Secondary complications of spinal cord injury (SCI) are a burden to affected individuals and the rest of society. There is limited evidence of the economic burden or cost of complications in SCI populations in Canada, however, which is necessary for comparative economic analyses and decision analytic modeling of possible solutions to these common health problems. Comparative economic analyses can inform resource allocation decisions, but the outputs are only as good as the inputs. In this article, new evidence of the excess or incremental costs of urinary tract infection (UTI) and pressure ulceration (PU) in acute traumatic SCI from an exploratory case series analysis of admissions to a Level I specialized Canadian spine facility (2008-2013) is presented. Participants in a national SCI registry were case-control matched (1:1) on the predicted probability of experiencing UTI or PU during initial acute SCI admission. The excess costs of UTI and PU are estimated as the mean of the differences in total direct acute SCI admission costs (length of stay, accommodation, nursing, pharmacy) from the perspective of the admitting facility between participants matched or paired on demographic and SCI characteristics. Even relatively minor UTI and PU, respectively, added an average of $7,790 (standard deviation [SD] $6,267) and $18,758 (SD $27,574) to the direct cost of acute SCI admission in 2013 Canadian dollars (CAD). This case series analysis established evidence of the excess costs of UTI and PU in acute SCI admissions, which will support decision-informing analyses in SCI.
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http://dx.doi.org/10.1089/neu.2016.4934 | DOI Listing |
Fluids Barriers CNS
January 2025
Adelaide Spinal Research Group & Centre for Orthopaedics and Trauma Research, Faculty of Health and Medical Sciences, The University of Adelaide, Level 7, Adelaide Health and Medical Sciences Building, North Terrace, Adelaide, SA, 5005, Australia.
Background: Traumatic spinal cord injury (SCI) causes spinal cord swelling and occlusion of the subarachnoid space (SAS). SAS occlusion can change pulsatile cerebrospinal fluid (CSF) dynamics, which could have acute clinical management implications. This study aimed to characterise SAS occlusion and investigate CSF dynamics over 14 days post-SCI in the pig.
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January 2025
CIBER Cardiovascular, Madrid, Spain.
Soluble ST2 (sST2) is released in response to vascular congestion, inflammation, and pro-fibrotic stimuli. In heart failure (HF), elevated levels of sST2 are associated with a higher risk of adverse clinical outcomes. Emerging evidence suggests that carbohydrate antigen 125 (CA125) may act as a ligand that modulates the inflammatory response.
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January 2025
Division of Nephrology, The First People's Hospital of Kashi, Kashi, China.
Sci Rep
January 2025
Department of Pathology, Dokkyo Medical University School of Medicine and Graduate School of Medicine, 880 Kitakobayashi, Mibu, Shimotsugagun, Tochigi, 321-0293, Japan.
Although alveolar hyperoxia exacerbates lung injury, clinical studies have failed to demonstrate the beneficial effects of lowering the fraction of inspired oxygen (FO) in patients with acute respiratory distress syndrome (ARDS). Atelectasis, which is commonly observed in ARDS, not only leads to hypoxemia but also contributes to lung injury through hypoxia-induced alveolar tissue inflammation. Therefore, it is possible that excessively low FO may enhance hypoxia-induced inflammation in atelectasis, and raising FO to an appropriate level may be a reasonable strategy for its mitigation.
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January 2025
Medicine, University of Washington, Seattle, Washington, USA.
Objectives: To study neutrophil gelatinase-associated lipocalin (NGAL) levels in peripheral blood in SLE, and to propose a mechanism by which neutrophils secrete NGAL on stimulation with immune complexes (IC).
Methods: NGAL was measured by ELISA in two independent Swedish SLE cohorts acting as exploratory and validation cohort (n=124 and n=308, respectively), disease controls (n=38) and healthy controls (n=77). NGAL levels were measured in supernatant from IC-stimulated neutrophils in the presence or absence of a toll-like receptor 8 inhibitor (TLR8i).
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