The prognostic importance of traumatic axonal injury on early MRI: the Trondheim TAI-MRI grading and quantitative models.

OBJECTIVES: We analysed magnetic resonance imaging (MRI) findings after traumatic brain injury (TBI) aiming to improve the grading of traumatic axonal injury (TAI) to better reflect the outcome. METHODS: Four-hundred sixty-three patients (8-70 years) with mild (n = 158), moderate (n = 129), or severe (n = 176) TBI and early MRI were prospectively included. TAI presence, numbers, and volumes at predefined locations were registered on fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging, and presence and numbers on T2*GRE/SWI. Presence and volumes of contusions were registered on FLAIR. We assessed the outcome with the Glasgow Outcome Scale Extended. Multivariable logistic and elastic-net regression analyses were performed. RESULTS: The presence of TAI differed between mild (6%), moderate (70%), and severe TBI (95%). In severe TBI, bilateral TAI in mesencephalon or thalami and bilateral TAI in pons predicted worse outcomes and were defined as the worst grades (4 and 5, respectively) in the Trondheim TAI-MRI grading. The Trondheim TAI-MRI grading performed better than the standard TAI grading in severe TBI (pseudo-R2 0.19 vs. 0.16). In moderate-severe TBI, quantitative models including both FLAIR volume of TAI and contusions performed best (pseudo-R2 0.19-0.21). In patients with mild TBI or Glasgow Coma Scale (GCS) score 13, models with the volume of contusions performed best (pseudo-R2 0.25-0.26). CONCLUSIONS: We propose the Trondheim TAI-MRI grading (grades 1-5) with bilateral TAI in mesencephalon or thalami, and bilateral TAI in pons as the worst grades. The predictive value was highest for the quantitative models including FLAIR volume of TAI and contusions (GCS score <13) or FLAIR volume of contusions (GCS score ≥ 13), which emphasise artificial intelligence as a potentially important future tool. CLINICAL RELEVANCE STATEMENT: The Trondheim TAI-MRI grading reflects patient outcomes better in severe TBI than today's standard TAI grading and can be implemented after external validation. The prognostic importance of volumetric models is promising for future use of artificial intelligence technologies. KEY POINTS: Traumatic axonal injury (TAI) is an important injury type in all TBI severities. Studies demonstrating which MRI findings that can serve as future biomarkers are highly warranted. This study proposes the most optimal MRI models for predicting patient outcome at 6 months after TBI; one updated pragmatic model and a volumetric model. The Trondheim TAI-MRI grading, in severe TBI, reflects patient outcome better than today's standard grading of TAI and the prognostic importance of volumetric models in all severities of TBI is promising for future use of AI.

Standardized reporting for Head CT Scans in patients suspected of traumatic brain injury (TBI): An international expert endeavor.

BACKGROUND AND PURPOSE: Traumatic brain injury (TBI) is a major source of health loss and disability worldwide. Accurate and timely diagnosis of TBI is critical for appropriate treatment and management of the condition. Neuroimaging plays a crucial role in the diagnosis and characterization of TBI. Computed tomography (CT) is the first-line diagnostic imaging modality typically utilized in patients with suspected acute mild, moderate and severe TBI. Radiology reports play a crucial role in the diagnostic process, providing critical information about the location and extent of brain injury, as well as factors that could prevent secondary injury. However, the complexity and variability of radiology reports can make it challenging for healthcare providers to extract the necessary information for diagnosis and treatment planning. METHODS/RESULTS/CONCLUSION: In this article, we report the efforts of an international group of TBI imaging experts to develop a clinical radiology report template for CT scans obtained in patients suspected of TBI and consisting of fourteen different subdivisions (CT technique, mechanism of injury or clinical history, presence of scalp injuries, fractures, potential vascular injuries, potential injuries involving the extra-axial spaces, brain parenchymal injuries, potential injuries involving the cerebrospinal fluid spaces and the ventricular system, mass effect, secondary injuries, prior or coexisting pathology).

Traumatic axonal injury: Relationships between lesions in the early phase and diffusion tensor imaging parameters in the chronic phase of traumatic brain injury.

This prospective study of traumatic brain injury (TBI) patients investigates fractional anisotropy (FA) from chronic diffusion tensor imaging (DTI) in areas corresponding to persistent and transient traumatic axonal injury (TAI) lesions detected in clinical MRI from the early phase. Thirty-eight patients (mean 24.7 [range 13-63] years of age) with moderate-to-severe TBI and 42 age- and sex-matched healthy controls were included. Patients underwent 1.5-T clinical MRI in the early phase (median 7 days), including fluid-attenuated inversion recovery (FLAIR) and T2* gradient echo (T2*GRE) sequences. TAI lesions from the early phase were characterized as nonhemorrhagic or microhemorrhagic. In the chronic phase (median 3 years), patients and controls were imaged at 3 T with FLAIR, T2*GRE, T1, and DTI sequences. TAI lesions were classified as transient or persistent. The FLAIR/T2*GRE images from the early phase were linearly registered to the FA images from the chronic phase and lesions manually segmented on the FA-registered FLAIR/T2*GRE images. For regions of interest (ROIs) from both nonhemorrhagic and microhemorrhagic lesion, we found a significant linear trend of lower mean FA from ROIs in healthy controls to ROIs in patients without either nonhemorrhagic or microhemorrhagic lesions and further to transient and finally persistent lesion ROIs (P < 0.001). Histogram analyses showed lower FA in persistent compared with transient nonhemorrhagic lesion ROIs (P < 0.001), but this was not found in microhemorrhagic lesion ROIs (P = 0.08-0.55). The demonstrated linear trend of lower FA values from healthy controls to persistent lesion ROIs was found in both nonhemorrhagic and microhemorrhagic lesions and indicates a gradual increasing disruption of the microstructure. Lower FA values in persistent compared with transient lesions were found only in nonhemorrhagic lesions. Thus, clinical MRI techniques are able to depict important aspects of white matter pathology across the stages of TBI. © 2016 Wiley Periodicals, Inc.

Intracranial Pressure During Pressure Control and Pressure-Regulated Volume Control Ventilation in Patients with Traumatic Brain Injury: A Randomized Crossover trial.

INTRODUCTION: Mechanical ventilation with control of partial arterial CO2 pressures (PaCO2) is used to treat or stabilize intracranial pressure (ICP) in patients with traumatic brain injury (TBI). Pressure-regulated volume control (PRVC) is a ventilator mode where inspiratory pressures are automatically adjusted to deliver the patient a pre-set stable tidal volume (TV). This may result in a more stable PaCO2 and thus a more stable ICP compared with conventional pressure control (PC) ventilation. The aim of this study was to compare PC and PRVC ventilation in TBI patients with respect to ICP and PaCO2. METHODS: This is a randomized crossover trial including eleven patients with a moderate or severe TBI who were mechanically ventilated and had ICP monitoring. Each patient was administered alternating 2-h periods of PC and PRVC ventilation. The outcome variables were ICP and PaCO2. RESULTS: Fifty-two (26 PC, 26 PRVC) study periods were included. Mean ICP was 10.8 mmHg with PC and 10.3 mmHg with PRVC ventilation (p = 0.38). Mean PaCO2 was 36.5 mmHg (4.87 kPa) with PC and 36.1 mmHg (4.81 kPa) with PRVC (p = 0.38). There were less fluctuations in ICP (p = 0.02) and PaCO2 (p = 0.05) with PRVC ventilation. CONCLUSIONS: Mean ICP and PaCO2 were similar for PC and PRVC ventilation in TBI patients, but PRVC ventilation resulted in less fluctuation in both ICP and PaCO2. We cannot exclude that the two ventilatory modes would have impact on ICP in patients with higher ICP values; however, the similar PaCO2 observations argue against this.

Lesion Frequency Distribution Maps of Traumatic Axonal Injury on Early Magnetic Resonance Imaging After Moderate and Severe Traumatic Brain Injury and Associations to 12 Months Outcome.

Traumatic axonal injury (TAI) is a common finding on magnetic resonance imaging (MRI) in patients with moderate-severe traumatic brain injury (TBI), and the burden of TAI is associated with outcome in this patient group. Lesion mapping offers a way to combine imaging findings from numerous individual patients into common lesion maps where the findings from a whole patient cohort can be assessed. The aim of this study was to evaluate the spatial distribution of TAI lesions on different MRI sequences and its associations to outcome with use of lesion mapping. Included prospectively were 269 patients (8-70 years) with moderate or severe TBI and MRI within six weeks after injury. The TAI lesions were evaluated and manually segmented on fluid-attenuated inversed recovery (FLAIR), diffusion weighted imaging (DWI), and either T2* gradient echo (T2*GRE) or susceptibility weighted imaging (SWI). The segmentations were registered to the Montreal Neurological Institute space and combined to lesion frequency distribution maps. Outcome was assessed with Glasgow Outcome Scale Extended (GOSE) score at 12 months. The frequency and distribution of TAI was assessed qualitatively by visual reading. Univariable associations to outcome were assessed qualitatively by visual reading and also quantitatively with use of voxel-based lesion-symptom mapping (VLSM). The highest frequency of TAI was found in the posterior half of corpus callosum. The frequency of TAI was higher in the frontal and temporal lobes than in the parietal and occipital lobes, and in the upper parts of the brainstem than in the lower. At the group level, all voxels in mesencephalon had TAI on FLAIR. The patients with poorest outcome (GOSE scores ≤4) had higher frequencies of TAI. On VLSM, poor outcome was associated with TAI lesions bilaterally in the splenium, the right side of tectum, tegmental mesencephalon, and pons. In conclusion, we found higher frequency of TAI in posterior corpus callosum, and TAI in splenium, mesencephalon, and pons were associated with poor outcome. If lesion frequency distribution maps containing outcome information based on imaging findings from numerous patients in the future can be compared with the imaging findings from individual patients, it would offer a new tool in the clinical workup and outcome prediction of the patient with TBI.

Diffusion Tensor and Kurtosis Imaging Findings the First Year following Mild Traumatic Brain Injury.

Despite enormous research interest in diffusion tensor imaging and diffusion kurtosis imaging (DTI; DKI) following mild traumatic brain injury (MTBI), it remains unknown how diffusion in white matter evolves post-injury and relates to acute MTBI characteristics. This prospective cohort study aimed to characterize diffusion changes in white matter the first year after MTBI. Patients with MTBI (n = 193) and matched controls (n = 83) underwent 3T magnetic resonance imaging (MRI) within 72 h and 3- and 12-months post-injury. Diffusion data were analyzed in three steps: 1) voxel-wise comparisons between the MTBI and control group were performed with tract-based spatial statistics at each time-point; 2) clusters of significant voxels identified in step 1 above were evaluated longitudinally with mixed-effect models; 3) the MTBI group was divided into: (A) complicated (with macrostructural findings on MRI) and uncomplicated MTBI; (B) long (1-24 h) and short (< 1 h) post-traumatic amnesia (PTA); and (C) other and no other concurrent injuries to investigate if findings in step 1 were driven mainly by aberrant diffusion in patients with a more severe injury. At 72 h, voxel-wise comparisons revealed significantly lower fractional anisotropy (FA) in one tract and significantly lower mean kurtosis (Kmean) in 11 tracts in the MTBI compared with control group. At 3 months, the MTBI group had significantly higher mean diffusivity in eight tracts compared with controls. At 12 months, FA was significantly lower in four tracts and Kmean in 10 tracts in patients with MTBI compared with controls. There was considerable overlap in affected tracts across time, including the corpus callosum, corona radiata, internal and external capsule, and cerebellar peduncles. Longitudinal analyses revealed that the diffusion metrics remained relatively stable throughout the first year after MTBI. The significant group*time interactions identified were driven by changes in the control rather than the MTBI group. Further, differences identified in step 1 did not result from greater diffusion abnormalities in patients with complicated MTBI, long PTA, or other concurrent injuries, as standardized mean differences in diffusion metrics between the groups were small (0.07 ± 0.11) and non-significant. However, follow-up voxel-wise analyses revealed that other concurrent injuries had effects on diffusion metrics, but predominantly in other metrics and at other time-points than the effects observed in the MTBI versus control group analysis. In conclusion, patients with MTBI differed from controls in white matter integrity already 72 h after injury. Diffusion metrics remained relatively stable throughout the first year after MTBI and were not driven by deviating diffusion in patients with a more severe MTBI.

A longitudinal MRI study of traumatic axonal injury in patients with moderate and severe traumatic brain injury.

OBJECTIVE: To study the evolution of traumatic axonal injury (TAI) detected by structural MRI in patients with moderate and severe traumatic brain injury (TBI) during the first year and relate findings to outcome. METHODS: 58 patients with TBI (Glasgow Coma Scale score 3-13) were examined with MRI at a median of 7 days, 3 months and 12 months post injury. TAI lesions were evaluated blinded and categorised into three stages based on location: hemispheres, corpus callosum and brainstem. Lesions in T2* weighted gradient echo (GRE), fluid attenuated inversion recovery (FLAIR) and diffusion weighted imaging (DWI) were counted and FLAIR lesion volumes were estimated. Inter-rater reliability score was calculated. Outcome was assessed 12 months post injury using the Glasgow Outcome Scale Extended. RESULTS: In the initial MRI, 31% had brainstem lesions compared with 17% at 3 months (p=0.008). In the FLAIR sequences, number and volumes of lesions were reduced from early to 3 months (p<0.001). In T2*GRE sequences, the number of lesions persisted at 3 months but was reduced at 12 months (p=0.007). The number of lesions in DWI and volume of FLAIR lesions on early MRI predicted worse clinical outcome in adjusted analyses (p<0.05). CONCLUSION: This is the first study to demonstrate and quantify attenuation of non-haemorrhagic TAI lesions on structural MRI during the first 3 months after TBI; most importantly, the disappearance of brainstem lesions. Haemorrhagic TAI lesions attenuate first after 3 months. Only early MRI findings predicted clinical outcome after adjustment for other prognostic factors. Hence valuable clinical information may be missed if MRI is performed too late after TBI.

Acute Diffusion Tensor and Kurtosis Imaging and Outcome following Mild Traumatic Brain Injury.

In this prospective cohort study, we investigated associations between acute diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI) metrics and persistent post-concussion symptoms (PPCS) 3 months after mild traumatic brain injury (mTBI). Adult patients with mTBI (n = 176) and community controls (n = 78) underwent 3 Tesla magnetic resonance imaging (MRI) within 72 h post-injury, estimation of cognitive reserve at 2 weeks, and PPCS assessment at 3 months. Eight DTI and DKI metrics were examined with Tract-Based Spatial Statistics. Analyses were performed in the total sample in uncomplicated mTBI only (i.e., without lesions on clinical MRI), and with cognitive reserve both controlled for and not. Patients with PPCS (n = 35) had lower fractional anisotropy (in 2.7% of all voxels) and kurtosis fractional anisotropy (in 6.9% of all voxels), and higher radial diffusivity (in 0.3% of all voxels), than patients without PPCS (n = 141). In uncomplicated mTBI, only fractional anisotropy was significantly lower in patients with PPCS. Compared with controls, patients with PPCS had widespread deviations in all diffusion metrics. When including cognitive reserve as a covariate, no significant differences in diffusion metrics between patients with and without PPCS were present, but patients with PPCS still had significantly higher mean, radial, and axial diffusivity than controls. In conclusion, patients who developed PPCS had poorer white matter microstructural integrity acutely after the injury, compared with patients who recovered and healthy controls. Differences became less pronounced when cognitive reserve was controlled for, suggesting that pre-existing individual differences in axonal integrity accounted for some of the observed differences.

Traumatic axonal injury on clinical MRI: association with the Glasgow Coma Scale score at scene of injury or at admission and prolonged posttraumatic amnesia.

OBJECTIVE: The aim in this study was to investigate if MRI findings of traumatic axonal injury (TAI) after traumatic brain injury (TBI) are related to the admission Glasgow Coma Scale (GCS) score and prolonged duration of posttraumatic amnesia (PTA). METHODS: A total of 490 patients with mild to severe TBI underwent brain MRI within 6 weeks of injury (mild TBI: median 2 days; moderate to severe TBI: median 8 days). The location of TAI lesions and measures of total TAI lesion burden (number and volume of lesions on FLAIR and diffusion-weighted imaging and number of lesions on T2*-weighted gradient echo or susceptibility-weighted imaging) were quantified in a blinded manner for clinical information. The volume of contusions on FLAIR was likewise recorded. Associations between GCS score and the location and burden of TAI lesions were examined with multiple linear regression, adjusted for age, Marshall CT score (which includes compression of basal cisterns, midline shift, and mass lesions), and alcohol intoxication. The predictive value of TAI lesion location and burden for duration of PTA > 28 days was analyzed with multiple logistic regression, adjusted for age and Marshall CT score. Complete-case analyses of patients with TAI were used for the regression analyses of GCS scores (n = 268) and PTA (n = 252). RESULTS: TAI lesions were observed in 58% of patients: in 7% of mild, 69% of moderate, and 93% of severe TBI cases. The TAI lesion location associated with the lowest GCS scores were bilateral lesions in the brainstem (mean difference in GCS score -2.5), followed by lesions bilaterally in the thalamus, unilaterally in the brainstem, and lesions in the splenium. The volume of TAI on FLAIR was the measure of total lesion burden most strongly associated with the GCS score. Bilateral TAI lesions in the thalamus had the largest predictive value for PTA > 28 days (OR 16.2, 95% CI 3.9-87.4). Of the measures of total TAI lesion burden, the FLAIR volume of TAI predicted PTA > 28 days the best. CONCLUSIONS: Bilateral TAI lesions in the brainstem and thalamus, as well as the total volume of TAI lesions on FLAIR, had the strongest association with the GCS score and prolonged PTA. The current study proposes a first step toward a modified classification of TAI, with grades ranked according to their relation to these two measures of clinical TBI severity.

Association of cause of injury and traumatic axonal injury: a clinical MRI study of moderate and severe traumatic brain injury.

OBJECTIVE: The authors investigated the association between the cause of injury and the occurrence and grade of traumatic axonal injury (TAI) on clinical MRI in patients with moderate or severe traumatic brain injury (TBI). METHODS: Data for a total of 396 consecutive patients, aged 7-70 years, with moderate or severe TBI admitted to a level 1 trauma center were prospectively registered. Data were included for analysis from the 219 patients who had MRI performed within 35 days (median 8, IQR 4-17 days) and for whom cause of injury was known. Cause of injury was registered as road traffic accident (RTA) or fall (both with respective subcategories), alpine skiing or snowboarding accident, or violence. The MRI protocol consisted of T2*-weighted gradient echo, FLAIR, and diffusion-weighted imaging scans. TAI lesions were evaluated in a blinded manner and categorized into 3 grades, hemispheric/cerebellar white matter (grade 1), corpus callosum (grade 2), and brainstem (grade 3). The absence of TAI was analyzed as grade 0. Contusions and mass lesions on CT were also registered. RESULTS: Cause of injury did not differ between included and nonincluded patients. TAI was found in 83% of patients in the included group after RTAs and 62% after falls (p < 0.001). Observed TAI grades differed between the subcategories of both RTAs (p = 0.004) and falls (p = 0.006). Pedestrians in RTAs, car drivers/passengers in RTAs, and alpine skiers had the highest prevalence of TAI (89%-100%) and the highest TAI grades (70%-82% TAI grades 2-3). TAI was found in 76% of patients after falls from > own height (45% TAI grade 2-3), 63% after falls down the stairs (26% TAI grade 2-3), and 31% after falls from ≤ own height (12% TAI grade 2-3). Moreover, 53% of patients with TAI after RTAs and 68% with TAI after falls had cortical contusions or mass lesions on CT. CONCLUSIONS: This prospective study of moderate and severe TBI is to the authors' knowledge the first clinical MRI study to demonstrate both the high prevalence and grade of TAI after most of the different types of RTAs, alpine skiing accidents, and falls from a height. Importantly, TAI was also common following more low-energy trauma such as falls down the stairs or from own height. Physicians managing TBI patients in the acute phase should be aware of the possibility of TAI no matter the cause of injury and also when the CT scan shows cortical contusions or mass lesions.

Time of Injury and Relation to Alcohol Intoxication in Moderate-to-Severe Traumatic Brain Injury: A Decade-Long Prospective Study.

BACKGROUND: Knowledge about the causes and time of injury for traumatic brain injury (TBI) is important for the development of efficient prevention policies. We aimed to study time of injury and relation to alcohol intoxication for moderate-to-severe TBI in a level 1 trauma center in Norway. METHODS: From October 2004 to September 2014, 493 consecutive patients (≥16 years) with moderate (Glasgow Coma Scale [GCS] score 9-13) and severe TBI (GCS score 3-8) were prospectively included in the Trondheim TBI Study (222 patients with moderate and 270 patients with severe TBI). RESULTS: Mean age was 47 years (standard deviation 21 years). Positive blood alcohol concentration (BAC) was found in 29%, and median BAC was 41.5 mmol/L (interquartile range 28.7-54.3), equal to 1.91‰. Admissions were more frequent on Saturdays (relative risk [RR] 2.67, 95% confidence interval [CI] 1.87-3.80) and Sundays (RR 2.10, 95% CI 1.45-3.03) compared with Mondays, and positive BAC was more common on weekends than weekdays (43% vs. 16%). Furthermore, admissions were more frequent in June (RR 2.26, 95% CI 1.44-3.55), July (RR 2.07, 95% CI 1.31-3.28), and December (RR 2.07, 95% CI 1.31-3.28) compared with January. The number of patients with positive BAC was greatest in December (RR 5.75, 95% CI 1.99-16.63), and 70% of these were caused by falls. CONCLUSIONS: Our findings demonstrate that moderate-to-severe TBI admissions display a clear weekly and seasonal variation and that alcohol is an important modifiable risk factor for moderate-to-severe TBI.

Incidence and mortality of moderate and severe traumatic brain injury in children: A ten year population-based cohort study in Norway.

OBJECTIVE: In this study we wanted to estimate population-based rates of incidence and mortality of moderate and severe traumatic brain injury (TBI) in children in one specific region in Norway. METHODS: In the region there are seven acute care hospitals (ACHs) in addition to a Level 1 trauma centre. Of 702 869 inhabitants (2014), 145 395 were children aged 0-16 years. Data were collected during ten years (2004-2014). All children aged 0-16 years with moderate (Glasgow Coma Scale [GCS] score 9-13) or severe (GCS score ≤ 8) TBI admitted to the Level 1 trauma centre were prospectively included. Children treated outside the Level 1 trauma centre were retrospectively included from the ACHs. Children who died from TBI prehospitally were included from the National Cause of Death Registry. Poisson regression was used to estimate incidence rate ratios (with a 95% confidence interval) comparing age, sex, and time periods. RESULTS: A total of 71 children with moderate or severe TBI were identified. Crude incidence rates were 2·4 (95% CI 1·7-3·3) for moderate and 2·5 (95% CI 1·8-3·4) for severe TBI per 100 000 person-years (py). Mortality rate from TBI was 1·2 (95% CI 0·7-1·9) per 100 000 py, and 88% were prehospital deaths. CONCLUSION: The incidence rates and mortality of moderate and severe TBI were low compared to international reports. Most likely explained by successful national prevention of TBI.

Patients with Mild Traumatic Brain Injury Recruited from Both Hospital and Primary Care Settings: A Controlled Longitudinal Magnetic Resonance Imaging Study.

With an emphasis on traumatic axonal injury (TAI), frequency and evolution of traumatic intracranial lesions on 3T clinical magnetic resonance imaging (MRI) were assessed in a combined hospital and community-based study of patients with mild traumatic brain injury (mTBI). The findings were related to post-concussion symptoms (PCS) at 3 and 12 months. Prospectively, 194 patients (16-60 years of age) were recruited from the emergency departments at a level 1 trauma center and a municipal outpatient clinic into the Trondheim mTBI follow-up study. MRI was acquired within 72 h (n = 194) and at 3 (n = 165) and 12 months (n = 152) in patients and community controls (n = 78). The protocol included T2, diffusion weighted imaging, fluid attenuated inversion recovery (FLAIR), and susceptibility weighted imaging (SWI). PCS was assessed with British Columbia Post Concussion Symptom Inventory in patients and controls. Traumatic lesions were present in 12% on very early MRI, and in 5% when computed tomography (CT) was negative. TAI was found in 6% and persisted for 12 months on SWI, whereas TAI lesions on FLAIR disappeared or became less conspicuous on follow-up. PCS occurred in 33% of patients with lesions on MRI and in 19% in patients without lesions at 3 months (p = 0.12) and in 21% with lesions and 14% without lesions at 12 months (p = 0.49). Very early MRI depicted cases of TAI in patients with mTBI with microbleeds persisting for 12 months. Patients with traumatic lesions may have a more protracted recovery, but the study was underpowered to detect significant differences for PCS because of the low frequency of trauma-related MRI lesions.

Relationship of "dose" of intracranial hypertension to outcome in severe traumatic brain injury.

OBJECT: It has recently been suggested that the degree of intracranial pressure (ICP) above the treatment goal can be estimated by the area under the curve (AUC) of ICP versus time in patients with severe traumatic brain injury (TBI). The objective of this study was to determine whether the calculated "ICP dose"-the ICP AUC-is related to mortality rate, outcome, and Marshall CT classification. METHODS: Of 135 patients (age range 1-82 years) with severe TBI treated during a 5-year period at the authors' institution, 113 patients underwent ICP monitoring (84%). Ninety-three patients with a monitoring time>24 hours were included for analysis of ICP AUC calculated using the trapezoidal method. Computed tomography scans were assessed according to the Marshall TBI classification. Patients with Glasgow Outcome Scale scores at 6 months and >3 years were separated into 2 groups based on outcome. RESULTS: Sixty patients (65%) had ICP values>20 mm Hg, and 12 (13%) developed severe intracranial hypertension and died secondary to herniation. A multiple regression analysis adjusting for Glasgow Coma Scale score, age, pupillary abnormalities and Injury Severity Scale score demonstrated that the ICP AUC was a significant predictor of poor outcome at 6 months (p=0.034) and of death (p=0.035). However, it did not predict long-term outcome (p=0.157). The ICP AUC was significantly higher in patients with Marshall head injury Categories 3 and 4 (24 patients) than in those with Category 2 (23 patients, p=0.025) and Category 5 (46 patients, p=0.021) TBIs using the worst CT scan obtained. CONCLUSIONS: The authors found a significant relationship between the dose of ICP, the worst Marshall CT score, and patient outcome, suggesting that the AUC method may be useful in refining and improving the treatment of ICP in patients with TBI.

Best practice guidelines for blunt cerebrovascular injury (BCVI).

Blunt cerebrovascular injury (BCVI) is a non-penetrating injury to the carotid and/or vertebral artery that may cause stroke in trauma patients. Historically BCVI has been considered rare but more recent publications indicate an overall incidence of 1-2% in the in-hospital trauma population and as high as 9% in patients with severe head injury. The indications for screening, treatment and follow-up of these patients have been controversial for years with few clear recommendations. In an attempt to provide a clinically oriented guideline for the handling of BCVI patients a working committee was created. The current guideline is the end result of this committees work. It is based on a systematic literature search and critical review of all available publications in addition to a standardized consensus process. We recommend using the expanded Denver screening criteria and CT angiography (CTA) for the detection of BCVI. Early antithrombotic treatment should be commenced as soon as considered safe and continued for at least 3 months. A CTA at 7 days to confirm or discard the diagnosis as well as a final imaging control at 3 months should be performed.