Vascular injury and orthopaedics.
Ontology highlight
ABSTRACT:
SUBMITTER: Parvizi J
PROVIDER: S-EPMC6287961 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC6977530 | biostudies-literature
Project description:There is a growing interest in the application of artificial intelligence (AI) to orthopaedic surgery. This review aims to identify and characterise research in this field, in order to understand the extent, range and nature of this work, and act as springboard to stimulate future studies. A scoping review, a form of structured evidence synthesis, was conducted to summarise the use of AI in orthopaedics. A literature search (1946-2019) identified 222 studies eligible for inclusion. These studies were predominantly small and retrospective. There has been significant growth in the number of papers published in the last three years, mainly from the USA (37%). The majority of research used AI for image interpretation (45%) or as a clinical decision tool (25%). Spine (43%), knee (23%) and hip (14%) were the regions of the body most commonly studied. The application of artificial intelligence to orthopaedics is growing. However, the scope of its use so far remains limited, both in terms of its possible clinical applications, and the sub-specialty areas of the body which have been studied. A standardized method of reporting AI studies would allow direct assessment and comparison. Prospective studies are required to validate AI tools for clinical use.
| S-EPMC8610245 | biostudies-literature
Project description: Not available
| S-EPMC6128312 | biostudies-literature
Project description:The novel Coronavirus (COVID-19) pandemic has placed an immense strain on health care systems and orthopedic surgeons across the world. To limit the spread, federal and state governments mandated the cancellation of all nonurgent surgical cases to address surging hospital admissions and manage workforce and resource reallocation. During the pandemic surge, thousands of surgical cancellations have been required. We outline our experience through the onset and advance of the surge, detail our incident response and discuss the transition toward recovery. Level of Evidence: Level V.
| S-EPMC7245196 | biostudies-literature
Project description:Good inpatient handover ensures patient safety and continuity of care. An adjunct to this is the patient list which is routinely managed by junior doctors. These lists are routinely created and managed within Microsoft Excel or Word. Following the merger of two orthopaedic departments into a single service in a new hospital, it was felt that a number of safety issues within the handover process needed to be addressed. This quality improvement project addressed these issues through the creation and implementation of a new patient database which spanned the department, allowing trouble free, safe, and comprehensive handover. Feedback demonstrated an improved user experience, greater reliability, continuity within the lists and a subsequent improvement in patient safety.
| S-EPMC4645854 | biostudies-literature
Project description:BackgroundThe integrity of endothelial monolayer is a sine qua non for vascular homeostasis and maintenance of tissue-fluid balance. However, little is known about the signaling pathways regulating regeneration of the endothelial barrier after inflammatory vascular injury.Methods and resultsUsing genetic and pharmacological approaches, we demonstrated that endothelial regeneration selectively requires activation of p110γPI3K signaling, which thereby mediates the expression of the endothelial reparative transcription factor Forkhead box M1 (FoxM1). We observed that FoxM1 induction in the pulmonary vasculature was inhibited in mice treated with a p110γ-selective inhibitor and in Pik3cg(-/-) mice after lipopolysaccharide challenge. Pik3cg(-/-) mice exhibited persistent lung inflammation induced by sepsis and sustained increase in vascular permeability. Restoration of expression of either p110γ or FoxM1 in pulmonary endothelial cells of Pik3cg(-/-) mice restored endothelial regeneration and normalized the defective vascular repair program. We also observed diminished expression of p110γ in pulmonary vascular endothelial cells of patients with acute respiratory distress syndrome, suggesting that impaired p110γ-FoxM1 vascular repair signaling pathway is a critical factor in persistent leaky lung microvessels and edema formation in the disease.ConclusionsWe identify p110γ as the critical mediator of endothelial regeneration and vascular repair after sepsis-induced inflammatory injury. Thus, activation of p110γ-FoxM1 endothelial regeneration may represent a novel strategy for the treatment of inflammatory vascular diseases.
| S-EPMC4792690 | biostudies-literature
Project description:The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25-30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood-brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.
| S-EPMC4827373 | biostudies-literature
Project description:IntroductionWith a recent resurgence of the 2019 coronavirus disease (COVID-19) cases globally, an increasing number of healthcare systems are adopting telemedicine as an alternative method of healthcare delivery in a bid to decrease disease transmission. Continued care of orthopaedic patients in the outpatient setting during the coronavirus disease of 2019 era can prove challenging without a systematic workflow, adequate logistics, and careful patient selection for teleconsultation. The aim of this paper is to describe our single-centre experience with the application of telemedicine in our orthopaedic practice, and its effectiveness in maintaining outpatient follow-up of orthopaedic patients.MethodologyWe describe our centre's telemedicine model of care for orthopaedic patients on the outpatient follow-up - which includes workforce assembly, population health and target patients, logistics and communications, and overall workflow - with roles and responsibilities of involved people portrayed in detail.ResultsFeedback from both patients and orthopaedic surgeons reflected high satisfaction rates with care provided, noting minimal communication and clinical barriers compared to face-to-face consultations. Whilst not without limitations, our protocol allowed for rapid adoption of telemedicine in line with a national-wide initiative to digitize healthcare.DiscussionThe implementation of teleconsultation services at our orthopaedic centre has provided an effective method of healthcare delivery while enforcing social distancing measures - which proves vital in combating the spread of COVID-19 and ushering in a new normal.
| S-EPMC9111019 | biostudies-literature
Project description:Traumatic microbleeds are small foci of hypointensity seen on T2*-weighted MRI in patients following head trauma that have previously been considered a marker of axonal injury. The linear appearance and location of some traumatic microbleeds suggests a vascular origin. The aims of this study were to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe the pathology underlying traumatic microbleeds in an index patient. Patients presenting to the emergency department following acute head trauma who received a head CT were enrolled within 48 h of injury and received a research MRI. Disability was defined using Glasgow Outcome Scale-Extended ≤6 at follow-up. All magnetic resonance images were interpreted prospectively and were used for subsequent analysis of traumatic microbleeds. Lesions on T2* MRI were stratified based on 'linear' streak-like or 'punctate' petechial-appearing traumatic microbleeds. The brain of an enrolled subject imaged acutely was procured following death for evaluation of traumatic microbleeds using MRI targeted pathology methods. Of the 439 patients enrolled over 78 months, 31% (134/439) had evidence of punctate and/or linear traumatic microbleeds on MRI. Severity of injury, mechanism of injury, and CT findings were associated with traumatic microbleeds on MRI. The presence of traumatic microbleeds was an independent predictor of disability (P < 0.05; odds ratio = 2.5). No differences were found between patients with punctate versus linear appearing microbleeds. Post-mortem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages, predominately seen in perivascular space. Evidence of axonal injury was not observed in co-localized histopathological sections. Traumatic microbleeds were prevalent in the population studied and predictive of worse outcome. The source of traumatic microbleed signal on MRI appeared to be iron-laden macrophages in the perivascular space tracking a network of injured vessels. While axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who could benefit from new therapies targeting the injured vasculature and secondary injury to parenchyma.
| S-EPMC6821371 | biostudies-literature
Project description:BackgroundEndothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury.Methods and resultsThe role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects.ConclusionWe found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS.
| S-EPMC5806471 | biostudies-literature