4,049 research outputs found
The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.
No full textAdhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. Implications: This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful
Leukocyte adhesion molecule profiles and outcome after traumatic brain injury.
No full textAdhesion molecules have an important role in leukocyte migration into tissue after injury. We hypothesised that changes in ICAM-1 and L-selectin expression after traumatic brain injury would result in altered serum concentrations of these molecules, which would be related to injury severity and outcome. We investigated arterial and jugular venous concentrations of ICAM-1 and L-selectin in 22 patients. The Glasgow Coma Score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken at designated times after brain injury: on admission, at 24 hours, 48 hours and 96 hours. Glasgow Outcome Scores at 6 months were obtained. Mean serum concentrations of ICAM-1 were normal on admission, but became significantly increased by 96 hours (p = 0.018). Mean L-selectin concentrations wre markedly below controls at all time points (p < 0.001). There were no significant differences between jugular venous and arterial concentrations of either ICAM-1 or L-selectin. Serum ICAM-1 was significantly related to neurological outcome (p < 0.001) and to the Glasgow Coma Score (p < 0.001). These changes in adhesion molecules expression may be important in the pathophysiology of secondary injury. The highly significant relationship between serum ICAM-1 and neurological outcome suggests that drugs which antagonize adhesion molecule activity may improve outcome after traumatic brain injury
The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury
No full textAdhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. Implications: This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful
Leukocyte adhesion molecule profiles and outcome after traumatic brain injury
No full textAdhesion molecules have an important role in leukocyte migration into tissue after injury. We hypothesised that changes in ICAM-1 and L-selectin expression after traumatic brain injury would result in altered serum concentrations of these molecules, which would be related to injury severity and outcome. We investigated arterial and jugular venous concentrations of ICAM-1 and L-selectin in 22 patients. The Glasgow Coma Score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken at designated times after brain injury: on admission, at 24 hours, 48 hours and 96 hours. Glasgow Outcome Scores at 6 months were obtained. Mean serum concentrations of ICAM-1 were normal on admission, but became significantly increased by 96 hours (p = 0.018). Mean L-selectin concentrations wre markedly below controls at all time points (p < 0.001). There were no significant differences between jugular venous and arterial concentrations of either ICAM-1 or L-selectin. Serum ICAM-1 was significantly related to neurological outcome (p < 0.001) and to the Glasgow Coma Score (p < 0.001). These changes in adhesion molecules expression may be important in the pathophysiology of secondary injury. The highly significant relationship between serum ICAM-1 and neurological outcome suggests that drugs which antagonize adhesion molecule activity may improve outcome after traumatic brain injury
Ventilatory strategies for patients with acute brain injury
No full textPURPOSE OF REVIEW:
The ventilation of patients with acute brain injuries can present significant challenges. Frequently, guidelines recommending management strategies for patients with traumatic brain injuries come into conflict with what is now considered best ventilatory practice. In this review, we will explore many of these areas of conflict.
RECENT FINDINGS:
The use of ventilatory strategies to control partial pressure of carbon dioxide in patients with traumatic brain injury is associated with the development of acute lung injury. Analysis of the International Mission for Prognosis And Clinical Trial (IMPACT) database has confirmed the association between hypoxia and poor neurological outcome. Although a recent meta-analysis has suggested a survival benefit for steroids in acute lung injury, the use of steroids has been associated with a worsening of outcome in patients with traumatic brain injuries and their effects on the brain have not been fully elucidated.
SUMMARY:
There are unlikely to be randomized controlled trials advising how best to ventilate patients with acute brain injuries because of the heterogeneous nature of such injuries. Hypoxia should be avoided. The more widespread use of multimodal brain monitoring, including brain tissue oxygen and cerebral blood flow monitoring, may allow clinicians to tolerate a higher arterial partial pressure of carbon dioxide than has been traditional, allowing a less injurious ventilatory strategy. Modest positive end-expiratory pressure can be used. In severe respiratory failure, most 'rescue' strategies have been attempted in patients with acute brain injuries. Choice of rescue therapy at present is best decided on a case-by-case basis in conjunction with local expertise
Long-term quality-of-life impairment in patients with more than 1-year COVID-19-related olfactory dysfunction.
No full textClinical factors influencing olfactory performance in patients with persistent COVID-19 smell loss longer than 1 year
No full textObjectives: Factors affecting persistence of COVID-19-related olfactory dysfunction (OD) remain partially unknown. We aim to evaluate the clinical factors which could influence olfactory performance in patients with persistent COVID-19-related smell loss. Methods: A retrospective analysis of 100 patients with persistent COVID-19-related OD was performed between October 2020 and December 2022 at a single-center long-COVID smell clinic. All subjects underwent smell assessment using Sniffin' Sticks (S'S) extended test, nasal endoscopy, nasal airflow evaluation (peak nasal inspiratory flow [PNIF]), allergy test (skin prick test [SPT]) for common aeroallergens, MRI of the head and patient-reported outcome measures (PROMs—VAS, SF-36, Short QOD-NS, SNOT-22). Based on S'S score, subjects were divided into normosmics (TDI ≥ 30.75) and dysosmics (TDI < 30.75). Results: The median age was 42 years and the median length of patient-reported OD was 1.4 years. 20 patients (20.0%) were normosmic at the time of S'S assessment. Dysosmic patients were found to have significantly lower scores at the SF-36 health domains for energy/fatigue (p =.0004) and emotional wellbeing (p =.04) when compared to normosmics. A moderate correlation (r =.45–.59) between S'S scores and some PROMs was also demonstrated. At the multivariate analysis higher PNIF scores positively influenced odor threshold (p =.001) while positivity to SPT negatively influenced odor identification (p =.04). Conclusions: Impairment of nasal airflow and sensitivity to aeroallergens can negatively affect olfactory performance in COVID-19-related OD. Long-COVID smell loss deeply affects QoL although recovery of olfaction can bring it back to a normal range. Level of Evidence: IV
Ventilatory strategies for patients with acute brain injury
No full textPURPOSE OF REVIEW:
The ventilation of patients with acute brain injuries can present significant challenges. Frequently, guidelines recommending management strategies for patients with traumatic brain injuries come into conflict with what is now considered best ventilatory practice. In this review, we will explore many of these areas of conflict.
RECENT FINDINGS:
The use of ventilatory strategies to control partial pressure of carbon dioxide in patients with traumatic brain injury is associated with the development of acute lung injury. Analysis of the International Mission for Prognosis And Clinical Trial (IMPACT) database has confirmed the association between hypoxia and poor neurological outcome. Although a recent meta-analysis has suggested a survival benefit for steroids in acute lung injury, the use of steroids has been associated with a worsening of outcome in patients with traumatic brain injuries and their effects on the brain have not been fully elucidated.
SUMMARY:
There are unlikely to be randomized controlled trials advising how best to ventilate patients with acute brain injuries because of the heterogeneous nature of such injuries. Hypoxia should be avoided. The more widespread use of multimodal brain monitoring, including brain tissue oxygen and cerebral blood flow monitoring, may allow clinicians to tolerate a higher arterial partial pressure of carbon dioxide than has been traditional, allowing a less injurious ventilatory strategy. Modest positive end-expiratory pressure can be used. In severe respiratory failure, most 'rescue' strategies have been attempted in patients with acute brain injuries. Choice of rescue therapy at present is best decided on a case-by-case basis in conjunction with local expertise
Book Discussion : PJ Powers
No full textThe UJ Campus Health Services and the Student Affairs Division in partnership with the UJ Library invite you to meet PJ Powers (Thandeka) the co-author of the book HERE I AM About the book: Here I Am, written with Marianne Thamm, is an intimate and hilarious account of the life and times of one of this country’s most recognisable and enduring performers. From the dizzying heights of international stardom to the dark depths of her struggle with alcohol, this is a must-read to explore the heady mix of politics and music of the time. More than just a story about the personal journey of one of South Africa’s most beloved music icons, this extraordinary memoir of PJ Powers – or Thandeka, as she was affectionately renamed by Soweto crowds – is set against the turbulent backdrop of South Africa’s recent political history. It features a gallery of political leaders and international celebrities, including the likes of Nelson Mandela, Graça Machel, Chris Hani, Joaquim Chissano, Queen Elizabeth II, Brenda Fassie, Sharon Stone and Robert De Niro. Facilitator: Prof Alban Burke, Director – PsyCad, University of Johannesburg PJ Powers will also perform a few songs on the day. Date: 27 August 2015 Time: 16:30 for 17:00 Venue: Auditorium (6th Floor), APK Library, University of Johannesburg (corner Kingsway and University Road, Auckland Park) RSVP: By Wednesday, 26 August 2015 to Theodorah Modise on [email protected] / 011 559 226
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