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      Early Detection of Acute Chest Syndrome Through Electronic Recording and Analysis of Auscultatory Percussion

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          Abstract

          Acute chest syndrome (ACS) is the leading cause of death among people with sickle cell disease. ACS is clinically defined and diagnosed by the presence of a new pulmonary infiltrate on chest imaging with accompanying fever and respiratory symptoms like hypoxia, tachypnea, and shortness of breath. However, the characteristic chest x-ray (CXR) findings necessary for a clinical diagnosis of ACS can be difficult to detect, as is determining which patient needs a CXR. This makes early detection difficult; but it is critical in order to limit ACS severity and subsequent fatalities. This research project looks to apply percussion and auscultation techniques that can provide an immediate diagnosis of acute pulmonary conditions by using an automated standard percussive input and electronic auscultation for computational analysis of the measured signal. Measurements on sickle cell patients having ACS, vaso-occlusive crisis (VOC), and regular clinic visits (healthy) were recorded and analyzed. Average intensity of sound transmission through the chest and lungs was determined in the ACS and healthy subject groups, revealing an average of 10–14 dB decrease in sound intensity in the ACS group compared to the healthy group. A random under-sampling boosted tree classification model identified with 94% accuracy the positive ACS and healthy observations. The analysis also revealed unique measurable changes in a small number of cases clinically classified as complicated VOC, which later developed into ACS. This suggests the developed approach may also have early predictive capability, identifying patients at risk for developing ACS prior to current clinical practice.

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          Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group.

          The acute chest syndrome is the leading cause of death among patients with sickle cell disease. Since its cause is largely unknown, therapy is supportive. Pilot studies with improved diagnostic techniques suggest that infection and fat embolism are underdiagnosed in patients with the syndrome. In a 30-center study, we analyzed 671 episodes of the acute chest syndrome in 538 patients with sickle cell disease to determine the cause, outcome, and response to therapy. We evaluated a treatment protocol that included matched transfusions, bronchodilators, and bronchoscopy. Samples of blood and respiratory tract secretions were sent to central laboratories for antibody testing, culture, DNA testing, and histopathological analyses. Nearly half the patients were initially admitted for another reason, mainly pain. When the acute chest syndrome was diagnosed, patients had hypoxia, decreasing hemoglobin values, and progressive multilobar pneumonia. The mean length of hospitalization was 10.5 days. Thirteen percent of patients required mechanical ventilation, and 3 percent died. Patients who were 20 or more years of age had a more severe course than those who were younger. Neurologic events occurred in 11 percent of patients, among whom 46 percent had respiratory failure. Treatment with phenotypically matched transfusions improved oxygenation, with a 1 percent rate of alloimmunization. One fifth of the patients who were treated with bronchodilators had clinical improvement. Eighty-one percent of patients who required mechanical ventilation recovered. A specific cause of the acute chest syndrome was identified in 38 percent of all episodes and 70 percent of episodes with complete data. Among the specific causes were pulmonary fat embolism and 27 different infectious pathogens. Eighteen patients died, and the most common causes of death were pulmonary emboli and infectious bronchopneumonia. Infection was a contributing factor in 56 percent of the deaths. Among patients with sickle cell disease, the acute chest syndrome is commonly precipitated by fat embolism and infection, especially community-acquired pneumonia. Among older patients and those with neurologic symptoms, the syndrome often progresses to respiratory failure. Treatment with transfusions and bronchodilators improves oxygenation, and with aggressive treatment, most patients who have respiratory failure recover.
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            RUSBoost: A Hybrid Approach to Alleviating Class Imbalance

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              Management of ground-glass opacities: should all pulmonary lesions with ground-glass opacity be surgically resected?

              Pulmonary nodules with ground-glass opacity (GGO) are frequently observed and will be increasingly detected. GGO can be observed in both benign and malignant conditions, including lung cancer and its preinvasive lesions. Atypical adenomatous hyperplasia and adenocarcinoma in situ are typically manifested as pure GGOs, whereas more advanced adenocarcinomas may include a larger solid component within the GGO region. The natural history of GGOs has been gradually clarified. Approximately 20% of pure GGOs and 40% of part-solid GGOs gradually grow or increase their solid component, whereas others remain unchanged for years. Therefore, it remains unclear whether all pulmonary lesions with GGO should be surgically resected or whether lesions without changes may not require resection. To distinguish GGOs with growth from those without growth, a 3-year follow-up observation period is a reasonable benchmark based on the data that the volume-doubling time (VDT) of pure GGOs ranges from approximately 600 to 900 days and that of part-solid GGOs ranges from 300 to 450 days. Future studies on the genetic differences between GGOs with growth and those without growth will help establish an appropriate management algorithm.
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                Author and article information

                Contributors
                Journal
                IEEE J Transl Eng Health Med
                IEEE J Transl Eng Health Med
                0063400
                JTEHM
                IJTEBN
                IEEE Journal of Translational Engineering in Health and Medicine
                IEEE
                2168-2372
                2020
                30 September 2020
                : 8
                : 4900108
                Affiliations
                [1 ]departmentRichard and Loan Hill Department of Bioengineering, institutionUniversity of Illinois at Chicago, institutionringgold 14681; ChicagoIL60607USA
                [2 ]departmentDepartment of Medicine, institutionUniversity of Illinois at Chicago, institutionringgold 14681; ChicagoIL60612USA
                [3 ]institutionJesse Brown VA; ChicagoIL60612USA
                Article
                4900108
                10.1109/JTEHM.2020.3027802
                7571866
                33094035
                a0c5ed31-1529-4503-aacf-f49d80d5f340
                Copyright @ 2020

                This work is licensed under a Creative Commons Attribution 4.0 License. For more information, see https://creativecommons.org/licenses/by/4.0/

                History
                : 11 May 2020
                : 10 September 2020
                : 27 September 2020
                : 08 October 2020
                Page count
                Figures: 4, Tables: 0, Equations: 1, References: 17, Pages: 8
                Funding
                Funded by: NIH through the University of Illinois at Chicago Clinical and Translational Science Award, fundref 10.13039/100006108;
                Award ID: UL1 TR002003
                Funded by: Pilot Grant Program;
                Award ID: 2018-04
                This work was supported in part by the NIH through the University of Illinois at Chicago Clinical and Translational Science Award under Grant UL1 TR002003, and in part by the Pilot Grant Program under Grant 2018-04.
                Categories
                Article

                acoustic,stethoscope,percussion,lung,acute chest syndrome,sickle cell disease,machine learning,diagnosis

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