Systemic complications after head injury: a clinical review

Lim, Hoon; Smith, Martin

doi:10.1111/j.1365-2044.2007.04998.x

Cited by 106 publications

(70 citation statements)

References 94 publications

(137 reference statements)

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“…Previous studies have indeed demonstrated that extracranial complications contribute to almost two-thirds of all deaths after severe TBI [3, 4]. As is known, the most frequently seen extracranial complications following TBI is infection [5]. The incidence of infection following TBI is obviously higher than other noncranial insults such as polytrauma, burn injury, and major surgery [6].…”

Section: Introductionmentioning

confidence: 99%

Acute Traumatic Brain Injury Induces CD4+ and CD8+ T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Yang

Chen

et al. 2019

Neuroimmunomodulation

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Objective: Traumatic brain injury (TBI) induces immunosuppression in the acute phase, and the activation of the sympathetic nervous system (SNS) might play a role in this process, but the mechanism involved is unknown. Herein, we explored the impact of acute (a)TBI on the peripheral immune system and its correlation with the SNS and the T cell exhaustion marker, PD-1 (programmed cell death-1). Methods: Flow cytometry (FCM) was performed to analyze the expression of T cell markers and intracellular cytokines, interferon-γ and tumor necrosis factor-α, and the T cell exhaustion marker, PD-1, in the peripheral blood mononuclear cells (PBMCs) of TBI rats. Enzyme-linked immunosorbent assay (ELISA) was performed to analyze the concentration of norepinephrine (NE) in the serum. Propranolol was administrated to block the SNS in vivo and NE stimulation was used to imitate the activation of the SNS in vitro. Results: We found that the concentration of NE was significantly elevated after TBI, and the dysfunction of CD4⁺ and CD8⁺ T cells was reversed by the SNS blocker propranolol in vivo and imitated by the SNS neurotransmitter NE in vitro. The expression of PD-1 on CD4⁺ and CD8⁺ T cells was upregulated after aTBI, which was reversed by propranolol administration in vivo and imitated by NE stimulation in vitro. Furthermore, the PD-1 blocker reversed the dysfunction of CD4⁺ and CD8⁺T cells in vitro. Conclusion: Our findings demonstrated that aTBI activated the SNS, and further upregulated the expression of PD-1 on CD4⁺ and CD8⁺ T cells, which, in turn, impaired their function and contributed to immunosuppression.

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Section: Introductionmentioning

confidence: 99%

Acute Traumatic Brain Injury Induces CD4+ and CD8+ T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Yang

Chen

et al. 2019

Neuroimmunomodulation

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“…Although the clinical differences were not statistically significant, these data suggest alterations in the immune status which may not be directly related to the overall injury severity. Non-neurological organ dysfunctions via neuroendocrine pathways have been recognized to be a common complication after TBI (16). Moreover, TBI in itself has been demonstrated to induce inflammation, as expressed by the release of diverse pro-inflammatory cytokines (TNF-a, IL-1b, -6 and -8) along with metabolic alterations in the early post-traumatic state, both systemically and in remote organs such as the gut (17,18).…”

Section: Discussionmentioning

confidence: 99%

Severe head injury promotes early caspase-dependent apoptosis in peripheral blood monocytes from multiply injured patients

Tschoeke

Drogies

Meyer

et al. 2009

Journal of Organ Dysfunction

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Objective. To investigate the influence of traumatic brain injury (TBI) on immune function and viability of human peripheral monocytes in polytraumatized patients. Material and methods. This was a prospective, randomized, controlled clinical study conducted in a Level I trauma center. Multiply injured patients (n 042; mean age 42.4915.5 years) with a mean Injury Severity Score (ISS) of 32.399.6 were compared to healthy controls (n 020; mean age 36.398.4 years). The methods used were clinical evaluation, scoring of injury severity (ISS, abbreviated injury scores), multiple organ dysfunction score, realtime reverse transcription polymerase chain reaction, Western blotting and fluorescent-activated cell sorting analyses of negatively isolated monocytes. The main outcome measures were overall clinical outcome, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) staining, expression of the Fas and tumor necrosis factor receptor I, expression of the mitochondrial proteins Bax and Bcl-2, caspase-8, -9 and -3/7 activity and the level of C5a throughout a 5-day post-trauma observation period. Results. Apoptosis of peripheral blood monocytes was evident in both patient cohorts, as demonstrated by positive TUNEL staining and significant increases in caspase-3/7 activation. Trauma patients with TBI ('TBI patients) presented with a higher incidence of sepsis. Moreover, only 'TBI patients demonstrated significant upregulation of pro-apoptotic mediators (increased Fas receptor) and downregulation of anti-apoptotic mediators (decreased Bcl-2) via caspase-dependent signaling (increased caspase-8 and -9) when compared to both trauma patients without TBI ((TBI patients) and healthy controls. In contrast, (TBI patients demonstrated significantly higher plasma concentrations of anaphylatoxin C5a on Day 0. Conclusions. Multiply injured patients show significant monocyte apoptosis, which may particularly promote the development of post-traumatic complications in a caspase-dependent manner in 'TBI patients. The role of increased C5a and complement-associated monocyte apoptosis in (TBI patients requires further investigation.

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“…The intensive care management of head injury associated with nonneurological organ dysfunction and failure presents a significant challenge, because optimum treatment for the failing systemic organ system may have potentially adverse effects on the injured brain and vice versa. 10 Respiratory complications are most frequent, occurring in up to 80% of patients, with those with the severest injury being most at risk. Ventilator-acquired pneumonia is a particular problem and occurs in 45-60% of patients.…”

Section: General Aspects Of Carementioning

confidence: 99%

“…10 They represent risk factors that are potentially amenable to treatment, and early recognition and prompt intervention may improve outcome. The intensive care management of head injury associated with nonneurological organ dysfunction and failure presents a significant challenge, because optimum treatment for the failing systemic organ system may have potentially adverse effects on the injured brain and vice versa.…”

Section: General Aspects Of Carementioning

confidence: 99%

Critical care management of head injury

Dunn¹,

Smith²

2008

Anaesthesia & Intensive Care Medicine

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The intensive care management of head injury requires a coordinated, comprehensive and multidisciplinary approach to treatment. crucial to management is the prevention of secondary brain injury by avoidance of systemic physiological disturbances, such as hypotension and hypoxae mia, and maintenance of adequate cerebral perfusion and oxygenation. There have been marked improvements in the treatment of patients with severe traumatic brain injury over the last decade, leading to a reduction in both mortality and morbidity. advances in management in the pre hospital setting and in the a&e department have now been extended into the intensive care unit. The management of head injury has undergone extensive revision as evidence accumulates that established practices are not as effective or innocuous as previously believed. Management protocols have evolved with international consensus, providing guide lines that assist clinicians in delivering optimal care. improved diagnos tic and monitoring modalities are improving our understanding of the pathobiology of head injury and allowing the delivery of individualized therapeutic interventions.Keywords cerebral perfusion pressure; head injury; intracranial pressure; neurointensive care Traumatic brain injury (TBI) is a major cause of mortality and morbidity, particularly in young people. The overall incidence is around 450 per 100,000 for all head injuries and 40 per 100,000 for moderate and severe injury. TBI is more common in males than females and in those of lower socioeconomic status. It accounts for 1% of overall deaths and 15% of deaths in the 15-45-year age group. The causes are multifactorial and include road traffic accidents (40-50%), falls (18%) and assaults (10%).

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Systemic complications after head injury: a clinical review

Cited by 106 publications

References 94 publications

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Acute Traumatic Brain Injury Induces CD4<sup>+</sup> and CD8<sup>+</sup> T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

Severe head injury promotes early caspase-dependent apoptosis in peripheral blood monocytes from multiply injured patients

Critical care management of head injury

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