Long-Term Outcomes after Severe Traumatic Brain Injury in Older Adults. A Registry-based Cohort Study.

Rationale: Older adults (≥65 yr old) account for an increasing proportion of patients with severe traumatic brain injury (TBI), yet clinical trials and outcome studies contain relatively few of these patients.Objectives: To determine functional status 6 months after severe TBI in older adults, changes in this status over 2 years, and outcome covariates.Methods: This was a registry-based cohort study of older adults who were admitted to hospitals in Victoria, Australia, between 2007 and 2016 with severe TBI. Functional status was assessed with Glasgow Outcome Scale Extended (GOSE) 6, 12, and 24 months after injury. Cohort subgroups were defined by admission to an ICU. Features associated with functional outcome were assessed from the ICU subgroup.Measurements and Main Results: The study included 540 older adults who had been hospitalized with severe TBI over the 10-year period; 428 (79%) patients died in hospital, and 456 (84%) died 6 months after injury. There were 277 patients who had not been admitted to an ICU; at 6 months, 268 (97%) had died, 8 (3%) were dependent (GOSE 2-4), and 1 (0.4%) was functionally independent (GOSE 5-8). There were 263 patients who had been admitted to an ICU; at 6 months, 188 (73%) had died, 39 (15%) were dependent, and 32 (12%) were functionally independent. These proportions did not change over longer follow-up. The only clinical features associated with a lower rate of functional independence were Injury Severity Score ≥25 (adjusted odds ratio, 0.24 [95% confidence interval, 0.09-0.67]; P = 0.007) and older age groups (P = 0.017).Conclusions: Severe TBI in older adults is a condition with very high mortality, and few recover to functional independence.

Mortality After Traumatic Brain Injury in Elderly Patients: A New Scoring System.

BACKGROUND: Traumatic brain injury (TBI) remains a life-threatening condition characterized by growing incidence worldwide, particularly in the aging population, in which the primary goal of treatment appears to be avoidance of chronic institutionalization. METHODS: To identify independent predictors of 30-day mortality or vegetative state in a geriatric population and calculate an intuitive scoring system, we screened 480 patients after TBI treated at a single department of neurosurgery over a 2-year period. We analyzed data of 214 consecutive patients aged ≥65 years, including demographics, medical history, cause and time of injury, neurologic state, radiologic reports, and laboratory results. A predictive model was developed using logistic regression modeling with a backward stepwise feature selection. RESULTS: The median Glasgow Coma Scale (GCS) score on admission was 14 (interquartile range, 12-15), whereas the 30-day mortality or vegetative state rate amounted to 23.4%. Starting with 20 predefined features, the final prediction model highlighted the importance of GCS motor score (odds ratio [OR], 0.17; 95% confidence interval [CI], 0.09-0.32); presence of comorbid cardiac, pulmonary, or renal dysfunction or malignancy (OR, 2.86; 9 5% CI, 1.08-7.61); platelets ≤100 × 109 cells/L (OR, 13.60; 95% CI, 3.33-55.49); and red blood cell distribution width coefficient of variation ≥14.5% (OR, 2.91; 95% CI, 1.09-7.78). The discovered coefficients were used for nomogram development. It was further simplified to facilitate clinical use. The proposed scoring system, Elderly Traumatic Brain Injury Score (eTBI Score), yielded similar performance metrics. CONCLUSIONS: The eTBI Score is the first scoring system designed specifically for older adults. It could constitute a framework for clinical decision-making and serve as an outcome predictor. Its capability to stratify risk provides reliable criteria for assessing efficacy of TBI management.

Application of a Grading System in the Treatment of Frontal Lobe Contusion in High-Altitude Regions.

OBJECTIVE: With the development of frontal contusion, patients may rapidly deteriorate or even die. Experience in the treatment of frontal contusion in high-altitude regions is limited; thus, we explore a grading system for the treatment of frontal lobe contusion. METHODS: A total of 446 patients with frontal contusions in a high-altitude regions were reviewed retrospectively. We combined the patients' computed tomography scans of the head and clinical features for grading. The score determined the treatment and whether the bone flap was removed. If the patient's condition deteriorated, and the score was greater than 1, the patient was treated surgically. At the same time, the risk factors of deterioration were analyzed. Finally, the Glasgow Outcome Scale of conservative treatment and surgical treatment groups was analyzed. RESULTS: Among the 446 patients, 254 were conservatively treated, and 28 worsened and underwent surgical treatment. In total, 122 patients received an operation. Logistic regression analysis indicated that scattered hematoma, anterior angle of the ventricle, and hemoglobin concentration were risk factors. The postoperative Glasgow Outcome Scale of conservative treatment and surgical treatment groups was analyzed; the good healing rate of the conservative treatment group was 91.12%, the good healing rate of the retain-bone flap surgical group was 75%, and the good healing rate of the remove-bone flap surgical group was 63.33%. The failure rates of the groups were 9.38% and 7.78%, respectively. CONCLUSIONS: This grading system could guide frontal contusion treatment, which could help patients to achieve a good healing rate and reduce the failure rate.

Normobaric hyperoxia does not improve derangements in diffusion tensor imaging found distant from visible contusions following acute traumatic brain injury.

We have previously shown that normobaric hyperoxia may benefit peri-lesional brain and white matter following traumatic brain injury (TBI). This study examined the impact of brief exposure to hyperoxia using diffusion tensor imaging (DTI) to identify axonal injury distant from contusions. Fourteen patients with acute moderate/severe TBI underwent baseline DTI and following one hour of 80% oxygen. Thirty-two controls underwent DTI, with 6 undergoing imaging following graded exposure to oxygen. Visible lesions were excluded and data compared with controls. We used the 99% prediction interval (PI) for zero change from historical control reproducibility measurements to demonstrate significant change following hyperoxia. Following hyperoxia DTI was unchanged in controls. In patients following hyperoxia, mean diffusivity (MD) was unchanged despite baseline values lower than controls (p < 0.05), and fractional anisotropy (FA) was lower within the left uncinate fasciculus, right caudate and occipital regions (p < 0.05). 16% of white and 14% of mixed cortical and grey matter patient regions showed FA decreases greater than the 99% PI for zero change. The mechanistic basis for some findings are unclear, but suggest that a short period of normobaric hyperoxia is not beneficial in this context. Confirmation following a longer period of hyperoxia is required.

[APPLICATION OF ALLOGENIC TISSUE OF THE FETAL BRAIN CORTEX AND THE OLFACTORY BULB TISSUE FOR TREATMENT OF THE BRAIN CONTUSION IN RATS].

Impact of the allogenic tissue transplantation of the fetal cerebral large hemispheres and the оlfactory bulb tissue (OBT) on the healing processes after the brain contusion was studied in experiment. The investigation was performed on mongrel male rats: in laboratory animals of the first group in the first day after open penetrating local cerebral trauma (OPLCT) the allogenic fetal nervous tissue fragment was transplanted into the formatted tissue defect; for the second group ­ in the first day after cerebral trauma the allogenic OBT fragment was transplanted into the formatted tissue defect; and for the third group (control) - the OPLCT was done without further transplantation of tissues. The impact of the allogenic fetal nervous tissue transplantation was demonstrated by more active participation of glial cells during the healing process course, and the OBT transplantation was followed by activation of neoangiogenesis processes , mainly in the injured brain. The experimental simulation choosed permits to study the possibilities of application of neurogenic tissues in the brain contusion treatment, and to determine the therapy tactics.

Mild Hypothermia Promotes Pericontusion Neuronal Sprouting via Suppressing Suppressor of Cytokine Signaling 3 Expression after Moderate Traumatic Brain Injury.

Mild therapeutic hypothermia is a candidate for the treatment of traumatic brain injury (TBI). However, the role of mild hypothermia in neuronal sprouting after TBI remains obscure. We used a fluid percussion injury (FPI) model to assess the effect of mild hypothermia on pericontusion neuronal sprouting after TBI in rats. Male Sprague-Dawley rats underwent FPI or sham surgery, followed by mild hypothermia treatment (33°C) or normothermia treatment (37°C) for 3 h. All the rats were euthanized at 7 days after FPI. Neuronal sprouting that was confirmed by an increase in growth associated protein-43 (GAP-43) expression was evaluated using immunofluorescence and Western blot assays. The expression levels of several intrinsic and extrinsic sprouting-associated genes such as neurite outgrowth inhibitor A (NogoA), phosphatase and tensin homolog (PTEN), and suppressor of cytokine signaling 3 (SOCS3) were analyzed by quantitative real-time polymerase chain reaction (RT-PCR). Our results revealed that mild hypothermia significantly increased the expression level of GAP-43 and dramatically suppressed the expression level of interleukin-6 (IL-6) and SOCS3 at 7 days after FPI in the ipsilateral cortex compared with that of the normothermia TBI group. These data suggest that post-traumatic mild hypothermia promotes pericontusion neuronal sprouting after TBI. Moreover, the mechanism of hypothermia-induced neuronal sprouting might be partially associated with decreased levels of SOCS3.

Isoflurane-Associated Mydriasis Mimicking Blown Pupils in a Patient Treated in a Neurointensive Care Unit.

We report a misinterpretation of bilateral mydriasis as blown pupils related to elevated intracranial pressure (ICP) under volatile sedation with isoflurane (Anesthetic Conserving Device [AnaConDa], Hudson RCI, Uppland Vasby, Sweden) in a 59-year-old patient with a severe traumatic brain injury with frontal contusion. The patient showed bilateral mydriasis and a missing light reflex 8 hours after changing sedation from intravenous treatment with midazolam and esketamine to volatile administration of isoflurane. Because cranial computed tomography ruled out signs of cerebral herniation, we assumed the bilateral mydriasis was caused by isoflurane and reduced the isoflurane supply. Upon this reduction the mydriasis regressed, suggesting the observed mydriasis was related to an overdose of isoflurane. Intensivists should be aware of the reported phenomenon to avoid unnecessary diagnostic investigations that might harm the patient. We recommend careful control of the isoflurane dose when fixed and dilated pupils appear in patients without other signs of elevated ICP.

Selective Brain Hypothermia Mitigates Brain Damage and Improves Neurological Outcome after Post-Traumatic Decompressive Craniectomy in Mice.

Hypothermia and decompressive craniectomy (DC) have been considered as treatment for traumatic brain injury. The present study investigates whether selective brain hypothermia added to craniectomy could improve neurological outcome after brain trauma. Male CD-1 mice were assigned into the following groups: sham; DC; closed head injury (CHI); CHI followed by craniectomy (CHI+DC); and CHI+DC followed by focal hypothermia (CHI+DC+H). At 24 h post-trauma, animals were subjected to Neurological Severity Score (NSS) test and Beam Balance Score test. At the same time point, magnetic resonance imaging using a 9.4 Tesla scanner and subsequent volumetric evaluation of edema and contusion were performed. Thereafter, the animals were sacrificed and subjected to histopathological analysis. According to NSS, there was a significant impairment among all the groups subjected to trauma. Animals with both trauma and craniectomy performed significantly worse than animals with craniectomy alone. This deleterious effect disappeared when additional hypothermia was applied. BBS was significantly worse in the CHI and CHI+DC groups, but not in the CHI+DC+H group, compared to the sham animals. Edema and contusion volumes were significantly increased in CHI+DC animals, but not in the CHI+DC+H group, compared to the DC group. Histopathological analysis showed that neuronal loss and contusional blossoming could be attenuated by application of selective brain hypothermia. Selective brain cooling applied post-trauma and craniectomy improved neurological function and reduced structural damage and may be therefore an alternative to complication-burdened systemic hypothermia. Clinical studies are recommended in order to explore the potential of this treatment.

Derivation of a Predictive Score for Hemorrhagic Progression of Cerebral Contusions in Moderate and Severe Traumatic Brain Injury.

BACKGROUNDS: After traumatic brain injury (TBI), hemorrhagic progression of contusions (HPCs) occurs frequently. However, there is no established predictive score to identify high-risk patients for HPC. METHODS: Consecutive patients who were hospitalized (2008-2013) with non-penetrating moderate or severe TBI were studied. The primary outcome was HPC, defined by both a relative increase in contusion volume by ≥30 % and an absolute increase by ≥10 mL on serial imaging. Logistic regression models were created to identify independent risk factors for HPC. The HPC Score was then derived based on the final model. RESULTS: Among a total of 286 eligible patients, 61 (21 %) patients developed HPC. On univariate analyses, HPC was associated with older age, higher initial blood pressure, antiplatelet medications, anticoagulants, subarachnoid hemorrhage (SAH) subdural hematoma (SDH), skull fracture, frontal contusion, larger contusion volume, and shorter interval from injury to initial CT. In the final model, SAH (OR 6.33, 95 % CI, 1.80-22.23), SDH (OR 3.46, 95 % CI, 1.39-8.63), and skull fracture (OR 2.67, 95 % CI, 1.28-5.58) were associated with HPC. Based on these factors, the HPC Score was derived (SAH = 2 points, SDH = 1 point, and skull fracture = 1 point). This score had an area under the receiver operating curve of 0.77. Patients with a score of 0-2 had a 4.0 % incidence of HPC, while patients with a score of 3-4 had a 34.6 % incidence of HPC. CONCLUSIONS: A simple HPC Score was developed for early risk stratification of HPC in patients with moderate or severe TBI.

Effects of Brain Temperature on Cerebrovascular Autoregulation During the Acute Stage of Severe Traumatic Brain Injury.

The pressure reactivity index (PRx) is calculated as a moving correlation coefficient between intracranial pressure (ICP) and mean arterial blood pressure (MABP), and this analytical value is viewed as reflecting a vasomotor response to MABP variability. At present, the factors influencing the PRx value during the acute stage of traumatic brain injury (TBI) are not known. We observed significant cases where changes in the calculated value of PRx seemed to be influenced by changes in brain temperature during the course of acute stage TBI. In one case, a patient was treated for 72 h with therapeutic brain hypothermia after a decompressive hemicraniectomy. During the hypothermic condition, the mean value of PRx was -0.019; however, after gradual rewarming, the value of PRx increased drastically, and the mean value during the rewarming period, when the brain temperature exceeded 35 °C, was 0.331. Similarly, in another case where the patient underwent therapeutic brain hypothermia, the PRx showed a mean value of -0.038 during the hypothermic condition, and a mean value of 0.052 during the rewarming period. In both cases, a trend toward a negative correlation between ICP and MABP during brain hypothermia shifted to a positive correlation upon rewarming.