Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 1.880
Filtrar
1.
Medicine (Baltimore) ; 99(49): e22452, 2020 Dec 04.
Artigo em Inglês | MEDLINE | ID: mdl-33285671

RESUMO

RATIONALE: Limb-kinetic apraxia (LKA) is a disorder of movement execution that is a result of injury to the corticofugal tracts (CFTs) from the secondary motor area. We report on a patient with traumatic brain injury (TBI) and complete monoplegia due to LKA, which was mainly ascribed to injury of the CFT from the secondary motor area using diffusion tensor tractography. PATIENT CONCERNS: A 35-year-old male was struck by a car from the side during riding an autocycle and received direct head trauma as a result of falling to ground. He lost consciousness for approximately 1 month and experienced continuous post-traumatic amnesia after the accident. The patient's Glasgow Coma Scale score was 3 and he showed quadriparesis including complete monoplegia of his left arm since the onset of TBI. DIAGNOSES: The patient diagnosed complete monoplegia due to LKA after traumatic brain injury. INTERVENTIONS: He underwent conservative management for TBI followed by rehabilitation at approximately 2 months after onset. OUTCOMES: At 32-month after onset, weakness on left arm (Manual Muscle Test [MMT]:0) and partial weakness of left leg (MMT:3). OUTCOMES: Results of electromyography and nerve conduction studies of left extremities were normal. Motor evoked potential values obtained from the abductor pollicis brevis muscle (APB) were: right APB latency 22.3msec, amplitude 1.6mV; left APB latency 22.8msec, amplitude 1.5mV. After 2 weeks of administration of dopaminergic drugs for improvement of LKA, left arm weakness had recovered to level that permitted movement against gravity (MMT:3). Diffusion tensor tractography at 32-month after onset showed right corticospinal tract discontinuation at the pontine level and partial tearing of the left corticospinal tract at the subcortical white matter. In addition, the left CFT from the supplementary motor area showed partial tearing at the subcortical white matter. LESSONS: The LKA due to injury of the left supplementary motor area-CFT was demonstrated in a patient with complete monoplegia following TBI. Accurate diagnosis of LKA is important for successful rehabilitation because LKA is known to respond to dopaminergic drug treatment.


Assuntos
Apraxia Ideomotora/complicações , Lesões Encefálicas Traumáticas/complicações , Hemiplegia/etiologia , Adulto , Escala de Coma de Glasgow , Hemiplegia/reabilitação , Humanos , Masculino
3.
Artigo em Inglês | MEDLINE | ID: mdl-33233364

RESUMO

BACKGROUND: Traumatic brain injury (TBI) is commonly associated with cardiac dysfunction, which may be reflected by abnormal electrocardiograms (ECG) and/or contractility. TBI-related cardiac disorders depend on the type of cerebral injury, the region of brain damage and the severity of the intracranial hypertension. Decompressive craniectomy (DC) is commonly used to reduce intra-cranial hypertension (ICH). Although DC decreases ICH rapidly, its effect on ECG has not been systematically studied. The aim of this study was to analyze the changes in ECG in patients undergoing DC. METHODS: Adult patients without previously known cardiac diseases treated for isolated TBI with DC were studied. ECG variables, such as: spatial QRS-T angle (spQRS-T), corrected QT interval (QTc), QRS and T axes (QRSax and Tax, respectively), STJ segment and the index of cardio-electrophysiological balance (iCEB) were analyzed before DC and at 12-24 h after DC. Changes in ECG were analyzed according to the occurrence of cardiac arrhythmias and 28-day mortality. RESULTS: 48 patients (17 female and 31 male) aged 18-64 were studied. Intra-cranial pressure correlated with QTc before DC (p < 0.01, r = 0.49). DC reduced spQRS-T (p < 0.001) and QTc interval (p < 0.01), increased Tax (p < 0.01) and changed STJ in a majority of leads but did not affect QRSax and iCEB. The iCEB was relatively increased before DC in patients who eventually experienced cardiac arrhythmias after DC (p < 0.05). Higher post-DC iCEB was also noted in non-survivors (p < 0.05), although iCEB values were notably heart rate-dependent. CONCLUSIONS: ICP positively correlates with QTc interval in patients with isolated TBI, and DC for relief of ICH reduces QTc and spQRS-T. However, DC might also increase risk for life-threatening cardiac arrhythmias, especially in ICH patients with notably prolonged QTc before and increased iCEB after DC.


Assuntos
Arritmias Cardíacas/etiologia , Lesões Encefálicas Traumáticas/cirurgia , Craniectomia Descompressiva/métodos , Hipertensão Intracraniana/cirurgia , Adolescente , Adulto , Arritmias Cardíacas/fisiopatologia , Lesões Encefálicas Traumáticas/complicações , Eletrocardiografia , Feminino , Humanos , Hipertensão Intracraniana/etiologia , Pressão Intracraniana , Masculino , Pessoa de Meia-Idade , Resultado do Tratamento , Adulto Jovem
4.
Medicine (Baltimore) ; 99(43): e22742, 2020 Oct 23.
Artigo em Inglês | MEDLINE | ID: mdl-33120775

RESUMO

The treatment of severe traumatic brain injury (TBI) with brain herniation is challenging because outcomes are often associated with high mortality and morbidity. Our aim was to identity factors contributing to decompressive craniectomy (DC) and evaluate treatment outcomes in patients with severe TBI with brain herniation.In this retrospective study, we analyzed medical records of severe TBI with brain herniation from May 2009 to December 2013. We reviewed their demographic data, mechanism of injury, Glasgow Coma Scale (GCS) score, pupil status, computed tomography findings, surgical treatment methods, time interval between brain herniation and surgery, as well as outcomes. GCS and pupil status are clinical parameters for detecting increase intracranial pressure while brain parenchyma bulged above the inner plate of the skull during operation indicated brain swelling as well as increased intracranial pressure on which basis the decision to perform DC or craniotomy was determined intraoperatively.One hundred ninety-four patients were included in the study. We performed DC in 143 of the patients while 51 of them we performed craniotomy. There were no statistically significant differences in the age, gender, or injury mechanism between the 2 groups. GCS, pupillary dilation, midline shift, hematoma type and timing of surgery were associated with DC. Nevertheless, logistic regression analysis revealed that hematoma type and timing of surgery were significantly associated with favorable DC outcomes (P < .001 and P = .023). Subdural hematoma and timing of surgery >1 hour were both identified as risk factors for DC. Six months after TBI, 34.0% of patients exhibited favorable outcomes. Overall mortality rate was 30.4%. Age, GCS, pupil dilation, hematoma type, and timing of surgery were all associated with patient outcomes. Further logistic regression analysis revealed that, lower GCS, bilateral pupil dilation, timing of surgery >1 hour, and advanced age were independent risk factors for poor outcomes (P = .001, P = .037, P = .028, and P = .001, respectively).Our study revealed that, DC is not mandatory for all TBI patients with brain herniation. Nevertheless, DC decreases mortality rate in severe TBI patients with brain herniation. Subdural hematoma and timing of surgery >1 hour are key indicators for DC. Lower GCS, bilateral pupil dilation, delayed timing of surgery and advance age are indicators of poor outcomes.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Craniotomia , Encefalocele/etiologia , Encefalocele/cirurgia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Pré-Escolar , Craniectomia Descompressiva , Feminino , Humanos , Escala de Gravidade do Ferimento , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Resultado do Tratamento , Adulto Jovem
5.
Proc Natl Acad Sci U S A ; 117(44): 27667-27675, 2020 11 03.
Artigo em Inglês | MEDLINE | ID: mdl-33087571

RESUMO

Chronic neurodegeneration in survivors of traumatic brain injury (TBI) is a major cause of morbidity, with no effective therapies to mitigate this progressive and debilitating form of nerve cell death. Here, we report that pharmacologic restoration of the blood-brain barrier (BBB), 12 mo after murine TBI, is associated with arrested axonal neurodegeneration and cognitive recovery, benefits that persisted for months after treatment cessation. Recovery was achieved by 30 d of once-daily administration of P7C3-A20, a compound that stabilizes cellular energy levels. Four months after P7C3-A20, electron microscopy revealed full repair of TBI-induced breaks in cortical and hippocampal BBB endothelium. Immunohistochemical staining identified additional benefits of P7C3-A20, including restoration of normal BBB endothelium length, increased brain capillary pericyte density, increased expression of BBB tight junction proteins, reduced brain infiltration of immunoglobulin, and attenuated neuroinflammation. These changes were accompanied by cessation of TBI-induced chronic axonal degeneration. Specificity for P7C3-A20 action on the endothelium was confirmed by protection of cultured human brain microvascular endothelial cells from hydrogen peroxide-induced cell death, as well as preservation of BBB integrity in mice after exposure to toxic levels of lipopolysaccharide. P7C3-A20 also protected mice from BBB degradation after acute TBI. Collectively, our results provide insights into the pathophysiologic mechanisms behind chronic neurodegeneration after TBI, along with a putative treatment strategy. Because TBI increases the risks of other forms of neurodegeneration involving BBB deterioration (e.g., Alzheimer's disease, Parkinson's disease, vascular dementia, chronic traumatic encephalopathy), P7C3-A20 may have widespread clinical utility in the setting of neurodegenerative conditions.


Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Lesões Encefálicas Traumáticas/tratamento farmacológico , Carbazóis/farmacologia , Cognição/efeitos dos fármacos , Doenças Neurodegenerativas/tratamento farmacológico , Fármacos Neuroprotetores/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Comportamento Animal/fisiologia , Barreira Hematoencefálica/citologia , Barreira Hematoencefálica/patologia , Barreira Hematoencefálica/ultraestrutura , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/patologia , Carbazóis/uso terapêutico , Células Cultivadas , Doença Crônica/tratamento farmacológico , Cognição/fisiologia , Modelos Animais de Doenças , Células Endoteliais , Endotélio Vascular/citologia , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/patologia , Humanos , Masculino , Camundongos , Microscopia Eletrônica , Microvasos/citologia , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/patologia , Doenças Neurodegenerativas/fisiopatologia , Fármacos Neuroprotetores/uso terapêutico , Cultura Primária de Células , Sobreviventes
6.
Medicine (Baltimore) ; 99(43): e22879, 2020 Oct 23.
Artigo em Inglês | MEDLINE | ID: mdl-33120830

RESUMO

Cerebral edema is a frequent and serious complication in traumatic brain injury (TBI) patients. The objective is to study the effect of dexamethasone in patients with brain contusions, and to assess its effect on the vasogenic component of the pericontusional edema.Prospective-observational study to quantify, using magnetic resonance imaging, the volume of the edema before and after 10 days of dexamethasone in patients with brain contusions. Using diffusion tensor imaging, we have examined the effect of dexamethasone on fractional anisotropy (FA) and apparent diffusion coefficient (ADC). To assess changes, the pre- and post-treatment values for each patient were compared using a paired-samples Student t test.We included 30 TBI patients, 15 in each group. The volume of the vasogenic edema in the group of patients treated with dexamethasone decreased from 22 to 19 mL and this decrease was statistically significant (P < .05). Nevertheless, in the non-steroids group the volume of the vasogenic edema increased from 11 to 15 mL. There was a significant decrease in the ADC value (from 1.78-1.59; P < .05); and a significant increase in the FA value (0.09-0.11; P < .05) in the patients treated with dexamethasone.Using diffusion tensor imaging we have shown in a selected group of TBI patients with vasogenic pericontusional edema, a reduction of edema volume, a decrease in the ADC and an increase in the FA after treatment with dexamethasone. However, we have no data if such results are beneficial in terms of improving functional outcome.


Assuntos
Anti-Inflamatórios/uso terapêutico , Edema Encefálico/tratamento farmacológico , Lesões Encefálicas Traumáticas/complicações , Dexametasona/uso terapêutico , Imagem de Tensor de Difusão/métodos , Adulto , Idoso , Anisotropia , Anti-Inflamatórios/administração & dosagem , Edema Encefálico/diagnóstico por imagem , Edema Encefálico/etiologia , Estudos de Casos e Controles , Dexametasona/administração & dosagem , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Espanha/epidemiologia
7.
Neurocirugía (Soc. Luso-Esp. Neurocir.) ; 31(5): 216-222, sept.-oct. 2020. tab
Artigo em Inglês | IBECS | ID: ibc-195154

RESUMO

OBJECTIVES: To evaluate the incidence of severe potassium disturbances during barbiturate coma therapy in patients with severe traumatic brain injury (TBI), and the characteristics of these patients. METHODS: The study comprised 37 patients with severe TBI who were treated for barbiturate coma between 2015 and 2017 in level 3 intensive care units of two hospitals. RESULTS: No potassium disturbance occurred in 14 patients. Seventeen patients developed mild-moderate hypokalemia (2.6-3.5 mEq/L), and 6 patients developed severe hypokalemia (< 2.5 mEq/L) following the induction of barbiturate therapy. The incidence of mild-to-severe barbiturate-induced hypokalemia was 62.2% and the rate of severe hypokalemia was 16.2%. The mean potassium supply per day during thiopentone therapy was statistically significantly different between patients with mild-to-moderate hypokalemic and those with severe hypokalemic (p < 0.001). Four of 6 patients with severe hypokalemia developed rebound hyperkalemia exceeding 6mEq/L following the cessation of barbiturate infusion. The nadir potassium concentration was 1.5 mEq/L and the highest value was 6.8 mEq/L. The mean time to reach nadir potassium concentrations was 2.8 days. The mortality rate of the 6 patients was 66.7%. Of the 2 survivors of severe hypokalemia, the Glasgow Outcome Scale (GOS) on discharge and the extended GOS one year after the trauma were 5 and 8 respectively. CONCLUSIONS: Severe hypokalemia refractory to medical treatment and rebound hyperkalemia is a serious adverse effect of thiopentone coma therapy in patients with severe TBI. Excessive and aggressive potassium replacement during the barbiturate-induced hypokalemia period must be avoided. Weaning barbiturate treatment over time may be advantageous in the management of severe serum potassium disturbances


OBJETIVOS: Evaluar la incidencia de alteraciones graves de los niveles de potasio durante el coma terapéutico inducido por barbitúricos en pacientes con lesiones cerebrales traumáticas (LCT) graves y las características de estos pacientes. MÉTODOS: El estudio incluyó 37 pacientes con LCT grave que habían sido tratados mediante coma terapéutico inducido por barbitúricos entre 2015 y 2017 en unidades de cuidados intensivos de nivel 3 de dos hospitales. RESULTADOS: En 14 pacientes no se observaron alteraciones de los niveles de potasio. Diecisiete pacientes desarrollaron hipopotasemia leve o moderada (2,6-3,5 mEq/l), y 6 pacientes desarrollaron hipopotasemia grave (< 2,5 mEq/l) después de la inducción de la terapia con barbitúricos. La incidencia de hipopotasemia de leve a grave inducida por barbitúricos fue del 62,2% y la tasa de hipopotasemia grave fue del 16,2%. El aporte medio de potasio al día durante el tratamiento con tiopentona fue diferente de forma estadísticamente significativa entre los pacientes con hipopotasemia leve o moderada y entre los que tenían hipopotasemia grave (p < 0,001). Cuatro de los 6 pacientes con hipopotasemia grave desarrollaron hiperpotasemia de rebote que superó los 6 mEq/l después de la suspensión de la infusión de barbitúricos. La concentración mínima de potasio fue de 1,5 mEq/l y el valor máximo de potasio fue de 6,8 mEq/l. El tiempo medio hasta alcanzar las concentraciones mínimas de potasio fue de 2,8 días. La tasa de mortalidad de los 6 pacientes fue del 66,7%. En los 2 supervivientes con hipopotasemia grave, los resultados de la Escala de Resultados de Glasgow (Glasgow Outcome Scale, GOS) en el alta y la GOS extendida un año después del traumatismo fueron 5 y 8, respectivamente


Assuntos
Humanos , Masculino , Feminino , Adolescente , Adulto Jovem , Adulto , Pessoa de Meia-Idade , Hipopotassemia/induzido quimicamente , Hiperpotassemia/induzido quimicamente , Coma/induzido quimicamente , Barbitúricos/efeitos adversos , Lesões Encefálicas Traumáticas/tratamento farmacológico , Barbitúricos/uso terapêutico , Lesões Encefálicas Traumáticas/complicações , Potássio/sangue , Mortalidade , Eletroencefalografia
8.
Lakartidningen ; 1172020 10 05.
Artigo em Sueco | MEDLINE | ID: mdl-33021328

RESUMO

Traumatic brain injury (TBI) is a leading cause of death and disability. Progressive intracranial bleeding is common in TBI and worsens outcome. The multicentre, randomized placebo-controlled CRASH-3 study enrolling 12,737 patients showed that early, <3h, administration of tranexamic acid (TXA) decreased mortality in mild-moderate TBI patients. In accordance with large previous trials, thromboembolic complications were not increased. In view of the favourable safety profile of TXA and the devastating effects from intracranial bleeds, the authors argue that TXA be administered within 3h post-injury to moderate-severe TBI patients, and in mild TBI to those with intracranial haemorrhage on acute CT.


Assuntos
Antifibrinolíticos , Concussão Encefálica , Lesões Encefálicas Traumáticas , Ácido Tranexâmico , Antifibrinolíticos/efeitos adversos , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/tratamento farmacológico , Método Duplo-Cego , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Ácido Tranexâmico/efeitos adversos
9.
J Clin Neurosci ; 79: 237-240, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-33070903

RESUMO

Traumatic brain injuries (TBI) and its sequelae are becoming one of the most pressing public health concerns worldwide. It is one of the leading causes of increased morbidity and mortality. The primary insult to the brain can cause ischemic brain injury, paralysis, concussions, death, and other serious complications. Brain injury also involves other systems through a secondary pathway resulting in multiple complications during and after hospitalization. The focus of our article is to assess the literature available on traumatic brain injury and intestinal dysfunctional to highlight the aspects of epidemiology, pathophysiology, and different diagnostic approaches for early diagnosis of gut dysfunction. We review studies done in both humans and animals, to better understand this underrated topic, as it costs billions of dollars to the healthcare industry because of delayed diagnosis.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Gastroenteropatias/etiologia , Animais , Lesões Encefálicas Traumáticas/patologia , Lesões Encefálicas Traumáticas/fisiopatologia , Gastroenteropatias/patologia , Gastroenteropatias/fisiopatologia , Humanos
12.
Medicine (Baltimore) ; 99(39): e22375, 2020 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-32991457

RESUMO

BACKGROUND: Depressive disorder has gradually become one of the most commonly reported disabling psychiatric complication that occurs after traumatic brain injury (TBI). Currently classical antidepressant medications may not have the same effectiveness in patients with TBI as in patients without TBI. Non-pharmacological interventions have been considered to be effective for managing depressive symptoms or treating depressive disorder. But to date the comparative effectiveness of various types of non-pharmacological interventions has been synthesized in few studies, the evidence remains inconclusive. Thus, the purpose of this systematic review and network meta-analyses is to summarize high-quality evidence and identify the most effective non-pharmacological intervention when applied to treat the depressive disorder in patients after TBI. METHODS: The comprehensive literature search in electronic database including PubMed, Ovid Medline, Cochrane Library, Web of Science database, Embase Database, China National Knowledge Infrastructure (CNKI), and Wanfang Data Chinese database from inception to the search date. Only high-quality randomized controlled trials (RCTs) that have used non-pharmacological interventions to treat depressive disorder after TBI will be considered. Two independent reviewers will identify eligible studies, extract and manage data information, and then determine methodical quality of included studies. Overall efficacy will be assessed as primary outcome. Secondary outcomes involved treatment response, remission rate, overall acceptability, tolerability of treatment, social functioning, occurrence of adverse events, and suicide-related outcome. Cochrane risk of bias assessment tool will be adopted to assess the risk of bias. Study heterogeneity will be measured by the I statistic. Traditional pairwise meta-analyses will be performed using STATA, while WinBUGS with GeMTC package of R software will be used to carry out network meta-analysis. RESULTS: This systematic review will examine the relative efficacy, effectiveness, safety, tolerability and acceptability of non-pharmacological interventions, and then to identify the most effective non-pharmacological intervention for depressive disorder after TBI. EXPECTED CONCLUSION: Our work could be used to give clinical recommendations for practice guideline developers, psychiatrist, neurologist, policymakers, researchers as well as individual with depressive disorder after TBI, and will also identify gaps in knowledge that could be the subject of future research. ETHICS AND DISSEMINATION: Neither ethics approval nor patient informed consent is necessary since this protocol was designed based on the existing literature. The results will be disseminated electronically or in print through publications in peer-reviewed scientific journal. INPLASY REGISTRATION: INPLASY202080022.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Transtorno Depressivo/terapia , Transtorno Depressivo/etiologia , Humanos , Metanálise como Assunto , Revisões Sistemáticas como Assunto
14.
PLoS One ; 15(9): e0234749, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32966291

RESUMO

Traumatic brain injury (TBI) can lead to neurodegeneration in the injured circuitry, either through primary structural damage to the neuron or secondary effects that disrupt key cellular processes. Moreover, traumatic injuries can preferentially impact subpopulations of neurons, but the functional network effects of these targeted degeneration profiles remain unclear. Although isolating the consequences of complex injury dynamics and long-term recovery of the circuit can be difficult to control experimentally, computational networks can be a powerful tool to analyze the consequences of injury. Here, we use the Izhikevich spiking neuron model to create networks representative of cortical tissue. After an initial settling period with spike-timing-dependent plasticity (STDP), networks developed rhythmic oscillations similar to those seen in vivo. As neurons were sequentially removed from the network, population activity rate and oscillation dynamics were significantly reduced. In a successive period of network restructuring with STDP, network activity levels returned to baseline for some injury levels and oscillation dynamics significantly improved. We next explored the role that specific neurons have in the creation and termination of oscillation dynamics. We determined that oscillations initiate from activation of low firing rate neurons with limited structural inputs. To terminate oscillations, high activity excitatory neurons with strong input connectivity activate downstream inhibitory circuitry. Finally, we confirm the excitatory neuron population role through targeted neurodegeneration. These results suggest targeted neurodegeneration can play a key role in the oscillation dynamics after injury.


Assuntos
Lesões Encefálicas Traumáticas/fisiopatologia , Simulação por Computador , Modelos Neurológicos , Rede Nervosa/fisiopatologia , Doenças Neurodegenerativas/fisiopatologia , Potenciais de Ação , Encéfalo/fisiologia , Encéfalo/fisiopatologia , Lesões Encefálicas Traumáticas/complicações , Humanos , Rede Nervosa/fisiologia , Doenças Neurodegenerativas/etiologia , Plasticidade Neuronal , Neurônios/patologia , Neurônios/fisiologia
15.
Medicine (Baltimore) ; 99(35): e21655, 2020 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-32871879

RESUMO

BACKGROUND: To compare the effects of 3% hypertonic saline solution and 20% mannitol solution on intracranial hypertension. METHODS: WAN-FANGDATA, CNKI, and CQVIP databases were searched, and relevant literatures of randomized controlled trials comparing 3% hypertonic saline solution with mannitol in reducing intracranial hypertension from 2010 to October 2019 were collected. Meta-analysis was performed using RevMan software. RESULTS: As a result, 10 articles that met the inclusion criteria were finally included. A total of 544 patients were enrolled in the study, 270 in the hypertonic saline group and 274 in the mannitol group. There was no significant difference in the decrease of intracranial pressure and the onset time of drug between the 2 groups after intervention (all P > .05). There was a statistically significant difference between the hypertonic saline group and the mannitol group in terms of duration of effect in reducing intracranial pressure (95% confidence interval: 0.64-1.05, Z = 8.09, P < .00001) and cerebral perfusion pressure after intervention (95% confidence interval: 0.15-0.92, Z = 2.72, P = .007). CONCLUSION: Both 3% hypertonic saline and mannitol can effectively reduce intracranial pressure, but 3% hypertonic saline has a more sustained effect on intracranial pressure and can effectively increase cerebral perfusion pressure.


Assuntos
Lesões Encefálicas Traumáticas/tratamento farmacológico , Diuréticos Osmóticos/uso terapêutico , Hipertensão Intracraniana/tratamento farmacológico , Manitol/uso terapêutico , Solução Salina Hipertônica/uso terapêutico , Lesões Encefálicas Traumáticas/complicações , Diuréticos Osmóticos/farmacologia , Humanos , Hipertensão Intracraniana/etiologia , Pressão Intracraniana/efeitos dos fármacos , Manitol/farmacologia , Solução Salina Hipertônica/farmacologia
16.
Medicine (Baltimore) ; 99(38): e22004, 2020 Sep 18.
Artigo em Inglês | MEDLINE | ID: mdl-32957318

RESUMO

BACKGROUND: Mannitol and hypertonic saline (HTS) are effective in reducing intracranial pressure (ICP) after severe traumatic brain injury (TBI). However, their efficacy on the ICP has not been evaluated rigorously. OBJECTIVE: To evaluate the efficacy of repeated bolus dosing of HTS and mannitol in similar osmotic burdens to treat intracranial hypertension (ICH) in patients with severe TBI. METHODS: The authors used an alternating treatment protocol to evaluate the efficacy of HTS with that of mannitol given for ICH episodes in patients treated for severe TBI at their hospital during 2017 to 2019. Doses of similar osmotic burdens (20% mannitol, 2 ml/kg, or 10% HTS, 0.63 ml/kg, administered as a bolus via a central venous catheter, infused over 15 minutes) were given alternately to the individual patient with severe TBI during ICH episodes. The choice of osmotic agents for the treatment of the initial ICH episode was determined on a randomized basis; osmotic agents were alternated for every subsequent ICH episode in each individual patient. intracranial pressure (ICP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) were continuously monitored between the beginning of each osmotherapy and the return of ICP to 20 mm Hg. The duration of the effect of ICP reduction (between the beginning of osmotherapy and the return of ICP to 20 mm Hg), the maximum reduction of ICP and its time was recorded after each dose. Serum sodium and plasma osmolality were measured before, 0.5 hours and 3 hours after each dose. Adverse effects such as central pontine myelinolysis (CPM), severe fluctuations of serum sodium and plasma osmolality were assessed to evaluate the safety of repeated dosing of HTS and mannitol. RESULTS: Eighty three patients with severe TBI were assessed, including 437 ICH episodes, receiving 236 doses of HTS and 221 doses of mannitol totally. There was no significant difference between equimolar HTS and mannitol boluses on the magnitude of ICP reduction, the duration of effect, and the time to lowest ICP achieved (P > .05). The proportion of efficacious boluses was higher for HTS than for mannitol (P = .016), as was the increase in serum sodium (P = .038). The serum osmolality increased immediately after osmotherapy with a significant difference (P = .017). No cases of CPM were detected. CONCLUSION: Repeat bolus dosing of 10% HTS and 20% mannitol appears to be significantly and similarly effective for treating ICH in patients with severe TBI. The proportion of efficacious doses of HTS on ICP reduction may be higher than mannitol.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Diuréticos Osmóticos/uso terapêutico , Hipertensão Intracraniana/tratamento farmacológico , Hipertensão Intracraniana/etiologia , Manitol/uso terapêutico , Solução Salina Hipertônica/uso terapêutico , Adulto , Circulação Cerebrovascular/efeitos dos fármacos , Diuréticos Osmóticos/administração & dosagem , Diuréticos Osmóticos/efeitos adversos , Feminino , Humanos , Pressão Intracraniana/efeitos dos fármacos , Masculino , Manitol/administração & dosagem , Manitol/efeitos adversos , Pessoa de Meia-Idade , Solução Salina Hipertônica/administração & dosagem , Solução Salina Hipertônica/efeitos adversos , Índices de Gravidade do Trauma
17.
Artigo em Inglês | MEDLINE | ID: mdl-32932928

RESUMO

The aim of study is to investigate the risk of developing acquired cholesteatoma and external auditory canal (EAC) stenosis after traumatic brain injury (TBI) from the Taiwan National Health Insurance Research Database (NHIRD). Each subject was individually traced from their index date to identify those who received a diagnosis of acquired cholesteatoma and EAC stenosis. Cox regression analyses were applied to determine the risk of TBI-related acquired cholesteatoma and EAC stenosis. The follow-up data collected over 10 years were obtained from the TBI and comparison cohorts, of 455,834 and 911,668 patients, respectively. Multivariate analysis demonstrated that TBI significantly increased the risk of cholesteatoma (adjusted hazard ratio (HR), 1.777; 95% confidence interval (CI), 1.494-2.114, p < 0.001) and EAC stenosis (adjusted (HR), 3.549; 95% (CI), 2.713-4.644, p < 0.001). In our subgroup injury analysis, falls had the highest associated risk (4.308 times), followed by traffic injuries (66.73%; 3.718 times that of the control group). Otolaryngologists should not neglect the clinical importance and carefully investigate the possibility of subsequent cholesteatoma and EAC stenosis, which leads to hearing impairment in patients with TBI. Our research also shows the important role in preventing TBI, especially as a result of traffic injuries and falls.


Assuntos
Lesões Encefálicas Traumáticas , Colesteatoma , Meato Acústico Externo , Adulto , Idoso , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/epidemiologia , Colesteatoma/epidemiologia , Estudos de Coortes , Constrição Patológica , Meato Acústico Externo/patologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Risco , Taiwan/epidemiologia
18.
Sci Rep ; 10(1): 15057, 2020 09 14.
Artigo em Inglês | MEDLINE | ID: mdl-32929099

RESUMO

Systemic and local posttraumatic responses are often monitored on mRNA expression level using quantitative real-time PCR (qRT-PCR), which requires normalisation to adjust for confounding sources of variability. Normalisation requests reference (housekeeping) genes stable throughout time and divergent experimental conditions in the tissue of interest, which are crucial for a reliable and reproducible gene expression analysis. Although previous animal studies analysed reference genes following isolated trauma, this multiple-trauma gene expression analysis provides a notable study analysing reference genes in primarily affected (i.e. bone/fracture callus and hypothalamus) and secondarily affected organs (i.e. white adipose tissue, liver, muscle and spleen), following experimental long bone fracture and traumatic brain injury. We considered tissue-specific and commonly used top-ranked reference candidates from different functional groups that were evaluated applying the established expression stability analysis tools NormFinder, GeNorm, BestKeeper and RefFinder. In conclusion, reference gene expression in primary organs is highly time point as well as tissue-specific, and therefore requires careful evaluation for qRT-PCR analysis. Furthermore, the general application of Ppia, particularly in combination with a second reference gene, is strongly recommended for the analysis of systemic effects in the case of indirect trauma affecting secondary organs through local and systemic pathophysiological responses.


Assuntos
Lesões Encefálicas Traumáticas/genética , Fraturas do Fêmur/genética , Perfilação da Expressão Gênica/normas , Transcriptoma , Animais , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/metabolismo , Feminino , Fraturas do Fêmur/complicações , Fraturas do Fêmur/metabolismo , Perfilação da Expressão Gênica/métodos , Camundongos , Camundongos Endogâmicos C57BL , Especificidade de Órgãos , Padrões de Referência
19.
Am J Surg ; 220(6): 1503-1505, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-32980078

RESUMO

BACKGROUND: Levetiracetam and phenytoin are comparable for acute posttraumatic seizure(PTS) prophylaxis. Levetiracetam-induced hyponatremia has been reported in non-trauma patients. We studied hyponatremia in posttraumatic intracranial hemorrhage(ICH) patients receiving either drug. METHODS: Retrospective review of patients with ICH receiving PTS prophylaxis was performed. Patients were categorized by degree of sodium nadir: normal, mild, moderate, or severe, and analyzed by levetiracetam versus phenytoin. Patients were matched 2:1 regarding age and injury severity score(ISS). Incidence and treatment for hyponatremia was examined. RESULTS: 1735 ICH patients received PTS prophylaxis over an 8-year period. After exclusions and matching, there were 282 phenytoin and 564 levetiracetam patients. Age, ISS and initial sodium were comparable between the matched cohorts. There was no clinically significant difference in the rate or degree of hyponatremia. Treatment was more common in levetiracetam patients. DISCUSSION: There was a small but clinically insignificant difference in the incidence of hyponatremia in traumatic ICH patients receiving levetiracetam vs. phenytoin for PTS prophylaxis. There was an increased rate of intervention for hyponatremia in the levetiracetam group, possibly due to a coincidental preventive paradigm shift.


Assuntos
Anticonvulsivantes/efeitos adversos , Hiponatremia/induzido quimicamente , Hiponatremia/epidemiologia , Levetiracetam/efeitos adversos , Fenitoína/efeitos adversos , Convulsões/prevenção & controle , Adulto , Anticonvulsivantes/uso terapêutico , Lesões Encefálicas Traumáticas/complicações , Intervenção Médica Precoce , Feminino , Humanos , Incidência , Levetiracetam/uso terapêutico , Masculino , Pessoa de Meia-Idade , Fenitoína/uso terapêutico , Estudos Retrospectivos , Convulsões/etiologia , Adulto Jovem
20.
JAMA ; 324(10): 961-974, 2020 09 08.
Artigo em Inglês | MEDLINE | ID: mdl-32897344

RESUMO

Importance: Traumatic brain injury (TBI) is the leading cause of death and disability due to trauma. Early administration of tranexamic acid may benefit patients with TBI. Objective: To determine whether tranexamic acid treatment initiated in the out-of-hospital setting within 2 hours of injury improves neurologic outcome in patients with moderate or severe TBI. Design, Setting, and Participants: Multicenter, double-blinded, randomized clinical trial at 20 trauma centers and 39 emergency medical services agencies in the US and Canada from May 2015 to November 2017. Eligible participants (N = 1280) included out-of-hospital patients with TBI aged 15 years or older with Glasgow Coma Scale score of 12 or less and systolic blood pressure of 90 mm Hg or higher. Interventions: Three interventions were evaluated, with treatment initiated within 2 hours of TBI: out-of-hospital tranexamic acid (1 g) bolus and in-hospital tranexamic acid (1 g) 8-hour infusion (bolus maintenance group; n = 312), out-of-hospital tranexamic acid (2 g) bolus and in-hospital placebo 8-hour infusion (bolus only group; n = 345), and out-of-hospital placebo bolus and in-hospital placebo 8-hour infusion (placebo group; n = 309). Main Outcomes and Measures: The primary outcome was favorable neurologic function at 6 months (Glasgow Outcome Scale-Extended score >4 [moderate disability or good recovery]) in the combined tranexamic acid group vs the placebo group. Asymmetric significance thresholds were set at 0.1 for benefit and 0.025 for harm. There were 18 secondary end points, of which 5 are reported in this article: 28-day mortality, 6-month Disability Rating Scale score (range, 0 [no disability] to 30 [death]), progression of intracranial hemorrhage, incidence of seizures, and incidence of thromboembolic events. Results: Among 1063 participants, a study drug was not administered to 96 randomized participants and 1 participant was excluded, resulting in 966 participants in the analysis population (mean age, 42 years; 255 [74%] male participants; mean Glasgow Coma Scale score, 8). Of these participants, 819 (84.8%) were available for primary outcome analysis at 6-month follow-up. The primary outcome occurred in 65% of patients in the tranexamic acid groups vs 62% in the placebo group (difference, 3.5%; [90% 1-sided confidence limit for benefit, -0.9%]; P = .16; [97.5% 1-sided confidence limit for harm, 10.2%]; P = .84). There was no statistically significant difference in 28-day mortality between the tranexamic acid groups vs the placebo group (14% vs 17%; difference, -2.9% [95% CI, -7.9% to 2.1%]; P = .26), 6-month Disability Rating Scale score (6.8 vs 7.6; difference, -0.9 [95% CI, -2.5 to 0.7]; P = .29), or progression of intracranial hemorrhage (16% vs 20%; difference, -5.4% [95% CI, -12.8% to 2.1%]; P = .16). Conclusions and Relevance: Among patients with moderate to severe TBI, out-of-hospital tranexamic acid administration within 2 hours of injury compared with placebo did not significantly improve 6-month neurologic outcome as measured by the Glasgow Outcome Scale-Extended. Trial Registration: ClinicalTrials.gov Identifier: NCT01990768.


Assuntos
Antifibrinolíticos/administração & dosagem , Lesões Encefálicas Traumáticas/tratamento farmacológico , Ácido Tranexâmico/administração & dosagem , Adulto , Antifibrinolíticos/efeitos adversos , Encefalopatias/etiologia , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/mortalidade , Método Duplo-Cego , Serviços Médicos de Emergência , Feminino , Seguimentos , Escala de Coma de Glasgow , Humanos , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos , Gravidade do Paciente , Análise de Sobrevida , Tempo para o Tratamento , Ácido Tranexâmico/efeitos adversos
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA