Hawley v. Evans.
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Acquired Immunodeficiency Syndrome↗
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Unit-wide notification of ventilator disconnections.
The alarms generated by mechanical ventilators when patients become disconnected can blend in with other typical sounds of the intensive care unit. Ventilator alarms that go unnoticed for extended periods of time often result in permanent patient harm or death. We developed a unit-wide system to monitor ventilator disconnection alarms. When a disconnection is identified, the system takes control of every computer in the patient's intensive care unit and generates an enhanced audio and visual alert. This system was tested in four ICUs at LDS Hospital. Acceptance by medical personnel was very high and patient safety was improved through early intervention that avoided prolonged hypoxia. In addition, the system facilitated root cause analyses and new safety strategies.
Equipment Failure↗
Enhanced notification of critical ventilator events.
Mechanical ventilators are designed to generate alarms when patients become disconnected or experience other critical ventilator events. However, these alarms can blend in with other accustomed sounds of the intensive care unit. Ventilator alarms that go unnoticed for extended periods of time often result in permanent patient harm or death. We developed a system to monitor critical ventilator events through our existing hospital network. Whenever an event is identified, the new system takes control of every computer in the patient's intensive care unit and generates an enhanced audio and visual alert indicating that there is a critical ventilator event and identifies the room number. Once the alert is acknowledged or the event is corrected, all the computers are restored back to the pre-alert status and/or application. This paper describes the development and implementation of this system and reports the initial results, user acceptance, and the increase in valuable information and patient safety.
Computer Systems↗
Dynamics of a novel pathogen in an avian host: Mycoplasmal conjunctivitis in house finches.
In early 1994, a novel strain of Mycoplasma gallisepticum (MG)--a poultry pathogen with a world-wide distribution--emerged in wild house finches and within 3 years had reached epidemic proportions across their eastern North American range. The ensuing epizootic resulted in a rapid decline of the host population coupled with considerable seasonal fluctuations in prevalence. To understand the dynamics of this disease system, a multi-disciplinary team composed of biologists, veterinarians, microbiologists and mathematical modelers set forth to determine factors driving and influenced by this host-pathogen system. On a broad geographic scale, volunteer observers ("citizen scientists") collected and reported data used for calculating both host abundance and disease prevalence. The scale at which this monitoring initiative was conducted is unprecedented and it has been an invaluable source of data for researchers at the Cornell Laboratory of Ornithology to track the spread and magnitude of disease both spatially and temporally. At a finer scale, localized and intensive field studies provided data used to quantify the effects of disease on host demographic parameters via capture-mark-recapture modeling, effects of host behavior on disease and vice-versa, and the biological and genetic profiles of birds with known phenotypic characteristics. To balance the field-based component of the study, experiments were conducted with finches held in captivity to describe and quantify the effects of experimental infections on hosts in both individual and social settings. The confluence of these various elements of the investigation provided the foundation for construction of a general compartmentalized epidemiological model of the dynamics of the house finch-MG system. This paper serves several purposes including (i) a basic review of the pathogen, host, and epidemic cycle; (ii) an explanation of our research strategy; (iii) a basic review of results from the diverse multi-disciplinary approaches employed; and (iv) pertinent questions relevant to this and other wildlife disease studies that require further investigation.
Animals↗
Characterization of the genotypic and phenotypic spectrum of TCF7L2-related neurodevelopmental disorder (TRND).
PURPOSE: TCF7L2 (OMIM 602228; HGNC:11641) is a transcription factor and a critical effector of the Wnt/ β-Catenin pathway. In 2021, 11 pediatric patients with monoallelic predicted loss-of-function (pLOF) TCF7L2 variants and syndromic features were observed. Characterization of patients with pLOF TCF7L2 variants and neurodevelopmental features-herein referred to as TCF7L2-related neurodevelopmental disorder-is urgently needed. METHODS: We leveraged multiple methods (eg, GeneMatcher, DECIPHER, literature review, and public/private repositories) to identify an international cohort of 76 patients with pLOF TCF7L2 variants and neurodevelopmental features and phenotypically characterized them. We also retrospectively searched for an independent cohort of adults with pLOF TCF7L2 variants (n = 11) from more than 60,000 PennMedicine BioBank patients. RESULTS: Among 76 patients with pLOF TCF7L2 variants, speech delay (95.3%), craniofacial dysmorphisms (73.3%), ophthalmologic conditions (65.5%), autism (62.1%), and orthopedic abnormalities (52.6%) were the most commonly observed. Phenotypic differences did not cluster by variant type or genomic locus. Among PennMedicine BioBank patients, an association of nominal significance with type 2 diabetes with renal manifestations (odds ratio = 5.8; P = .03) was detected, warranting further investigation. CONCLUSION: This study represents the most comprehensive characterization of TCF7L2-related neurodevelopmental disorder to date, a novel neurodevelopmental disorder, defining its genotypic and phenotypic spectra. We opened a Simons Searchlight natural history study that is now available for patient enrollment to enhance the understanding of this condition.
Neurodevelopmental syndrome↗