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Postinjury Multiple Organ Failure Neurological Dysfunction in Multiple Organ Failure in Trauma

Postinjury Multiple Organ Failure : Neurological Dysfunction in Multiple Organ Failure in Trauma [Multiple organ failure (MOF) in trauma is defined as the progression to potentially reversible organ dysfunction involving two or more organ systems that were not involved in the primary traumatic insult (Cole, British J Surg 107:402–412, 2020). Neurological dysfunction is associated with prolonged MOF phenotypes and worse overall outcomes (Shepherd et al., Shock 47:429–435, 2017). The underlying pathological mechanisms of indirect neurological dysfunction in trauma are likely due to a cascade of neuroinflammation triggered by animbalance of pro- and anti-inflammatory mediators (Alam et al., EBioMedicine 37:547–556, 2018; Katsumi et al., Neuroimage Clin 27:102346, 2020). Acute cognitive dysfunction is a heralding sign of the onset of MOF and strongly associated with subsequent long-term chronic cognitive dysfunction and post-intensive care syndrome (PICS) (Ahmad and Teo, Ann Geriatr Med Res 25:72–78, 2021). Unfortunately, most scoring systems for MOF are poorly sensitive for detecting cognitive mild and moderate dysfunction and therefore the true prevalence of secondary neurological dysfunction in trauma is poorly described. Further, bedside identification of MODS associated neurological dysfunction is difficult to distinguish from neurodysfunction due to direct or indirect brain trauma or the confounding need for anaesthesia, sedation, or analgesia. Additionally, the lack of directed therapeutics decreases the clinical priority of discerning the precise driving cause of cognitive dysfunction in clinical practice. The mainstay of management is supportive bundles of care targeted at preventing further complications by sepsis surveillance and early treatment, supporting neurocognitive recovery through careful analgesia and sleep hygiene, and limiting exacerbating treatments like heavy sedation and prolonged ventilation (Marra, Crit Care Clin 33:225–243, 2017).] http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png

Postinjury Multiple Organ Failure Neurological Dysfunction in Multiple Organ Failure in Trauma

Part of the Hot Topics in Acute Care Surgery and Trauma Book Series
Editors: Balogh, Zsolt J.; Coimbra, Raul; Di Saverio, Salomone; Kirkpatrick, Andrew W.; Coccolini, Federico
Bierl, Cynthia
Postinjury Multiple Organ Failure — Mar 17, 2022
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Publisher
Springer International Publishing
Copyright
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
ISBN
978-3-030-92240-5
Pages
105 –112
DOI
10.1007/978-3-030-92241-2_10
Publisher site
See Chapter on Publisher Site

Abstract

[Multiple organ failure (MOF) in trauma is defined as the progression to potentially reversible organ dysfunction involving two or more organ systems that were not involved in the primary traumatic insult (Cole, British J Surg 107:402–412, 2020). Neurological dysfunction is associated with prolonged MOF phenotypes and worse overall outcomes (Shepherd et al., Shock 47:429–435, 2017). The underlying pathological mechanisms of indirect neurological dysfunction in trauma are likely due to a cascade of neuroinflammation triggered by animbalance of pro- and anti-inflammatory mediators (Alam et al., EBioMedicine 37:547–556, 2018; Katsumi et al., Neuroimage Clin 27:102346, 2020). Acute cognitive dysfunction is a heralding sign of the onset of MOF and strongly associated with subsequent long-term chronic cognitive dysfunction and post-intensive care syndrome (PICS) (Ahmad and Teo, Ann Geriatr Med Res 25:72–78, 2021). Unfortunately, most scoring systems for MOF are poorly sensitive for detecting cognitive mild and moderate dysfunction and therefore the true prevalence of secondary neurological dysfunction in trauma is poorly described. Further, bedside identification of MODS associated neurological dysfunction is difficult to distinguish from neurodysfunction due to direct or indirect brain trauma or the confounding need for anaesthesia, sedation, or analgesia. Additionally, the lack of directed therapeutics decreases the clinical priority of discerning the precise driving cause of cognitive dysfunction in clinical practice. The mainstay of management is supportive bundles of care targeted at preventing further complications by sepsis surveillance and early treatment, supporting neurocognitive recovery through careful analgesia and sleep hygiene, and limiting exacerbating treatments like heavy sedation and prolonged ventilation (Marra, Crit Care Clin 33:225–243, 2017).]

Published: Mar 17, 2022

Keywords: Delirium; Neuroinflammation; Acute confusion; Post-intensive care syndrome

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