BACKGROUND: Agitation occurs frequently among criticaly il patients admitted to the intensive care unit (ICU). We aimed to evaluate the frequency, predisposing factors and outcomes of agitation in trauma ICU. METHODS: A retrospective analysis was conducted to include patients who were admitted to the trauma ICU between April 2014 and March 2015. Data included patient's demographics, initial vitals, associated injuries, Ramsey Sedation Scale, Glasgow Coma Scale, head injury lesions, use of sedatives and analgesics, head interventions, ventilator days, and ICU length of stay. Patients were divided into two groups based on the agitation status. RESULTS: A total of 102 intubated patients were enrolled; of which 46 (45％) experienced agitation. Patients in the agitation group were 7 years younger, had significantly lower GCS and sustained higher frequency of head injuries (P<0.05). Patients who developed agitation were more likely to be prescribed propofol alone or in combination with midazolam and to have frequent ICP catheter insertion, longer ventilatory days and higher incidence of pneumonia (P<0.05). On multivariate analysis, use of propofol alone (OR=4.97; 95％CI=1.35–18.27), subarachnoid hemorrhage (OR=5.11; 95％CI=1.38–18.91) and ICP catheter insertion for severe head injury (OR=4.23; 95％CI=1.16–15.35) were independent predictors for agitation (P<0.01). CONCLUSION: Agitation is a frequent problem in trauma ICU and is mainly related to the type of sedation and poor outcomes in terms of prolonged mechanical ventilation and development of nosocomial pneumonia. Therefore, understanding the main predictors of agitation facilitates early risk-stratification and development of better therapeutic strategies in trauma patients.

No abstract available.
Cerebral Arteries* ; Hemodynamics* ; Ultrasonography*

Traumatic brain injury (TBI) remains a major cause of death and disability worldwide. Increasing evidence indicates that TBI is an important risk factor for neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. Despite improved supportive and rehabilitative care of TBI patients, unfortunately, all late phase clinical trials in TBI have yet to yield a safe and effective neuroprotective treatment. The disappointing clinical trials may be attributed to variability in treatment approaches and heterogeneity of the population of TBI patients as well as a race against time to prevent or reduce inexorable cell death. TBI is not just an acute event but a chronic disease. Among many mechanisms involved in secondary injury after TBI, emerging preclinical studies indicate that posttraumatic prolonged and progressive neuroinflammation is associated with neurodegeneration which may be treatable long after the initiating brain injury. This review provides an overview of recent understanding of neuroinflammation in TBI and preclinical cell-based therapies that target neuroinflammation and promote functional recovery after TBI.
Age Factors ; Animals ; Brain ; immunology ; Brain Injuries, Traumatic ; complications ; therapy ; Cell- and Tissue-Based Therapy ; methods ; Exosomes ; Extracellular Vesicles ; physiology ; Female ; Humans ; Inflammation ; etiology ; Lymphatic System ; physiology ; Male ; Neuroprotective Agents ; Sex Characteristics