This New Zealand study used a grounded theory methodology to explore the day-to-day occupations of family caregiving for children who had sustained a traumatic brain injury. Semi-structured interviews and participant observations were employed to gather data from five families including children of pre-school and school age and their parents. Constant comparative analysis of the data revealed a central caregiving category, Structuring For Security, which encompassed two simultaneous and interdependent caregiving processes. A model is presented illustrating the processes.Structuring For Security describes the way the parents' caregiving is directed towards building a framework that provides for the present and future safety and success of their children. Holding Things Together explains endeavours to contain the distressing events resulting from the accident, with a focus on protecting the children from physical and emotional dangers. Joining My Child With Others explains what is happening when parents set things up for their children to spend time in activity with other people. The two processes are mediated by support from others, and involve learning and use of practical knowledge about the child. Successful implementation of the processes results in parents' increasing awareness of their ability to cope, progress in the children, and children's successful participation with other people. Participation in the processes is ongoing, responding to change in the child and in the environment.The study findings suggest a basis for the development of a framework that families and clinicians might use to guide caregiving for children after a traumatic brain injury. The findings also indicate the importance of supporting parents in developing effective caregiving structures that fit with their concerns for their children's safety and success with others. Consideration needs to be given to policies that take into account the safety issues involved for children and the support needs of parents following the accident.

This New Zealand study used a grounded theory methodology to explore the day-to-day occupations of family caregiving for children who had sustained a traumatic brain injury. Semi-structured interviews and participant observations were employed to gather data from five families including children of pre-school and school age and their parents. Constant comparative analysis of the data revealed a central caregiving category, Structuring For Security, which encompassed two simultaneous and interdependent caregiving processes. A model is presented illustrating the processes.Structuring For Security describes the way the parents' caregiving is directed towards building a framework that provides for the present and future safety and success of their children. Holding Things Together explains endeavours to contain the distressing events resulting from the accident, with a focus on protecting the children from physical and emotional dangers. Joining My Child With Others explains what is happening when parents set things up for their children to spend time in activity with other people. The two processes are mediated by support from others, and involve learning and use of practical knowledge about the child. Successful implementation of the processes results in parents' increasing awareness of their ability to cope, progress in the children, and children's successful participation with other people. Participation in the processes is ongoing, responding to change in the child and in the environment.The study findings suggest a basis for the development of a framework that families and clinicians might use to guide caregiving for children after a traumatic brain injury. The findings also indicate the importance of supporting parents in developing effective caregiving structures that fit with their concerns for their children's safety and success with others. Consideration needs to be given to policies that take into account the safety issues involved for children and the support needs of parents following the accident.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. Linköping : Linköpings universitet, 2007.

Afhandling, Linköpings universitet, 2007.

INTRODUÇÃO: Estudos indicam que a morte encefálica está associada com alterações hemodinâmicas, hormonais e inflamatórias, comprometendo a viabilidade dos órgãos para o transplante. Porém, é necessário esclarecer quais destas alterações são decorrentes da morte encefálica e quais são devidas ao trauma associado. Este estudo tem por objetivo avaliar a microcirculação mesentérica, quantificar marcadores sistêmicos da resposta inflamatória, e analisar as alterações histopatológicas em ratos submetidos à morte encefálica comparados com ratos falso-operados. MÉTODOS: Ratos Wistar machos (300 50 g), anestesiados com isoflurano (5-2 %), foram intubados e mecanicamente ventilados (10 mL/kg, 70 ciclos/min). Através de uma trepanação, um cateter Fogarty® 4 F foi inserido no espaço intracraniano e rapidamente insuflado com 500 L de água para indução da morte encefálica. Após a indução da morte encefálica o anestésico foi retirado e os animais receberam solução salina 0,9 % endovenosa (2 mL/h). Animais falso-operados foram apenas trepanados. Pressão arterial média e frequência cardíaca foram monitoradas ao longo de todo tempo de experimento. Após 30, 180 ou 360 min, foram avaliados os seguintes parâmetros: 1) avaliação da perfusão e interação leucócito-endotélio na microcirculação mesentérica por técnica de microscopia intravital; 2) expressão de moléculas de adesão endoteliais (P-selectina e ICAM-1) por imunohistoquímica; 3) quantificação das citocinas (TNF-?, IL-1?, IL-6, e IL-10), quimiocinas (CINC-1 e CINC-2) e corticosterona séricas; 4) determinação do leucograma, hematócrito e gasometria; 5) avaliação histológica do coração, pulmão, fígado e rim. RESULTADOS: A morte encefálica resultou em imediato pico hipertensivo seguido de episódio de hipotensão, associado com queda na perfusão mesentérica para aproximadamente 30% de microvasos com fluxo sanguíneo normal (p<0,0001). A interação dos leucócitos com o endotélio apresentou um menor número de leucócitos rollers (p<0,0001), com maior migração leucocitária (p=0,03) para o tecido perivascular de ratos com morte encefálica, decorridos 180 min de experimento. A expressão de P-selectina não diferiu entre os grupos, enquanto que ICAM-1 teve sua expressão aumentada na terceira hora após a indução da morte encefálica (p<0,01). As concentrações séricas de citocinas e quimiocinas foram iguais entre animais com morte encefálica e falso-operados. Observou- se queda acentuada nos níveis séricos de corticosterona de animais com morte encefálica após 3 h de experimento (p<0,0001). O número de leucócitos totais nos animais com morte encefálica foi menor quando comparado com animais falso-operados (p<0,05), sendo observado aumento na razão neutrófilo/linfócito, após 3h de experimento, em ambos os grupos. Não foram observadas alterações significativas nos dados gasométricos e hematócrito. A morte encefálica induziu alterações histopatológicas nos quatro órgãos avaliados, sendo observada congestão vascular no coração (p=0,02) e pulmão (p=0,02), edema alveolar pulmonar (p=0,001), infiltrado leucocitário no fígado (p=0,01), e edema tubular renal (p=0,04). CONCLUSÕES: A morte encefálica desencadeou instabilidade hemodinâmica associada com hipoperfusão tecidual, além de queda na concentração de corticosterona endógena, resultando em aumento da expressão de ICAM-1 com maior migração de leucócitos na microcirculação mesentérica, além de leucopenia. Os órgãos sólidos apresentaram maior congestão vascular, sendo que os pulmões foram os órgãos mais comprometidos / BACKGROUND: Studies indicate that brain death is associated with hemodynamic, hormonal and inflammatory alterations, compromising the viability of organs to transplantation. However, it is necessary to clarify which of these alterations are consequences of brain death and which are due to brain death-associated trauma. This study aims to evaluate the mesenteric microcirculation, quantify systemic markers of the inflammatory response, and analyze the histopathological changes in rats submitted to brain death compared with sham operated animals. METHODS: Male Wistar rats (300 50 g) anesthetized with isoflurane (5-2 %) were intubated and mechanically ventilated (10 mL/kg, 70 breaths/min). Through trepanation, a Fogarty 4 F catheter was inserted intracranially and quickly inflated with 500 L of water to induce brain death. After brain death confirmation, anesthesia was stopped and the animals received 0.9 % saline solution intravenously (2 mL/h). Sham operated animals were just trepanned. Mean arterial blood pressure and heart rate were continuously monitored. After 30, 180 or 360 min, the following parameters were evaluated: 1) perfusion of microvessels and leukocyte- endothelial interactions in the mesenteric microcirculation by intravital microscopy; 2) expression of endothelial adhesion molecules (P-selectin and ICAM-1) by immunohistochemistry; 3) quantification of serum cytokines (TNF-?, IL-1?, IL-6 and IL-10), chemokines (CINC-1 and CINC-2), and corticosterone; 4) determination of white blood cell counts, hematocrit, and blood gases; 5) histological assessment of heart, lung, liver, and kidney. RESULTS: Brain death induced an immediate hypertensive peak followed by hypotension associated with a reduction in mesenteric perfusion to 30% of microvessels with normal blood flow (p<0.0001). Number of rolling leukocytes was reduced (p<0.0001), and migrated leukocytes to perivascular tissue increased after 180 min (p=0.03). The expression of P-selectin did not differ between groups, whereas the expression of ICAM-1 was increased 3 h after brain death induction (p<0.01). Increased serum concentrations of cytokines and chemokines were observed in both brain death and sham operated rats. Brain death rats showed a decrease in serum corticosterone levels after 3 h (p<0.0001). Total white blood cell counts in brain death rats was reduced when compared with sham operated rats (p<0.05), associated with an increase in neutrophil/lymphocyte ratio after 3 h in both groups. No significant changes in hematocrit and blood gases were observed. Brain death induced histopathological alterations in the evaluated organs: vascular congestion in the heart and lungs (p=0.02), pulmonary alveolar edema (p=0.001), leukocyte infiltration in the liver (p=0.01), and renal tubular edema (p=0.04). CONCLUSIONS: Brain death triggered hemodynamic instability associated with tissue hypoperfusion, and a decrease in the concentration of endogenous corticosterone, resulting in increased expression of ICAM-1 with increased migration of leukocytes at mesenteric microcirculation, associated with a paradoxical leukopenia. The main histopathological alteration in brain death rats was vascular congestion, and the lungs are the most compromised organs

INTRODUÇÃO: O Traumatismo Cranioencefálico (TCE) é uma das maiores causas de mortalidade e incapacidade em adultos em todo o mundo. Uma complicação frequente e precoce do TCE é o desenvolvimento de hipertensão intracraniana, cujo diagnóstico e tratamento intensivo geralmente requer monitorização invasiva da pressão intracraniana (PIC); o interesse científico neste campo é crescente. Neste contexto, estudos recentes têm demonstrado que é possível detectar hipertensão intracraniana de forma não-invasiva através da aferição ultrassonográfica do diâmetro da bainha do nervo óptico (BNO), utilizando-se ultrassonografia do nervo óptico (USNO) com insonação pela janela transorbitária. Não se sabe ainda, entretanto, se essa aferição do diâmetro da BNO por USNO tem um real significado prognóstico quando aplicada em pacientes na fase aguda de um TCE. Neste estudo, objetiva-se avaliar o valor prognóstico da aferição do diâmetro da BNO por USNO, avaliada na admissão, em pacientes vítimas de TCE moderado e grave. MÉTODOS: Avaliaramse prospectivamente pacientes vítimas de TCE moderado ou grave (pontuação < 15 na escala de coma de Glasgow [GCS] ou com lesão intracraniana aguda na tomografia de crânio) admitidos na Unidade de Emergência do HCFMRP-USP, com idades entre 18 e 80 anos, de fevereiro/2015 a julho/2015. Após consentimento livre e esclarecido, estes pacientes foram submetidos a avaliação clínica com escalas padronizadas (NOS-TBI), e radiológica (incluindo tomografia de crânio e USNO) e seguidos até sua alta para avaliação cega do seu desfecho funcional (avaliada pela escala modificada de Rankin [mRS]). Após análise univariada, utilizou-se regressão linear e regressão logística multivariada, para identificação de preditores independentes do déficit neurológico (NOS-TBI) e da incapacidade funcional na alta (mRS). Aplicou-se, ainda, curva ROC e estatística C para avaliar a acurácia da USNO em relação incapacidade grave ou óbito intra-hospitalar. RESULTADOS: 70 pacientes foram analisados, sendo 63 (90%) homens, idade média 37,5 ± 15,1 anos, sendo 32 (45%) pacientes com TCE grave e 29 (41%) causados por acidentes de trânsito. Na análise multivariada por regressão linear, o diâmetro médio da BNO (B=4,8; IC 95%: 0,51 a 9,1; p=0,029) e a gravidade do comprometimento do nível de consciência (GCS) na admissão (B=-1,97; IC 95%: -2,9 a -1,0; p<0,001) foram os únicos preditores independentes da severidade do déficit neurológico na alta pela escala NOS-TBI. Na regressão logística multivariada, o diâmetro médio da BNO (OR:2,1; IC 95%:1,1 a 3,9; p=0,021) foi independentemente associado com um escore de mRS>=4 à alta, mesmo após ajuste para idade e GCS na admissão. CONCLUSÕES: Uma maior distensão da bainha do nervo óptico nas primeiras 24 após TCE moderado a grave está independentemente associada a pior déficit neurológico e capacidade funcional à alta. Esses resultados sugerem que a USNO deve ser mais explorada como método com potencial para orientar medidas terapêuticas intensivas de neuroproteção e controle de hipertensão intracraniana na fase aguda do TCE. / BACKGROUND: Traumatic brain injury (TBI) is a major cause of mortality and disability among adults worldwide. Intracranial hypertension is a frequent and early complication in such patients and its diagnosis and intensive management often require invasive monitoring of intracranial pressure (ICP). In this context, recent studies have shown that it is possible to non-invasively detect intracranial hypertension by ultrasound measurement of optic nerve sheath diameter (ONSD), using optic nerve ultrasound (ONUS) with trans-orbital window insonation. It is still unclear, however, whether the ONSD measurement through ONUS has real prognostic significance when applied to patients in the acute phase of a TBI. In this study, we aimed to evaluate the prognostic value of ONSD measurement by ONUS at admission in patients with moderate and severe TBI. METHODS: We prospectively evaluated patients with moderate or severe TBI (score <15 Glasgow Coma Scale [GCS] or acute intracranial lesion on CT scan) admitted to the Emergency Unit of HCFMRP- USP, aged 18 to 80 years, from February / 2015 to July / 2015. After informed consent, these patients underwent clinical evaluation with standardized scales (NOS-TBI), and radiological (including CT scan and ONUS), and blinded functional outcome assessment at discharge (assed by modified Rankin Scale - mRS). After univariate analysis, we used linear regression and multivariate logistic regression to identify independent predictors of neurological deficit at discharge (NOS-TBI and mRS). We also used ROC Curves and C statistics to evaluate the accuracy of different ONSD cut-offs to identify severe disability and death at discharge. RESULTS: We analyzed 70 patients, 63 (90%) men, mean age 37.5 ± 15.1 years, 32 (45%) with severe TBI, 29 (41%) caused by traffic accidents. After multivariate linear regression analysis, the average diameter of the ONSD (B=4.8; IC 95%: 0.51 a 9.1; p=0.029) and the severity of consciousness impairment (GCS) at admission (B=-1,97; IC 95%: -2,9 a -1,0; p<0,001) were the only independent predictors of neurological deficit severity by the NOS-TBI scale at discharge. On multivariate logistic regression analysis, after age and GCS adjust, the mean ONSD was independently associated with a mRS>=4 at discharge. CONCLUSIONS: Increased distension of the optic nerve sheath in the first 24 after a moderate to severe TBI is independently associated with a worse neurological and functional outcome at discharge. Our results indicate that additional studies should be performed to test ONUS as a method with potential to guide intensive therapeutic measures of neuroprotection and intracranial hypertension control in the acute phase after TBI.

<p> Traumatic Brain Injury (TBI) is one of the most prevalent causes of injury in young adults,  and is a leading cause of hospitalization, disability, and even death. Although severe TBI can lead  to serious acute injury (such as brain hemorrhaging and skull fractures) and chronic disability, the vast majority (~80%) of TBIs are mild in nature, and do not present with such drastic symptoms.  As such, these mild TBIs may go undiagnosed or underreported. Without overt, acute symptoms,  mild TBIs may be particularly insidious as they are shown to correlate with increased risk of  chronic social and cognitive processing impairments, as well as the risk of developing  neurodegenerative diseases later in life. Additionally, many people who suffer TBIs, whether on  the sports field, field of battle, or even in everyday life, often are at increased risk of additional  TBIs, which likely increase the risk of life-long post injury complications. Given these risk factors,  there is a clear need to understand how mild TBIs affect the brain both acutely and chronically and  develop tactics to properly diagnose and treat mild injuries early.  In this dissertation, we argue for the potential use of Auditory Evoked Potentials (AEPs), a  clinically used noninvasive set of tests, as an effective route for improved diagnostics of mild TBIs.  To achieve this, we must first understand the relationship between underlying anatomical changes  and chronic deficits in mild injury. In blast induced TBIs, some of the most common sequalae,  both acutely and chronically, are auditory in nature. Temporary changes in hearing thresholds or  tinnitus are very common, but chronic impairments in more complex auditory processing tasks,  such as hearing speech-in-noise, are often reported as well. Although acute changes are likely due  to damage to the peripheral auditory system, there is mounting evidence suggesting damage to central auditory regions may play a clear role in chronic processing changes, however, this is still  poorly understood. Recent studies of concussions in sports medicine have found that impact  induced TBIs may produce long-term, but not acute, deficits in subtle auditory processing function  as well. Given its potential for ubiquitous damage following TBIs of multiple forms, understanding  the post-injury central auditory system can act as a window into the time-course and severity of  secondary biochemical changes and chronic processing issues seen following mild TBI.  Here we use a well-established rat blast TBI model to examine the acute and chronic time  course of auditory processing changes, as well as biochemical and anatomical changes. We show  a clear biphasic response of acute and chronic changes in auditory processing. Changes in  oxidative stress, inflammation, and inhibition/excitation show similar patterns within key regions  of the central auditory system (CAS), suggesting a link between AEP results and underlying  chronic damage. Our second objective was to design a more clinically relevant and consistent  animal model of free-range of motion impact induced TBI. Once developed, we examined similar  AEP and immunohistochemical tests to determine the degree of similarity of CAS changes in a  second form of TBI. Interesting, while AEP results suggest some long-term changes in auditory  processing, these were not identical to blast changes. Finally, we utilized a computational model  for axonal node damage to assess one method of potential damage resulting from the oxidative  stress changes post injury and provides a framework for future modeling techniques for improved  diagnosis and treatment. These results together suggest that AEPs have the potential to improve  diagnostics and monitoring tools in mild TBIs, regardless of injury type.  </p>

Background: Play is the child’s natural world. According to psychoanalytical studies, play has an important role in children’s development, and the absence of play during a child’s life could lead to severe pathological implications. Based on this theory and being aware that physiotherapy treatment programs could be long lasting, tiresome and lacking motivation for children, this literature review presents a perspective regarding the integration of play within physiotherapy programs and examines the physical and emotional outcomes during this integration. Aim: To investigate the outcomes of integrating play in physiotherapy for children with chronic health conditions. Method: The research strategy for this review was a thorough search of peer-reviewed articles in the databases CINAHL and AMED which include articles from the fields of allied and complementary medicine, as well as the database Scope Med. Participants were children with chronic health conditions, ranging from 2-18 years old. In the term ‘play’ virtual reality and video game activities were included due to the lack of research. In addition, articles from a previous literature review conducted by the author were also included in the present paper. Results: The focus of researchers on children with CP and the lack of evidence for children with other health conditions, the persistence of physiotherapists to assess mainly physical outcomes and not emotional needs of children, and the measurement tools used for this purpose are presented. Conclusions: For children with chronic health conditions who attend physiotherapy sessions, play could serve as a mediate and an appropriate developmental approach in order to achieve physical and emotional changes. There is a need for physiotherapists to balance physical and emotional needs, and have a more ‘human’ relationship, rather than a ‘bodily’ - strict professional relationship with children. Although the information presented in this review is not considered as sufficient to draw conclusions, it could serve as a first step for researchers to study this integration in greater depth, and to focus on children with conditions other than CP.

O traumatismo cranioencefálico (TCE) constitui um dos principais problemas de saúde pública mundial e as suas características variam de acordo com a população envolvida, sendo de suma importância o conhecimento de dados demográficos da mesma para que sejam adotadas medidas de prevenção efetivas. Tivemos como objetivos a descrição de dados demográficos e tomográficos em pacientes vítimas de TCE e a correlação entre idade, sexo, escala de Glasgow e dados tomográficos com a mortalidade em curto prazo. Neste estudo transversal e prospectivo realizado em pacientes vítimas de TCE admitidos na Unidade de Emergência Dr. Armando Lages, Maceió, Alagoas, foram incluídos 623 pacientes para descrição dos dados demográficos e 451 pacientes, para a análise de correlação; realizada por meio da Análise de Correlação de Spearman e de análise multivariada através de regressão logística. Foi constatada uma razão masculino/feminino geral de 3,54: 1 e a faixa etária mais acometida foi a de 21 a 30 anos. Os principais mecanismos do trauma foram os acidentes relacionados com meio de transporte motorizado (35,15%), as quedas (32,59%) e as agressões com ou sem armas (22,79%). As alterações mais comuns no TCE leve foram o hematoma subgaleal e/ou palpebral (48,5%), as fraturas (28,3%) e as contusões cerebrais (12,2%). No TCE moderado, as alterações mais freqüentes foram o hematoma subgaleal/palpebral (68,9%), fraturas (43,2%), contusão cerebral (33,7%) e hemorragia subaracnóide (HSA) (28,4%). No TCE grave, as anormalidades mais comuns foram a a HSA (71,1%), o hematoma subgaleal e/ou palpebral (68,9%), as fraturas (64,4%), contusões cerebrais (53,3%) e edema difuso (53,3%). As variáveis relacionadas com a mortalidade, por meio da análise univariada, foram a pontuação 3 na escala de Glasgow, presença de anormalidades tomográficas, de hematoma subdural (HSD), de HSA, apagamento/assimetria de cisternas basais, desvio da linha média, edema difuso, hemorragia intraventricular (HIV), presença de projétil ou estilhaços de arma de fogo. As variáveis sexo, faixa etária e hematoma extradural não apresentaram correlação estatisticamente significante com mortalidade neste estudo. As variáveis preditoras de mortalidade, na análise multivariada, foram valores baixos na escala de Glasgow, presença de anormalidades tomográficas, desvio da linha média e edema difuso. Em conclusão, os pacientes vítimas de TCE apresentaram uma predominância do masculino, numa razão M/F média de 3,54: 1,da faixa etária entre 21 a 30 anos e as causas mais freqüentes de TCE foram a queda de altura, o atropelamento e a agressão física. As características tomográficas mais freqüentes nos grupos de TCE leve e moderado foram: o hematoma subgaleal e/ou palpebral, fratura óssea e contusão cerebral. No TCE grave as lesões mais freqüentes foram a HSA, o hematoma subgaleal e/ou palpebral, fratura óssea, contusão cerebral e edema difuso. Os fatores relacionados com maior mortalidade na análise univariada foram: baixa pontuação na escala de Glasgow, pontuação 3 na escala de Glasgow, presença de anormalidades tomográficas, presença de HSA, presença de HSD, apagamento/assimetria de cisternas basais, desvio linha média, edema difuso, HIV e presença de projétil ou estilhaços de arma de fogo. Na análise multivariada: baixa pontuação na escala de Glasgow, presença de anormalidades tomográficas, presença de desvio da linha média, presença de edema difuso. / The traumatic brain injury (THI) is a major public health concern worldwide. Preventive measures to tackle the problem can be taken after analyzing demographic data and the types of injury affecting the population at hand. Our aim was to outline the demographic and tomographic data from THI victims and determine how tomography findings, age, gender, and Glasgow Coma Scale (GCS) are associated to short-term mortality. The THI patients in this cross-sectional and prospective study had been admitted to the Armando Lages Emergency Care Unit in Maceió, Alagoas. The study comprised 623 patients, who had been clinically diagnosed with THI. A total of 451 patients were included in the investigation into the correlation of computer tomography, age, gender, GCS, and mortality. Both the Spearman Correlation Analysis, and logistic regression multivariate analysis were used. The overall male:female ratio was 3.54, with 78.01% of the victims male and 21.99% female. Most patients fell within the 21 to 30 age bracket. Traffic accidents (35.15%) were the leading cause of head injury, followed by falls (32.59%), and physical assault (22.79%). Tomographic abnormalities were seen in 63.7% of victims of mild THI, the most common being subgaleal and eyelid hematoma (48.5%), skull fractures (28.3%), and cerebral contusion (12.2%). Moderate THI produced tomographic abnormalities in 83.4% of victims, the most frequent being subgaleal and eyelid hematoma (68.9%), fractures (43.2%), cerebral contusion (33.7%), and subarachnoid hemorrhage (SAH) (28.4%). Computer tomography of the skull showed alterations for all victims of severe THI, the most often being subgaleal and eyelid hematoma (68.9%), followed by SAH (71.1%), skull fractures (64.4%), cerebral contusion (53.3%), diffuse brain swelling (53.3%). Univariate analysis attested that a score 3 on the GCS, the presence of tomographic abnormalities, subdural hematoma (SDH), SAH, absent or compressed basal cisterns, midline shift, diffuse brain swelling, intraventricular hemorrhage (IVH), and the presence of a projectile or shell splinters had an statistically significant correlation with short-term mortality. In this study, gender, age group, and large extradural hematoma had no statistical significance as predictive factors for mortality. In a multivariate analysis, the variables that accounted for mortality were low GCS scores, the presence of tomographic abnormalities, midline shift, and diffuse brain swelling. It can be concluded that males were the predominant victims in THI cases, with the M:F ratio at 3.54. Most affected were individuals aged 21 to 30, and the most common causes of THI were falls, being run over by a vehicle, and physical assault. The most frequent tomographic characteristics in the mild and moderate THI cases were subgaleal and/or eyelid hematoma, skull fracture and cerebral contusion. The most common injuries in severe THI patients were subgaleal and/or eyelid hematoma, SAH, skull fracture, cerebral contusion, and diffuse brain swelling. The factors most closely linked to higher mortality after univariate analysis were low GCS scoring, a score 3 on the GCS, the presence of tomographic abnormalities, the presence of SAH, the presence of SDH, absent or compressed basal cisterns, midline shift, diffuse brain swelling, IVH, and the presence of a projectile or shell splinters. After multivariate analysis: low scoring on the GCS and the presence of tomographic abnormalities, midline shift, and diffuse brain swelling.