Effects of propofol on ischemia-reperfusion and traumatic brain injury.

Oxidative stress exacerbates brain damage following ischemia-reperfusion and traumatic brain injury (TBI). Management of TBI and critically ill patients commonly involves use of propofol, a sedation medication that acts as a general anesthetic with inherent antioxidant properties. Here we review available evidence from animal model systems and clinical studies that propofol protects against ischemia-reperfusion injury. However, evidence of propofol toxicity in humans exists and manifests as a rare complication, "propofol infusion syndrome" (PRIS). Evidence in animal models suggests that brain injury induces expression of the p75 neurotrophin receptor (p75NTR), which is associated with proapoptotic signaling. p75NTR-mediated apoptosis of neurons is further exacerbated by propofol's superinduction of p75NTR and concomitant inhibition of neurotrophin processing. Propofol is toxic to neurons but not astrocytes, a type of glial cell. Evidence suggests that propofol protects astrocytes from oxidative stress and stimulates astroglial-mediated protection of neurons. One may speculate that in brain injury patients under sedation/anesthesia, propofol provides brain tissue protection or aids in recovery by enhancing astrocyte function. Nevertheless, our understanding of neurologic recovery versus long-term neurological sequelae leading to neurodegeneration is poor, and it is also conceivable that propofol plays a partial as yet unrecognized role in long-term impairment of the injured brain.

Severe fungal infections following blunt traumatic injuries: A 5-year multicenter descriptive study.

INTRODUCTION: The aggressive and timely treatment of post-traumatic fungal infections is the most efficacious way to reduce morbidity and mortality. Compared to the military trauma population, studies reporting on fungal infections in civilian trauma are not well described. The purpose of this study was to describe characteristics of civilian trauma patients who developed fungal infections and to identify common risk factors and report any delays between injury and treatment. METHODS: This was a five-year (1/1/2013-3/1/2018) retrospective, descriptive study across six level 1 trauma centers. All consecutively admitted trauma patients (≥18 years) with laboratory-confirmed fungal wound infections were included. Patients with solely candida wound isolates were excluded. Patient demographics, clinical wound and infection characteristics, organisms cultured, treatment modalities, length of stay, in-hospital mortality, and any diagnostic or treatment delays were described. RESULTS: Of the 54,521 trauma patients screened for fungal infection, 12 were identified. All patients suffered major injuries after blunt trauma (abbreviated injury score 3-5) and sustained wound contamination, and in nine patients, the cause of injury was motor vehicle. Six had open wounds/fractures on admission. The geographical region with the highest rate of fungal infection was Texas (n = 7), followed by Kansas (N = 3), then Missouri (N = 2). First symptoms of infection (leukocytosis or fever (n = 10)) presented a median of 6.3 (4.1-9.8) days after injury. Wound management entailed a combination of debridements (n = 8), negative pressure wound therapy (n = 9), amputation (n = 6), and antifungal treatment (n = 10). All fungal isolates identified from the wound site were hyphomycetes. A median of 2.1 (1.8-4.0) days passed from diagnosis to first antifungal treatment, and 3 patients died. CONCLUSIONS: Our study shows the challenges surrounding diagnosis and treatment of fungal infections secondary to trauma. Non-specific fungal infection symptoms, such as leukocytosis and fever, typically presented a week after injury. Vigilance for investigating risk factors and infection symptoms may help clinicians with more timely management of trauma patients with a severe fungal infection.