than 35 years (OR: 1.22, 95% CI: 0.85, 1.74; pinteraction=0.019). Similarly, socioeconomic disparities in exacerbations were larger among those from ethnic minority groups (OR: 1.94, 95% CI: 1.40, 2.68) than white patients (OR: 1.24, 95% CI: 1.10, 1.39; pinteraction=0.012).Conclusion: We found worse disease control and increased exacerbation rates among patients with asthma from more deprived areas. There was evidence that the magnitude of socioeconomic disparities was elevated among older patients and those from ethnic minority groups. The drivers of these differences require further exploration.Keywords: asthma, socioeconomic status, disparities

In case of cochlear implantation seroma, hematoma, local wound infections or vertigo are rare but typical complications. In contrast, emphysema is seldom reported. They can occur after cochlear implantation both in the postoperative healing phase and years later. A therapeutic algorithm does not yet exist.We report on 3 patients with subcutaneous emphysema in the area of the receiver-stimulator. An unsystematic review of the literature of cases with emphysema after cochlear implantation highlights possible risk factors and the therapeutic options.The 3 cases developed subcutaneous emphysema 2-11 month after cochlear implantation due to nose blowing or CPAP therapy in obstructive sleep apnea. The current literature reports another 35 cases of emphysema after cochlear implantation. Air insufflation via the Eustachian tube is the most frequently described cause. Diseases of the nose and sinuses, tube dysfunction and obstructive sleep apnea are potential risk factors. Pressure bandage, puncture, tympanic tubes, and surgical revision are common treatments.Most emphysema can be controlled by conservative methods such as pressure bandaging and behavioral instruction. Punctures should be avoided due to the risk of upcoming infections. The prophylactic use of antibiotics seems dispensable. Surgical revision should be considered especially in cases of pneumocephalus with suspected leakage in the dura. The coverage of the mastoidectomy by a bony cap can be precautious and beneficial in cases with risk factors.Im Rahmen der Cochlea-Implantation (CI) zählen Serom- und Hämatombildung, Wundinfektion oder Schwindel zu den seltenen, aber typischen postoperativen Komplikationen. Emphyseme werden dagegen selten beobachtet. Sie können sowohl in der postoperativen Heilungsphase als auch Jahre später auftreten. Ein Therapiealgorithmus existiert bisher nicht.Wir berichten von 3 Patient*innen mit subkutanem Emphysem im Bereich des Signalprozessors aus dem eigenen Patientenkollektiv. In einem unsystematischen Review werden anschließend alle Studien mit Beschreibungen von Emphysemen nach CI hinsichtlich möglicher Risikofaktoren und therapeutischer Optionen untersucht.Bei den vorgestellten Patient*innen entwickelte sich 2–11 Monate postoperativ ein subkutanes Emphysem nach heftigem Schnäuzen bzw. im Rahmen einer cPAP-Therapie. In der Literatur finden sich weitere 35 Fälle von Emphysemen nach CI. Luftinsufflation über die Tube ist die häufigste Ursache. Erkrankungen der Nase und Nasennebenhöhlen, Tubenfunktionsstörungen und obstruktives Schlafapnoesyndrom sind potenzielle Risikofaktoren. Druckverband, Punktion und Paukendrainage gelten als gängige Behandlungsmethoden. In therapieresistenten Fällen oder bei ausgedehnten Emphysemen kann eine operative Revision sinnvoll sein.Die meisten Emphysembildungen sind durch konservative Maßnahmen beherrschbar. Punktionen sollten wegen möglicher Infektionen vermieden werden. Der prophylaktische Einsatz von Antibiotika scheint entbehrlich. Die operative Revision sollte bei Pneumozephalus mit Verdacht auf Leckage im Bereich der Dura erwogen werden. Die Abdeckung der Mastoidektomie mit einem Knochendeckel kann bei Risikokonstellation eine sinnvolle Maßnahme zur Prophylaxe postoperativer Emphyseme darstellen. .

Background: Limited data exist on the clinical and economic burden of chronic rhinosinusitis with nasal polyposis (CRSwNP). Objective: To describe patient characteristics, health-care resource utilization (HCRU), and health-care costs among patients with CRSwNP with and without comorbid asthma (primary analysis) and with surgical management of nasal polyps (secondary analysis). Methods: This was a retrospective study of patients diagnosed with CRSwNP conducted using administrative claims data from January 1, 2013, through March 31, 2019. Study outcomes were assessed over a 2-year follow-up. Results were stratified by baseline asthma status (primary analysis) and presented separately for patients with surgically managed CRSwNP (secondary analysis). Results: The primary analysis included 10,999 patients with CRSwNP (2649 with asthma, 8350 without asthma). Patients with versus without asthma had higher medication use, HCRU, and all-cause medical costs (mean ± standard deviation $34,667 ± $42,234 versus $27,122 ± $45,573; p < 0.001) across the full follow-up period. CRSwNP-related medical costs were significantly higher for patients with versus without asthma in year 2 of follow-up. In the surgical management analysis (n = 4943), most categories of medication use and CRSwNP-related HCRU declined from baseline levels during follow-up, and CRSwNP-related pharmacy costs in year 2 were less than half of baseline levels. Conclusion: Patients diagnosed with CRSwNP and asthma had a greater burden of illness than those without asthma. Higher CRSwNP-related medical costs in year 2 of follow-up for patients with asthma may indicate worsening symptoms over time. Among patients with surgically managed CRSwNP, HCRU and costs increased in year 1 of follow-up but decreased below baseline levels in year 2, potentially reflecting improved symptom severity.

Stephanie Chen,1 Marc Miravitlles,2 Chin Kook Rhee,3 Ian D Pavord,4 Rupert Jones,5 Victoria Carter,6 Benjamin Emmanuel,1 Marianna Alacqua,7 David B Price6,8 1BioPharmaceuticals Medical, Respiratory & Immunology, AstraZeneca, Gaithersburg, MD, USA; 2Pneumology Department, Hospital Universitari Vall d’Hebron, Vall d’Hebron Institut de Recerca (VHIR), Vall d’Hebron Barcelona Hospital Campus, CIBER de Enfermedades Respiratorias (CIBERES), Barcelona, Spain; 3College of Medicine, Seoul St Mary’s Hospital, the Catholic University of Korea, Seoul, South Korea; 4Oxford Respiratory NIHR BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK; 5Faculty of Health, University of Plymouth, Plymouth, UK; 6Observational and Pragmatic Research Institute, Singapore, Singapore; 7BioPharmaceuticals Medical, Respiratory & Immunology, AstraZeneca, Cambridge, UK; 8Centre of Academic Primary Care, Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UKCorrespondence: David B Price, Observational and Pragmatic Research Institute, 22 Sin Ming Lane, #06-76, Midview City, Singapore, 573969, Singapore, Tel +65 3105 1489, Email dprice@opri.sgBackground: Some patients with chronic obstructive pulmonary disease (COPD) experience frequent exacerbations despite maximal inhaled therapy (“triple therapy”), possibly leading to high health care resource utilization (HCRU).Aim: Describe characteristics, future HCRU, and mortality of patients with COPD who experience frequent exacerbations despite triple therapy; characterize individuals who may be candidates for biologic therapies.Methods: This descriptive observational study used primary care data of patients aged ≥ 40 years in the United Kingdom receiving maintenance therapy for COPD who had ≥ 1 year of data prior to index date and ≥ 1 year of follow-up data. We described these patients’ clinical and demographic characteristics, including blood eosinophil counts (BEC), pattern of exacerbations, hospitalizations, and corticosteroid exposure, as well as future exacerbations, hospitalizations, and death.Results: Of 43,753 patients with maintenance-treated COPD, 6480 experienced exacerbations despite ≥ 3 months of triple therapy. Of these, 5669 had available BEC: 1287 (22.7%) had BEC ≥ 250 cells/μL and ≥ 3 exacerbations in the year prior to the index date; 471 (36.6%) received ≥ 4 acute courses of oral corticosteroids. Patients with a pattern of high disease burden continued to have high disease burden: 51.1% experienced ≥ 3 exacerbations and 2.6% experienced ≥ 3 hospitalizations. Patients who experienced exacerbations despite triple therapy had a significantly higher risk of COPD-related death than other maintenance-treated patients (5.8% vs 2.1%).Conclusion: Nearly one-quarter of patients receiving triple therapy for COPD who experienced frequent exacerbations had elevated BEC and ≥ 3 exacerbations, suggesting a potential mechanism of persistent eosinophilic inflammation that could be a target for eosinophil-depleting biologic therapy.Keywords: chronic obstructive pulmonary disease, disease burden, eosinophils, exacerbations, health care resource utilization