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Nursing role on preventing secondary brain injury.

Secondary brain injury is a complicated, multifactorial process that results from hypoxemia, hypercapnia or hypocapnia, and increased ICP. Implementation of a traumatic brain injury protocol for patients with head injury including hemodynamic management, pulmonary care, maintenance of body temperature, control of the environment, positioning of patients, and seizure prophylaxis provides critical care nurses a proactive means to prevent or minimize the development of secondary brain injury in the emergency department.

Barbiturates↗

The role of artificial intelligence in the diagnosis and prognosis of traumatic brain injury based on brain CT scans: a systematic review.

Traumatic brain injury (TBI) is a leading cause of emergency department visits and a major contributor to injury-related mortality and long-term neurological disability. Non-contrast computed tomography (CT) is the gold-standard imaging modality for the rapid diagnosis of TBI. Clinical outcomes depend strongly on early detection and prompt acute management. Artificial intelligence (AI)-based models may support faster automated identification of traumatic findings and early prediction of patient prognosis. A systematic literature search was conducted in PubMed/MEDLINE, Scopus, IEEE Xplore, ACM Digital Library, and the Cochrane Library in accordance with PRISMA 2020 guidelines to evaluate AI-based models for automated detection of TBI-related findings on CT and for prediction of clinical outcomes. Risk of bias and applicability were assessed using QUADAS-2 for diagnostic accuracy studies and PROBAST + AI for prediction model studies. Twenty-two studies were included. Sixteen studies evaluated diagnostic tasks and 10 evaluated prognostic outcomes, with four studies contributing to both categories. Diagnostic performance was generally high, with many studies reporting AUC values approaching or exceeding 0.90, particularly for larger lesion volumes.Prognostic performance was more variable, with moderate to high discrimination and substantial heterogeneity. Only 9 studies incorporated independent external validation, and performance was frequently lower in external cohorts. All prognostic model studies were judged to be at high overall risk of bias using PROBAST + AI, and most diagnostic accuracy studies also demonstrated high or unclear risk of bias in at least one QUADAS-2 domain, most frequently in patient selection. AI-based models applied to brain CT demonstrate strong technical performance for both diagnostic and prognostic tasks in TBI. However, most studies relied on retrospective designs and lacked independent external validation which limits models generalizability and raises concern for potential overfitting. Prospective, multicenter studies with standardized methodologies and rigorous external validation are required before widespread clinical implementation.

Humans↗

Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

OBJECTIVE: We undertook a best-evidence synthesis on the incidence, risk factors and prevention of mild traumatic brain injury. METHODS: Medline, Cinahl, PsycINFO and Embase were searched for relevant articles. After screening 38,806 abstracts, we critically reviewed 169 studies on incidence, risk and prevention, and accepted 121 (72%). RESULTS: The accepted articles show that 70-90% of all treated brain injuries are mild, and the incidence of hospital-treated patients with mild traumatic brain injury is about 100-300/100,000 population. However, much mild traumatic brain injury is not treated at hospitals, and the true population-based rate is probably above 600/100,000. Mild traumatic brain injury is more common in males and in teenagers and young adults. Falls and motor-vehicle collisions are common causes. CONCLUSION: Strong evidence supports helmet use to prevent mild traumatic brain injury in motorcyclists and bicyclists. The mild traumatic brain injury literature is of varying quality, and the studies are very heterogeneous. Nevertheless, there is evidence that mild traumatic brain injury is an important public health problem, but we need more high-quality research into this area.

Adolescent↗

Rehabilitation and hypopituitarism after traumatic brain injury.

Traumatic brain injury (TBI) is a leading cause of death and disability in the United States (US). The severity of a TBI is difficult to assess, and therefore, accurate determination of the prognosis is difficult. The symptoms of a TBI involve most major medical systems, and share many similarities with the symptoms of hypopituitarism. Although more than two-thirds of patients with severe head injuries who die have structural abnormalities in the hypothalamus and the pituitary, pituitary function is not routinely assessed after head trauma. Thus, studies have shown that anterior pituitary hormone deficiencies are common following brain injury [Endocrinologist 11 (2001) 275; J. Clin. Endocrinol. Metab. 86 (2001) 2752]. Survivors of brain injury should be screened for such deficiencies so that replacement therapy can be initiated to optimize rehabilitation and outcome.

Brain Injuries↗

Clinician perspectives on decision-making capacity after acquired brain injury.

Acquired brain injury frequently alters an individual's ability to make health care decisions based on a clear understanding of the situation and options. This exploratory study investigated the ways health care providers address issues of decisionmaking capacity (DMC) on a daily, functional basis. 33 clinicians providing rehabilitation services to persons with acquired brain injury participated in 1 of 5 semi-structured focus groups. All 33 participants, representing 8 different occupations, agreed that DMC determinations affected their practice every day. Participants underscored a multidimensional rather than a unitary definition of DMC, with an emphasis on fluctuating capacities due to the injury. Important concerns were for the safety of the person with brain injury, the health care provider, and community members. Other themes included rehabilitation team involvement, family context, and professional socialization. Clinical determinations of DMC are context dependent and are affected by the abilities of the individual and the substance and consequences of the decision being made and include the concepts of regaining trust and reclaiming capacity.

Adult↗

Cerebral vascular and metabolic response to sustained systemic inflammation in ovine traumatic brain injury.

Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n = 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n = 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 +/- 4 mm Hg to 21 +/- 15 mm Hg (TBI/Endo) and from 10 +/- 3 mm Hg to 24 +/- 19 mm Hg (TBI) (means +/- SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO2, PaCO2, and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.

Animals↗

Course of functional improvement after stroke, spinal cord injury, and traumatic brain injury.

OBJECTIVE: To examine functional improvement patterns of persons with stroke, traumatic brain injury (TBI), and spinal cord injury (SCI). DESIGN: Statistical analysis of data from a multisite study evaluating rehabilitation outcomes. SETTING: Eight inpatient rehabilitation facilities. PARTICIPANTS: A total of 314 consecutive admissions of persons with stroke, SCI, and TBI who received acute medical rehabilitation between 1994 and 1998. INTERVENTION: Calibration of motor and cognitive items from the FIM instrument, grouping of cases by number of weeks of rehabilitation (length of stay [LOS] groups), and plotting of weekly averages across time. MAIN OUTCOME MEASURES: Weekly motor and cognitive functional status. RESULTS: With the exception of cognitive functioning for persons with SCI, LOS was related to initial functional status, with patients with greater disability having longer LOS (eg, initial motor status for persons with stroke was 48.3 for those with a 2-week stay, 36.8 for a 6-week stay, with the averages between decreasing monotonically). With the exception of cognitive gains for person with TBIs, the amount of functional gain during rehabilitation was essentially the same for all LOS groups (eg, the overall average total motor gain for persons with SCI is 22.3, with no patterns of increase or decrease across LOS groups); however, the rate of improvement in motor (but not cognitive) functioning differed across LOS groups, with patients with shorter stays having the greater rates of improvement (eg, the overall average weekly motor gain for persons with SCI was 3.6, with the averages by LOS group monotonically decreasing from 6.4 for those with 4-week stays to 2.7 for those with 9-week stays). CONCLUSIONS: When examined separately for persons grouped by LOS, functional status improved linearly during the rehabilitation stay, with differences in rate of improvement depending on initial functional status.

Adult↗

Psychosocial issues for spouses of brain injury survivors.

Brain injury has a profound effect on the family system. When the survivor is a spouse, the impact is especially devastating. Roles in the family are changed, responsibilities are shifted and economic stability is often challenged. The noninjured spouse frequently faces these difficult circumstances without the customary support of his or her marriage partner. The cognitive and behavioral changes which are associated with brain injury alter the survivor as a person. This creation of a "new" member of the family system necessitates major adjustments as this individual is reincorporated into the family. It is not unusual for friction to develop between the noninjured spouse and the in-laws. Because the experience of spouses is different from the experience of parents of persons with brain injury they may benefit from a mutual support group exclusively for spouses.

Brain Injuries↗

Differential reinforcement of other behavior (DRO) to reduce aggressive behavior following traumatic brain injury.

Severe brain injury can result in significant neurobehavioral and social functioning impairment. In rehabilitation settings, behavioral problems of aggression and nonadherence to therapeutic activities can pose barriers to maximal recovery of function. Behavioral interventions seem to be effective in reducing problem behavior among individuals recovering from severe brain trauma, but well-controlled studies examining the efficacy of such interventions are sparse. This article presents a single-case, multiple-baseline study of a differential reinforcement of other behavior (DRO) procedure in a 28-year-old, brain-injured male with aggressive behavior problems. The procedure successfully reduced the frequency of problem behavior by up to 74%, maintained at 1-month follow-up. Implications of this intervention for individuals with brain injury are discussed, and testing of this procedure using a between-group design seems indicated.

Adult↗

The impact of hypercarbia on the evolution of brain injury in a porcine model of traumatic brain injury and systemic hemorrhage.

Carbon dioxide is perhaps the most potent available modulator of cerebrovascular tone and thus cerebral blood flow (CBF). These experiments evaluate the impact of induced hypercarbia on the matching of blood flow and metabolism in the injured brain. We explore the hypothesis that hypercarbia will restore the relationship of CBF to metabolic demand, resulting in improved outcome following traumatic brain injury (TBI) and hemorrhage. A behavioral outcome score, hemodynamic, metabolic, and pathologic parameters were assessed in anesthetized and ventilated juvenile pigs. Animals were assigned to either normocarbia or hypercarbia and subdivided into TBI (via fluid percussion) with or without hemorrhage. The experimental groups were TBI; TBI + 40% hemorrhage (40%H); TBI + hypercarbia (CO2); and TBI + 40%H + CO2. Hemorrhaged animals were resuscitated with blood and crystalloid. Hypercarbia was induced immediately following TBI using 10% FiCO2. The normocarbic group demonstrated disturbance of the matching of CBF to metabolism evidenced by statistically significant increases in cerebral oxygen and glucose extraction. Hypercarbic animals showed falls in the same parameters, demonstrating improvement in the matching of CBF to metabolic demand. Parenchymal injury was significantly decreased in hypercarbic animals: 3/10 hypercarbic versus 6/8 normocarbic animals showed cerebral contusions at the gray/white interface (p = 0.05). The hypercarbic group had significantly better behavioral outcome scores, 10.5, versus 7.3 for the normocarbic groups (p = 0.005). The decreased incidence of cerebral contusion and improved behavioral outcome scores in our experiments appear to be mediated by better matching of cerebral metabolism and blood flow, suggesting that manipulations modulating the balance of blood flow and metabolism in injured brain may improve outcomes from TBI.

Animals↗

Rapid and widespread microglial activation induced by traumatic brain injury in rat brain slices.

In order to assess the role of circulating blood in early microglial activation after traumatic brain injury (TBI), controlled cortical impact injury was applied to adult rat brain slices (400 microm in thickness) and the microglial response was examined. The complement receptor (CR3) expression and morphological transformation of the microglia were evaluated by OX42 immunohistochemistry. At 5 min following injury, activated microglia with intense CR3 expression appeared throughout the hemisphere on the injured side. In contrast, the morphology and CR3 expression of the microglia on the contralateral side were indistinguishable from those of the resident ramified microglia seen in normal brains. At 30 min following injury, microglial activation was more pronounced on the injured side, while the microglia on the contralateral side still retained a ramified morphology. These results are consistent with our previous observations made in in vivo experiments, which indicate that, as the brain slice paradigm excludes variables arising from the circulating blood, the rapid and widespread microglial activation observed following TBI can not be attributed exclusively to the infiltration of blood-borne macrophages or molecules. Rather this activation is most likely caused by intrinsic mechanisms within the brain tissue, such as traumatic depolarization.

Animals↗

The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury.

Traumatic brain injury is a common occurrence in the United States, leading to approximately 190,000 deaths or long-term disabilities. Following the primary insult, secondary disturbances in cerebral blood flow (CBF) and metabolism may have deleterious effects on potentially viable neurons. Recent studies evaluating CBF immediately following head injury have revealed flows low enough to produce cerebral ischemia. Hyperventilation is used routinely to lower suspected increased intracranial pressure (ICP). Aggressive hyperventilation produces a marked reduction in CBF, which may give rise to or exacerbate cerebral ischemia, thus enhancing rather than reducing secondary injury. This article reviews the role of hyperventilation in the treatment of increased ICP and its impact on cerebral ischemia following traumatic brain injury.

Animals↗

Molecular mechanisms in the pathogenesis of traumatic brain injury.

Traumatic brain injury (TBI) is a serious neurodisorder commonly caused by car accidents, sports related events or violence. Preventive measures are highly recommended to reduce the risk and number of TBI cases. The primary injury to the brain initiates a secondary injury process that spreads via multiple molecular mechanisms in the pathogenesis of TBI. The events leading to both neurodegeneration and functional recovery after TBI are generalized into four categories: (i) primary injury that disrupts brain tissues; (ii) secondary injury that causes pathophysiology in the brain; (iii) inflammatory response that adds to neurodegeneration; and (iv) repair-regeneration that may contribute to neuronal repair and regeneration to some extent following TBI. Destructive multiple mediators of the secondary injury process ultimately dominate over a few intrinsic protective measures, leading to activation of cysteine proteases such as calpain and caspase-3 that cleave key cellular substrates and cause cell death. Experimental studies in rodent models of TBI suggest that treatment with calpain inhibitors (e.g., AK295, SJA6017) and neurotrophic factors (e.g., NGF, BDNF) can prevent neuronal death and dysfunction in TBI. Currently, there is still no precise therapeutic strategy for the prevention of pathogenesis and neurodegeneration following TBI in humans. The search continues to explore new therapeutic targets and development of promising drugs for the treatment of TBI.

Brain Injuries↗

[The influences of propofol on different kinds of brain injuries in rat brain slices].

OBJECTIVE: To investigate the effects of propofol on the three kinds of brain injuries induced by metabolic disorder, neurotoxicity of excitatory amino acid, and oxygen-derived free radicals in rat cerebral cortical and hippocampal slices. METHODS: Slices of rat cerebral cortex and hippocampus were made and incubated in normal artificial cerebrospinal fluid (nACSF). Then the rat cerebral cortical and hippocampal slices were divided into 2 categories: propofol group, the slices in which were co-incubated with 5, 50, or 100 micro mol/L propofol for 3 hours, and 3 experimental injury groups. Each experimental injury group was further subdivided into 3 subgroups including the slices of 4 rats. Two hours after normal incubation the slices were co-incubated with 2,3,5-triphenyltetrazolium chloride (TTC). Formazan, the red crystal product were extracted, and ELISA reader was used to read the absorbance at 490 nm (A(490)) so as to quantitatively evaluate the degree of injury. RESULTS: The values of A(490) of the slices co-incubated with propofol of different concentrations were not significantly different. Compared with those of the control subgroups, the values A490 were significantly decreased in the cerebral cortical and hippocampus slices damaged by OGD, glutamate, and H(2)O(2) injuries (all P < 0.01). The values of A(490) in the subgroups of low and middle concentrations (5 and 50 micro mol/L) of propofol plus OGD or glutamate injury were not significantly different from those of the subgroups of OGD or glutamate injury alone, both in cerebral cortical and hippocampal slices. However, the values of A(490) in the subgroups of high concentration of propofol (100 micro mol/L) plus OGD or glutamate injury was further decreased (P < 0.01). The values of A(490) in the subgroups of low and middle concentrations of propofol plus H(2)O(2) injury were significantly higher than those of the injury subgroup (all P < 0.01), however, however, the values of A490 in the high concentration propofol plus H(2)O(2) injury subgroup were significantly lower than those of the control group (all P < 0.01), even lower than that of the subgroup of H(2)O(2) injury alone. CONCLUSION: Propofol has a neuroprotective effect against hydrogen peroxide injury at low and middle concentrations. Propofol of low and middle concentrations does not improve the decrease of the value of A(490). however, propofol of high concentration augments the oxygen-glucose deprivation and glutamate injuries both in the rat cerebral cortical slices and hippocampal slices.

Animals↗

Epidemiology and outcomes of pediatric traumatic brain injury.

Traumatic brain injury is a leading cause of death and disability in the pediatric age group. Causes of injury vary with child developmental age, with more inflicted injuries in infants, fall-related injuries among toddlers, sports-related injuries among middle-school-aged children and motor vehicle crashes in older children. Prevention strategies exist for some pediatric traumatic brain injury; however, all suffer from lack of compliance and enforcement. Neuropsychological and behavioral outcomes for injured children vary with the severity of injury, child age at injury, premorbid child characteristics, family factors and the families' socioeconomic status. Each of these factors needs to be taken into account when designing rehabilitation strategies and assessing factors related to outcome.

Accidental Falls↗

A population-based outcomes study of persons hospitalized with traumatic brain injury: operations of the South Carolina Traumatic Brain Injury Follow-up Registry.

OBJECTIVE: To describe the design and operations of the South Carolina Traumatic Brain Injury (TBI) Follow-up Registry. DESIGN: Statewide prospective cohort study. SETTING: State of South Carolina. PARTICIPANTS: 2118 persons discharged from acute care hospitals after experiencing TBI. INTERVENTION: Telephone interviews. MAIN OUTCOME MEASURES: Service needs, alcohol and drug use, psychosocial health, health-related quality of life, functional status, symptoms of TBI, employment, global life satisfaction, and death. RESULTS: Selected initial and 1-year follow-up findings concerning demographic, insurance status, income, and employment factors. CONCLUSIONS: Population-based outcome studies that describe longer term problems associated with TBI, the need for services, and estimated disability could be useful to inform public policy.

Activities of Daily Living↗

Neuropsychiatric Aspects of Traumatic Brain Injury.

Traumatic brain injury (TBI) may produce a variety of neuropsychiatric problems, including impaired cognition, depression, mania, affective lability, irritability, anxiety, and psychosis. Despite the common occurrence of these symptoms following TBI, there are relatively few studies that provide clear guidance regarding management. Many symptoms (eg, irritability, affective lability, fatigue, sleep disturbance, and impaired cognition) are primarily consequences of brain injury rather than symptoms of a comorbid psychiatric disorder such as major depression. Although it is difficult to study the complicated treatments needed for such symptom complexes, we are able to recommend an approach to the evaluation and treatment of neuropsychiatric problems following traumatic brain injury. A thorough assessment of the patient is a prerequisite to the prescription of any treatment. This assessment should include a thorough developmental, psychiatric, and medication history; a detailed mental status examination; a complete neurologic examination; and quantification of neuropsychiatric symptoms using standardized and accepted inventories (eg, Neurobehavioral Rating Scale, Neuropsychiatric Inventory ). All symptoms must be evaluated in the context of the patient's premorbid history and current treatment because neuropsychiatric symptoms may be influenced by either factor or by both factors. Psychotherapy is an important component of the treatment of neuropsychiatric problems following TBI. Additionally, patients should be encouraged to become involved with local TBI support groups. When medications are prescribed, it is essential to use cautious dosing (low and slow) and empiric trials with continuous reassessment of symptoms using standardized scales and monitoring for drug-drug interactions. In general, medications with significant sedative, antidopaminergic, and anticholinergic properties should be avoided, and benzodiazepines should be used sparingly, if at all. Although patients with TBI may be particularly susceptible to adverse effects of psychopharmacologic medications, at times dosages similar to those used for the non-brain-injured psychiatric patient may be needed. When a single medication does not provide adequate relief of symptoms or cannot be tolerated at therapeutic doses, an alternative strategy is to augment the effect of one medication by using a second low-dose agent with a different mechanism of action.

Journal Article↗

Influence of Angiotensin-converting enzyme polymorphism on neuropsychological subacute performance in moderate and severe traumatic brain injury.

Traumatic brain injury (TBI) frequently results in cerebrovascular lesions that may increase secondary damage and cause neuropsychological impairment. Previous studies suggest an association among the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE), cardiovascular disease, and cognitive performance. Clinical and experimental studies have demonstrated the beneficial effects of ACE inhibitor treatment on vascular injury, hypertension, brain ischemia, and cognitive functioning. In a sample of 73 moderate and severe TBI patients, the authors assessed whether cognitive sequelae differed in relation to the ACE I/D polymorphism. D allele carrier patients performed worse than those with I/I polymorphism on tests involving attention and processing speed. Findings suggest that the physiopathological changes associated with TBI may have greater consequences in ACE D allele carriers.

Adolescent↗