Traumatic intracranial hemorrhages in facial fracture patients: review of 2,195 patients.

OBJECTIVE: Patients sustaining facial fractures are at risk for accompanying traumatic intracranial hematomas, which are a major cause of morbidity and mortality. Prompt recognition is crucial in improving patient survival and recovery. This study examined which simple clinical signs identify facial fracture patients at risk for intracranial hemorrhage before the performance of computed tomography. DESIGN AND METHODS: Retrospective study of 2,195 patients with facial fractures during a period of 7 years. By means of univariate and multivariate analysis clinical features potentially predictive for (a) intracranial hemorrhage and (b) surgery for intracranial hemorrhage were identified. SETTING: Critical care units of anesthesiology and neurology, general traumatology, and oral and maxillofacial surgery in a level I trauma university hospital. RESULTS: Seizures (OR 22.1) and vomiting/nausea (OR 20.2) were the strongest independent predictors of intracranial bleeding in facial fracture patients. For intracranial hemorrhages requiring surgical intervention closed head injuries (OR 9.75) and cranial vault fractures (OR 5.0) were the most significant risk factors. However, among those patients without vomiting/nausea and without seizures and without closed head injury ( n=1,628), 20 patients (1.2%) suffered intracranial hemorrhage, and six (0.37%) of them required surgical intervention. CONCLUSIONS: Simple clinical symptoms, such as seizures, vomiting/nausea, history of a closed head injury or cranial vault fractures are strong predictors for intracranial hemorrhage in facial fracture patients. The early consideration of such important indicators allows us to detect patients at elevated risk of an intracranial hematoma requiring surgical intervention.

Safety and efficacy of a novel intravascular cooling device to control body temperature in neurologic intensive care patients: a prospective pilot study.

OBJECTIVE: To determine the safety and efficacy of a novel intravascular cooling device (Cool Line catheter with Cool Gard system) to control body temperature (temperature goal <37 degrees C) in neurologic intensive care patients. DESIGN: A prospective, uncontrolled pilot study in 51 consecutive neurologic intensive care patients. SETTING: A neurologic intensive care unit at a tertiary care university hospital. PARTICIPANTS: Patients were 51 neurologic intensive care patients with an intracranial disease requiring a central venous catheter due to the primary (intracranial) disease. We excluded patients under the age of 19 yrs and those with active cardiac arrhythmia, full sepsis syndrome, bleeding diathesis and infection, or bleeding at the site of the intended catheter insertion. Male to female ratio was 31:20, and the median age was 55 yrs (range, 24-85 yrs). Forty-four of 51 patients (86.3%) had an initial Glasgow Coma Scale score of 3, three patients had a Glasgow Coma Scale score of 9, one patient presented with an initial Glasgow Coma Scale score of 11, two patients had an initial Glasgow Coma Scale score of 13, and one patient had an initial Glasgow Coma Scale score of 15. The mean initial tissue injury severity score was 45.1 and the median initial tissue injury severity score 45.0 (range, 19-70). INTERVENTIONS: Patients were enrolled prospectively in a consecutive way. Within 12 hrs after admission, the intravascular cooling device (Cool Line catheter) was placed, the temperature probe was located within the bladder (by Foley catheter), and the Cool Gard cooling device was initiated. This Cool Gard system circulates temperature-controlled sterile saline through two small balloons mounted on the distal end of the Cool Line catheter. The patient's blood is gently cooled as it is passed over the balloons. The Cool Gard system has been set with a target temperature of 36.5 degrees C. The primary purpose and end point of this study was to evaluate the cooling capacity of this intravascular cooling device. Efficacy is expressed by the calculation formula of fever burden, which is defined as the fever time product ( degrees C hours) under the fever curve. MEASUREMENTS AND MAIN RESULTS: The cooling device was in operation for a mean of 152.4 hrs. The ease of insertion was judged as easy in 42 of 51 patients; in a single patient, the catheter was malpositioned within the jugular vein, requiring early removal. The rate of infectious and noninfectious complications (nosocomial pneumonia, bacteremia, catheter-related ventriculitis, pulmonary embolism, etc.) was comparable to the rate usually observed in our neurologic intensive care patients with such severe intracranial diseases. The total fever burden within the entire study period of (on average) 152.4 hrs was 4.0 degrees C hrs/patient, being equivalent to 0.6 degrees C hrs/patient and day. Thirty of 51 patients showed an elevation of the body temperature (>37.9 degrees C) within 24 hrs after termination of the cooling study. One awake patient (subarachnoid hemorrhage, Glasgow Coma Scale score 15) experienced mild to moderate shivering throughout the entire period of 7 days. The mortality rate was 23.5%. CONCLUSION: This novel intravascular cooling device (Cool Line catheter and Cool Gard cooling device) was highly efficacious in prophylactically controlling the body temperature of neurologic intensive care patients with very severe intracranial disease (median Glasgow Coma Scale score, 3-15). Morbidity and mortality rates were consistent with the ranges reported in the literature for such neurologic intensive patients.

Early intensive care unit intervention for trauma care: what alters the outcome?

This review focuses on early management of multiple trauma patients with traumatic brain injury. Early usage of multislice computed tomography can substantially shorten the time spent on diagnostic workup in the emergency room and, therefore, speeds the initiation of lifesaving interventions for the control of hemorrhage. The important role of hemostatic angiographic embolization and its timing, in addition to surgical control of bleeding in patients suffering from pelvic fracture or organ lesions, is emphasized. The ongoing controversy regarding the strategy of fluid resuscitation is discussed. The concept of permissive hypotension seems to be promising but is absolutely contraindicated in patients with traumatic brain injury. Coagulation management should be guided by coagulation monitoring, including thromboelastography. A novel approach to reduce major bleeding is the application of recombinant factor VIIa. Strong effort should be directed toward the management of traumatic brain injury and the maintenance of cerebral perfusion pressure. The optimization of treatment of patients with multiple trauma, including brain injury, is a multidisciplinary task.

Temporal and spatial profile of Bid cleavage after experimental traumatic brain injury.

Apoptosis plays an essential role in the cascade of CNS cell degeneration after traumatic brain injury. However, the underlying mechanisms are poorly understood. The authors examined the temporal profile and cell subtype distribution of the proapoptotic protein Bid from 6 hours to 7 days after cortical impact injury in the rat. Increased protein levels of tBid were seen in the cortex ipsilateral to the injury site from 6 hours to 3 days after trauma. Immunohistologic examinations revealed expression of tBid in neurons, astrocytes, and oligodendrocytes from 6 hours to 3 days after impact injury, and concurrent assessment of DNA damage using TUNEL identified tBid-immunopositive cells with apoptoticlike morphology in the traumatized cortex. Moreover, Bid cleavage and activation of caspase-8 and caspase-9 occurred at similar time points and in similar brain regions (i.e., cortical layers 2 to 5) after impact injury. In contrast, there was no evidence of caspase-8 or caspase-9 processing or Bid cleavage in the ipsilateral hippocampus, contralateral cortex, and hippocampus up to 7 days after the injury. The results provide the first evidence of Bid cleavage in the traumatized cortex after experimental traumatic brain injury in vivo, and demonstrate that tBid is expressed in neurons and glial cells. Further, findings indicate that cleavage of Bid may be associated with the activation of the initiator caspase-8 and caspase-9. Finally, these data support the hypothesis that cleavage of Bid contributes to the apoptotic degeneration of different CNS cells in the injured cortex.