Early Antibiotic Administration is Independently Associated with Improved Survival in Traumatic Brain Injury

Dhillon, Navpreet K.; Adjamian, Norair; Fierro, Nicole M; Conde, Geena; Barmparas, Galinos; Ley, Eric J.

doi:10.1016/j.jss.2021.10.015

Cited by 7 publications

(5 citation statements)

References 32 publications

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“…This raises the question of whether infections represent a modifiable risk factor and therapeutic target to reduce or prevent epilepsy in this population. For example, systemic infections can be minimized through the implementation of non‐pharmacological infection control strategies, 62 while acute post‐injury prophylactic broad‐spectrum antibiotics to treat infections have been associated with improved survival 63 . Early screening for pneumonia in intubated trauma patients via assessment of bronchoalveolar lavage fluid has also been shown to reduce the incidence of ventilator‐associated pneumonia 64 .…”

Section: Discussionmentioning

confidence: 99%

“…For example, systemic infections can be minimized through the implementation of non‐pharmacological infection control strategies, 62 while acute post‐injury prophylactic broad‐spectrum antibiotics to treat infections have been associated with improved survival. 63 Early screening for pneumonia in intubated trauma patients via assessment of bronchoalveolar lavage fluid has also been shown to reduce the incidence of ventilator‐associated pneumonia. 64 Alongside previous reports of a high incidence of infections detected in patients with moderate and severe TBI, our findings suggest that minimizing the incidence of hospital‐acquired infections in patients after severe TBI as a means to potentially prevent poor outcomes including worse GOSE and the development of PTE in a subset of vulnerable individuals.…”

Section: Discussionmentioning

confidence: 99%

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Hospital‐acquired infections as a risk factor for post‐traumatic epilepsy: A registry‐based cohort study

Chen,

Laing,

et al. 2024

Epilepsia Open

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ObjectiveHospital‐acquired infections are a common complication for patients with moderate or severe traumatic brain injury (TBI), contributing to morbidity and mortality. As infection‐mediated immune responses can predispose towards epilepsy, we hypothesized that post‐injury hospital‐acquired infections increase the risk of post‐traumatic epilepsy (PTE).MethodsA retrospective cohort study of adults with moderate to severe TBI was conducted using data from the Victorian State Trauma Registry in Australia. Infections were identified from the International Statistical Classification of Diseases and Related Health Problems 10th Revision–Australian Modification (ICD‐10‐AM) codes, and diagnosis of PTE was determined by the Glasgow Outcome Scale – Extended questionnaire regarding epileptic fits at 24 months follow‐up.ResultsOf all TBI patients (n = 15 152), 24% had evidence of having had any type of infection, with the most common being pneumonia, urinary tract, and respiratory infections. Of those who responded to the PTE question at 24 months (n = 1361), 11% had developed PTE. Univariable analysis found that the incidence of PTE was higher in patients who had any type of infection compared to patients without an infection (p < 0.001). After adjustment for covariates associated with both development of PTE and risk of infection, multivariable analysis found a solid association between infection and PTE (adjusted RR = 1.59; 95% CI: 1.11–2.28; p = 0.011). Having any type of complicating infection acquired during admission was also associated with poor GOSE outcomes at subsequent follow‐ups (adjusted OR = 0.20; 95% CI: 0.11–0.35, p < 0.001).SignificanceThese findings suggest that hospital‐acquired infections contribute to PTE development after TBI. Future investigation into infections as a modifiable target to reduce poor outcomes after TBI is warranted.Plain Language SummaryHospital‐acquired infections are common in patients with traumatic brain injuries. A database study of adults with moderate or severe brain injuries in Australia examined whether these infections are associated with the development of epilepsy after a brain injury. 24% of patients had infections, with pneumonia and urinary tract infections being the most common. Of those surveyed 2 years after the injury, 11% developed post‐traumatic epilepsy. Patients with infections had a significantly higher risk of epilepsy, even when accounting for other known risk factors, and infections were also linked to poor outcomes more broadly. The study suggests that preventing hospital‐acquired infections could be a crucial target for improving outcomes after traumatic brain injuries.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hospital‐acquired infections as a risk factor for post‐traumatic epilepsy: A registry‐based cohort study

Chen,

Laing,

et al. 2024

Epilepsia Open

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“…Indeed, nearly 50% of hospitalized TBI patients require intensive care due to secondary brain injury risks [ 117 ]. These patients are prone to infections, necessitating mechanical ventilation [ 118 ], with approximately 40% receiving prophylactic antibiotics [ 119 ]. Moreover, almost 70% of moderate-to-severe TBI patients develop early multi-organ dysfunction [ 120 ].…”

Section: Gut–lung Interactionsmentioning

confidence: 99%

Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis

Ziaka,

Exadaktylos

2024

Crit Care

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It has been convincingly demonstrated in recent years that isolated acute brain injury (ABI) may cause severe dysfunction of peripheral extracranial organs and systems. Of all potential target organs and systems, the lung appears to be the most vulnerable to damage after ABI. The pathophysiology of the bidirectional brain–lung interactions is multifactorial and involves inflammatory cascades, immune suppression, and dysfunction of the autonomic system. Indeed, the systemic effects of inflammatory mediators in patients with ABI create a systemic inflammatory environment (“first hit”) that makes extracranial organs vulnerable to secondary procedures that enhance inflammation, such as mechanical ventilation (MV), surgery, and infections (“second hit”). Moreover, accumulating evidence supports the knowledge that gut microbiota constitutes a critical superorganism and an organ on its own, potentially modifying various physiological functions of the host. Furthermore, experimental and clinical data suggest the existence of a communication network among the brain, gastrointestinal tract, and its microbiome, which appears to regulate immune responses, gastrointestinal function, brain function, behavior, and stress responses, also named the “gut-microbiome–brain axis.” Additionally, recent research evidence has highlighted a crucial interplay between the intestinal microbiota and the lungs, referred to as the “gut-lung axis,” in which alterations during critical illness could result in bacterial translocation, sustained inflammation, lung injury, and pulmonary fibrosis. In the present work, we aimed to further elucidate the pathophysiology of acute lung injury (ALI) in patients with ABI by attempting to develop the “double-hit” theory, proposing the “triple-hit” hypothesis, focused on the influence of the gut–lung axis on the lung. Particularly, we propose, in addition to sympathetic hyperactivity, blast theory, and double-hit theory, that dysbiosis and intestinal dysfunction in the context of ABI alter the gut–lung axis, resulting in the development or further aggravation of existing ALI, which constitutes the “third hit.”

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“…Clinical findings from a recent study suggest that within 72 hours after severe trauma, patients with multiple injuries showed a decline in beneficial bacteria but an increase in Clostridiales and Enterococcus [23].Antibiotics (ABX) are frequently administered in intensive care units to prevent infections and sepsis in TBI patients, thereby reducing injury-related and hospital-acquired infections [24]. Early administration of ABX is associated with improved survival in TBI patients [25], and improves the TBI outcome [26]. In preclinical studies, a standard approach to deplete enteric bacteria with minimal systemic absorption is to administer a broad-spectrum ABX cocktail [27].…”

mentioning

confidence: 99%

Antibiotic treatment induces microbiome dysbiosis and reduction of neuroinflammation following traumatic brain injury in mice

Flinn,

Marshall,

Holcomb

et al. 2024

Preprint

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The gut microbiome is linked to brain pathology in cases of traumatic brain injury (TBI), yet the specific bacteria that are implicated are not well characterized. To address this gap, in this study, we induced traumatic brain injury (TBI) in male C57BL/6J mice using the controlled cortical impact (CCI) injury model. After 35 days, we administered a broad-spectrum antibiotics (ABX) cocktail (ampicillin, gentamicin, metronidazole, vancomycin) through oral gavage for 2 days to diminish existing microbiota. Subsequently, we inflicted a second TBI on the mice and analyzed the neuropathological outcomes five days later. Longitudinal analysis of the microbiome showed significant shifts in the diversity and abundance of bacterial genera during both acute and chronic inflammation. These changes were particularly dramatic following treatment with ABX and after the second TBI. ABX treatment did not affect the production of short-chain fatty acids (SCFA) but did alter intestinal morphology, characterized by reduced villus width and a lower count of goblet cells, suggesting potential negative impacts on intestinal integrity. Nevertheless, diminishing the intestinal microbiome reduced cortical damage, apoptotic cell density, and microglial/macrophage activation in the cortical and thalamic regions of the brain. Our findings suggest that eliminating colonized gut bacteria via broad-spectrum ABX reduces neuroinflammation and enhances neurological outcomes in TBI despite implications to gut health.

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Early Antibiotic Administration is Independently Associated with Improved Survival in Traumatic Brain Injury

Cited by 7 publications

References 32 publications

Hospital‐acquired infections as a risk factor for post‐traumatic epilepsy: A registry‐based cohort study

Hospital‐acquired infections as a risk factor for post‐traumatic epilepsy: A registry‐based cohort study

Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis

Antibiotic treatment induces microbiome dysbiosis and reduction of neuroinflammation following traumatic brain injury in mice

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