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Objective:To explore the establishment of the interconvertible injury parameters of same severe blast injury in mice at plain and plateau.Methods:A total of 157 C57BL/6 male mice were randomly divided into plain control group (8 mice), plain injury group (77 mice), plateau control group (8 mice) and plateau injury group (64 mice) according to random number table method. The mice in plateau control group and plateau blast injury group had been placed in animal experimental low-pressure oxygen chamber to simulate 4 000 meters plateau environment for 5 days in advance. Then the mice in plain blast injury group and plateau blast injury group were put into biological shock tube, respectively. Different pressures of the driving section were selected to establish the severe blast injury models in mice at plain and 4 000 meters plateau to reach approximately 70% mortality within 72 hours. The equivalent traumatic condition at 24 hours after blast injury in different groups was verified by the series of experiments including gross autopsy, lung wet/dry weight ratio (W/D), hematoxylin-eosin (HE) staining and histological scoring.Results:The mice mortality were basically consistent between the plain injury group (65%) and plateau injury group (75%) when 5.4 MPa and 4.0 MPa of the driving section pressures were chosen, respectively. Compared with the corresponding control groups, the lungs showed massive hemorrhage (patchy and diffuse) with significant pulmonary edema in both plain 5.4 MPa-injured group and the plateau 4.0 MPa-injured group at 24 hours after blast injury. Compared with the plateau control group, the pulmonary W/D ratio were significantly increased in the plateau injury group (5.579±0.646 vs. 4.476±0.076, P < 0.05), while the difference between plateau injury group and the plain control group was not statistically significant (5.303±1.020 vs. 4.015±0.144, P > 0.05). Also, compared with the corresponding control groups, the analysis of lung histopathological sections showed that there were several pathological changes including large alveolar rupture and fusion, thickened alveolar walls, and a small amount of inflammatory cell infiltration in the alveolar lumen in the groups of plain 5.4 MPa and plateau 4.0 MPa. In addition, the histopathological scores of lung in the groups of plain 5.4 MPa and plateau 4.0 MPa were significantly higher than that in corresponding control group (8.67±0.82 vs. 1.67±0.52, 9.00±1.10 vs. 2.17±0.41, both P < 0.05), however, there was no statistical difference for the above score between plain blast injury group and plateau blast injury group. Conclusions:The pressures of driving section 5.4 MPa and 4.0 MPa are injury parameters to establish equivalent severe blast injury in mice at plain and plateau, respectively, which can be converted to each other. This study provides support for the application and evaluation of prevention and treatment technology for severe blast injury in special environment.
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Objective: To establish an adult rat model of lung blast injury in laboratory for providing a reliable rat model for the diagnosis and treatment of lung blast injury. Methods: According to the different injury driving pressure of BST-I biological shock tube, 40 adult SD male rats aged 7 to 8 weeks were randomly divided into 4 groups (10 each): 4.5 MPa group, 4.8 MPa group, 5.0 MPa group and 5.5 MPa group. The general physiological and 24-hour survival status of rats in each group were recorded before and after modeling. The survived rats 24 h after modeling were anesthetized and then killed, and the chest anatomy was performed. The characteristics of lung injury were observed, the degree of lung tissue injury was graded using organ injury scaling (OIS) and abbreviated injury scale (AIS). Furthermore, the left lower part of lung tissue was taken for routine pathological section, and the degree of lung tissue injury was observed under light microscope. Results: All rats were successfully modeled and survived 24 h after injury, and showed shortness of breath and accelerated heart rate without hematuria and blood stool. There were significant differences among the four groups in bleeding rate of external auditory canal, anal temperature and pulmonary bleeding area (P5.0 MPa>4.8 MPa>4.5MPa. Under light microscope, rats in the four groups showed varying degrees of pulmonary hemorrhage, edema and atelectasis, and the lung tissue was ruptured. Conclusion: The stable adult SD rat models of mild, moderate, severe and extremely severe lung blast injury have been established.
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[Abstract] Objective To explore the regular pattern of the changes of vascular endothelial growth factor (VEGF) and neuropilin-1 (NRP-1) of rat model in early (<48h) blast lung injury (BLI) and the correlation of such changes to the degree of lung injury. Methods The rat model of lung blast injury was established with reducing three-way pipe and fixed pressure pneumatic simulation device. Forty SD rats were randomly divided into 5 groups: control group (C), 1h after blast (B1h), 6h after blast (B6h), 24h after blast (B24h) and 48h after blast (B48h) group. The data were collected of concentrations of VEGF and NRP-1 in serum and lung tissue. The degree of lung injury was estimated. Results The levels of NRP-1 increased in both serum and lung tissue (P<0.01) and the level of VEGF decreased in lung tissue (P<0.05) in control group than in B groups. The concentrations of NRP-1 in serum and lung tissue were highest, and of VEGF in lung tissue were lowest in the group B6h. The lung injury score was positively correlated with the levels of NRP-1 in lung tissue (r=0.429, P=0.014). In group B6h, the lung injury score was negatively correlated with the levels of VEGF in lung tissue (r=–0.769, P=0.013). In group B48h, both the lung injury score and the wet and dry ratios (W/D) of lung tissue were positively correlated with the concentrations of VEGF in serum (r=0.777, P=0.012 and r=0.687, P=0.030, respectively). Pulmonary interstitial vascular rupture, alveolar hemorrhage, alveolar epithelial cell and capillary injuries, and accompanied by inflammatory cell infiltration were the basic pathological changes of BLI. Conclusion The levels of NRP-1 and VEGF in serum and lung tissue may vary with time and are correlated with the degree of lung injury in early BLI.
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Objective To develop a new type of blast injury simulator to establish a mouse model of brain blast injury and study its damage mechanism. Methods Thirty healthy Kunming mice were randomly(random number) divided into the normal control group and brain blast injury model (TBI) group. A mouse model of traumatic brain injury was prepared by a self-developed explosive injury simulator. Morris water maze, Evans blue experiment and HE staining were used to observe the effects of shockwave exposure on spatial memory, blood-brain barrier, and pathological changes of brain tissues. T test was used for statistical analysis. Western blot method was used for detecting expression of brain injury markers Tau, S100β, Choline, inflammatory factors IL-1β, IL-4, IL-6, IL-10, NF-κB, apoptosis factors Bcl-2, Bax, Caspase3, and oxide protein stress-related factors IREα, MDA5, COX2 SOD1, and SOD2. Results Compared with the normal control group, (11.2±2.1) s, the time of searching platform in the TBI group was (54.6±8.4) s, was significantly longer (t=-19.330, P<0.05), and the EB exudation in the TBI group was 3.22 times (t=-13.903, P<0.05). Pathological staining revealed neuronal damage in the hippocampus, and TBI induced brain injury markers Tau(0.26±0.03 vs 0.46±0.04,t=-9.788, P<0.05), S100β(0.54±0.03 vs 0.74±0.02,t=-12.433, P<0.05) and Choline(0.54±0.05 vs 0.80±0.04, t=-7.970, P<0.05), inflammatory cytokines IL-1β(0.22±0.04 vs 0.31±0.05,t=-3.431, P<0.05), IL-4(0.65±0.02 vs 0.97±0.03, t=-18.927, P<0.05), IL-6(0.88±0.05 vs 1.07±0.08, t=-9.488, P<0.05) and NF-κB(0.80±0.06 vs 1.03±0.07,t=-4.507, P<0.05), and pro-apoptotic cytokines Bax(0.66±0.04 vs 0.78±0.04, t=-13.007, P<0.05) and Caspase3(0.44±0.03 vs 0.60±0.05, t=-4.472, P<0.05), oxidative stress-related factor pro IREα(0.72±0.06 vs 1.07±0.04, t=-9.665, P<0.05), MDA5(0.47±0.02 vs 0.77±0.02, t=-23.678, P<0.05) and expression of COX2(0.70±0.07 vs 0.86±0.02, t=-6.421, P<0.05), inhibition of inflammation inhibitory factor IL-10(1.14±0.06 vs 0.74±0.07, t=13.729, P<0.05), inhibition of apoptosis factors Bcl-2(0.72±0.05 vs 0.46±0.02, t=11.491, P<0.05) and inhibition of oxidative stress factors SOD1(1.17±0.05 vs 0.99±0.01, t=7.731, P<0.05) and SOD2(0.81±0.05 vs 0.61±0.04, t=10.257, P<0.05) expression. Conclusions The brain injury induced by blast exposure can induce spatial learning and memory loss, blood brain barrier disruption, neuronal damage hippocampus in mice, and promote the expression of brain injury markers, induce inflammation, oxidative stress and apoptosis. The self-developed explosive shock simulator successfully establishes a mouse brain blast injury model.
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The incidence of blast injury has increased recently. As the ear is the organ most sensitive to blast overpressure, the most frequent injuries seen after blast exposure are those affecting the ear. Blast overpressure affecting the ear results in sensorineural hearing loss, which is untreatable and often associated with a decline in the quality of life. Here, we review recent cases of blast-induced hearing dysfunction. The tympanic membrane is particularly sensitive to blast pressure waves, since such waves exert forces mainly at air-tissue interfaces within the body. However, treatment of tympanic membrane perforation caused by blast exposure is more difficult than that caused by other etiologies. Sensorineural hearing dysfunction after blast exposure is caused mainly by stereociliary bundle disruption on the outer hair cells. Also, a reduction in the numbers of synaptic ribbons in the inner hair cells and spiral ganglion cells is associated with hidden hearing loss, which is strongly associated with tinnitus or hyperacusis.
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Humanos , Traumatismos por Explosões/complicações , Orelha/lesões , Perda Auditiva Condutiva/etiologia , Perda Auditiva Neurossensorial/etiologia , Perfuração da Membrana Timpânica/complicaçõesRESUMO
Objective At present, the model of pulmonary blast injury is characterized by complexity, a certain degree of safety risks,and difficulty in obtaining the materials.This article aimed to establish a simple, safe and reusable primary pulmonary blast injury model in rats. Methods A total of 16 SD rats were randomly divided into control group and pulmonary blast injury group. In rats of control group, only ketamine(120 mg/kg)was injected intraperitoneally and hair was removed from chest.In pulmonary blast injury group,after the rats were fully anesthetized and depilated on chest,they were placed in a reducing T-pipe with only chest fully exposed,and the pneumatic simulated blasting device was adjusted to 0.4 Mpa.Taking locations about 2.5 cm from the intersection points of the median line of the sternum with left and right anterior axillary lines as targets,explosion were carried out respectively,fol-lowing the sequence of right chest 2 min prior to left chest.Lung pathology,lung water content,arterial blood gas analysis, and inter-leukin-6(IL-6)changes were observed. Results No obvious dam-age was found as to the appearance of chest in all rats after blast inju-ry.Transient purpura appeared in 37.5%(3/8)of the rats within 5 min after injury and disappeared within 1 h.On the spot,62.5%(5/8)of the rats presented 10-20 s of brief apnea and gradually recov-ered 6 h later.The lung tissue W/D,serum IL-6 level and lung tissue IL-6 level in pulmonary blast injury group were significantly greater than those in control group[(4.97±0.37)vs(4.62±0.07),(68.13± 59.40)vs(16.27 ±5.08)pg/mL,(487.04 ±30.57)vs(172.74 ±35.02)pg/mL],representing statistically significant difference(P<0.05).PaO2level in pulmonary blast injury group was significantly lower than that of control group,and the difference was statistically significant(P<0.05).After pulmonary blast injury, punctate and flaky hemorrhages were observed in the lesions of lung tissues,showing red hepatic changes.Lung interstitium was obviously thickened and alveoli collapsed under microscope.Erythrocytes and edema fluid in lung interstitium and alveoli exuded.Gas embolism in intersti-tial blood vessels was observed under microscope. Conclusion The lungs of rats after blast through simple T-pipe is typical of prima-ry pulmonary blast injury in pathological and pathophysiological manifestations, which proves the convenience and reliability of the modeling method.
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Objective To investigate the effects of Neuman System Model on acute stress disorder after severe blast injury. Methods In the nursing course of a severe blast injury patient, by using Neuman SystemModel, we evaluated the patient′s stress source according to five aspects, including physiology, psychology, society culture, development and spirit, and then through drafting the intervention program with the patient together, he was guided to take part in the management of their own symptoms, cognitive therapy was undertaken, and his parents were also assisted to create an effective supporting system. What′s more, level Ⅲ Neuman preventive measures were taken in the septal fibrosis and bridging. Results Satisfying results were acquired after sixty days′ interventions. The patient could almost properly face the blast injury, and discharge healthily. Conclusion Neuman System Model is really helpful in relieving the acute stress disorder of severe blast injury patients, so as to promote rehabilitation physically and mentally.
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Objective To study the characteristics and mechanism of mine blast injury that wading in shoal of different depths through an animal model.Methods Ninety-six healthy adult New Zealand white rabbits weighing 2.19 ± 0.12kg were randomly divided into land group (n=16),limb wading group (n=16,the water depth reaching up the middle of the thighs of rabbits),and chest wading group (n=16,the water depth reaching up the thoracic xiphoid),stress test group (n=30),fake injury group (n=18).Punctiform burster was used to simulate landmine.Electric ignited the simulated mine away,causing landmine explosion injury to rabbits' one-sided hind limbs in upright state.High-speed photography was used to observe the movement of water accompanying the simulated mine explosion.Arterial blood serum markers of myocardial injury (CK-MB,cTnⅠ) and nerve injury (MBP,NSE) were detected before injury,and 3,6 and 12h after injury,and echocardiography,electrocardiography,CT,DSA and other examinations were implemented at the same time.Survival animals were killed 12h after injury for anatomy to record their injuries to the limbs and distant organs.The histopathological examination was done to define the injury characteristics furthen Results Feet and distal tibia were broken,and closed femoral fractures and arterial damage were often found away from the stump in limb wading group.This type of injury was different from the mop-like tearing tissue in the land group.Chest,abdominal organs and the brain,spinal cord injury in wading group were more severe than those in land group.There were higher incidences of chest,abdominal organs and spinal cord injury in chest wading Group.Conclusion The energy transfer of underwater explosion is affected by water depth and limbs or trunk mutually,which is an important mechanism of the complex and serious injuries in the wading group.The wading depth is an important factor affecting severity of the injury.Based on characteristics and unique mechanism of wading explosion,emergency treatment and the principle of early treatment for injury warrant further explored.
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Objective It is a tough job to rescue batches of patients with severe blast injury .The article aimed to construct specific technique system management in the rescue of batches of patients with severe blast injury and evaluate its effects . Methods Retrospective analysis was made on 9 patients with severe blast injury who hospitalized simultaneously .According to the difficulties in the nursing process of treating severe blast injury such as management of respiratory tract , continuous renal replacement therapy , vascular access, nutritional supply, skin nursing, etc, specific technique system management was constructed to evaluate technical support key points at different phases , including personalized nursing scheme with disease progression , professional nursing instruction on key points of different phases from specialists as well as corresponding nursing decision and professional caring . Results Specific technique system management was applied in these 9 patients with severe blast injury .Only 1 patients developed ventilator related pneumonia when receiving mechanical ventilation and no procedure related complications occurred in the aspects of blood purification , skin management , vascular access and nutrition support .6 patients discharged from hospital after recovery . Conclusion Specific techniques and systemic management in batch treatment of severe bast injury patients could help collaborative nursing , improve the management of specific management and prevent complication .
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Objetivo: Determinar si pacientes con perforación timpánica causada por trauma por onda explosiva tienen un resultado quirúrgico peor que el encontrado en pacientes con perforación timpánica causada por otitis media crónica. Metodología: Estudio observacional analítico tipo cohorte prospectiva. Se comparó los resultados en timpanoplastia tipo I entre pacientes expuestos a trauma por onda explosiva (cohorte expuesta) y pacientes con perforación causada por otitis media crónica (cohorte no expuesta). Se incluyeron pacientes mayores de 18 años en quienes se utilizó técnica over-under de colocación de injerto de cartílago. Se excluyeron pacientes en quienes se utilizó otras técnicas quirúrgicas, a quienes se les practicó mastoidectomia u osciculoplastia, aquellos con perforaciones secundarias a otra etiología y quienes tenían colesteatoma. El tamaño de la muestra se calculó para la variable resultado anatómico y fue de 43 pacientes por cohorte. El estudio se terminó una vez se consiguió el tamaño de muestra propuesto. El análisis principal fue la comparación del resultado anatómico (estado del neo tímpano) y funcional (brecha aíre-hueso <10dB) entre las cohortes expuesta y no expuesta. Resultados: El estudio inició en agosto1 de 2011 y finalizó en julio 25 de 2013. No se encontró asociación entre la exposición bajo estudio y el fracaso anatómico, RR=4.0 [IC 95% RR = 0.47- 34.35]. Tampoco hubo asociación entre el fracaso anatómico y perforación timpánica ≥50%, localización anterior de la perforación timpánica e inflamación /infección al momento de la cirugía [IC 95% RR incluyó el valor 1]. Los pacientes de la cohorte expuesta tuvieron un RR=1.76 de fracaso funcional [IC 95% RR=1.19-2.59]. Conclusiones: El resultado anatómico de la timpanoplastia tipo I es equiparable entre los pacientes con perforación timpánica secundaria a trauma por onda explosiva respecto a aquellos con perforaciones timpánicas por otitis crónica. Sin embargo se observó un peor resultado funcional entre los pacientes víctimas de trauma por onda explosiva.
Objective: To determine whether patients with perforated eardrum caused by blast injury have a worse surgical outcome than that found in patients with perforated eardrum caused by chronic otitis media Methods: This is a prospective cohort study. We compared the results in type I tympanoplasty in patients exposed to blast injury (exposed cohort), and patients with perforation caused by chronic otitis media (unexposed cohort). We included patients older than 18 years in whom the over-under tympanoplasty technique was used, using cartilage graft. We excluded patients who underwent other surgical techniques, who underwent mastoidectomy and/or osciculoplastia, those with perforations secondary to other etiologies and those with cholesteatoma. The sample size was calculated for the variable anatomical outcome, and it was 43 patients per cohort. The study was finished once we reached the proposed sample size. The main outcome was the comparison of the anatomical outcome (status of the eardrum) and the functional outcome (air-bone gap <10 dB), between the exposed and unexposed cohorts. Results: The study began in August 1, 2011 and ended on July 25, 2013. There was no association between the exposure under study and the anatomical failure, RR=4.0 [IC 95% RR = 0.47-34.35]. There was also no association between the anatomical outcome and size of the perforated eardrum ≥ 50%, anterior tympanic membrane perforation and inflammation/infection at the time of surgery [IC 95%RR included the value 1]. The patients of the exposed cohort had a RR = 1.76 for functional failure, [IC 95% RR=1.19-2.59]. Conclusions: The anatomical outcome of type I tympanoplasty is comparable between patients with tympanic membrane perforation secondary to blast injury compared to those with chronic otitis media. However, we found a worse functional outcome among patients suffering from blast injury.
Objetivo: Avaliar se os pacientes com perfuração timpânica causada pelo trauma por onda explosiva tem um resultado cirúrgico pior do que os pacientes com perfuração timpânica causada pela otites media crônica. Metodologia: Estudo observacional analítico prospectivo. Foram comparados os resultados em timpanoplastia tipo I entre pacientes expostos ao trauma por onda explosiva (grupo exposto) e pacientes com perfuração por otites media crônica (grupo não exposto). Foram incluídos pacientes maiores de 18 anos utilizando a técnica over-under de colocação de implante de cartilagem. Foram excluídos os pacientes que utilizaram outras técnicas cirúrgicas, mastoidectomia ou ossiculoplastia, aqueles com perfurações secundarias a outra etiologia e os que tinham colesteatoma. O tamanho dà amostra foi calculada para a variável resultado anatômico e foi de 43 pacientes por grupo. O Estudo finalizou no momento que a amostra foi atingida. O análise principal foi a comparação do resultado anatômico (estado do neo-timpano) e funcional (lacuna aire-osso<10dB) entre os grupos exposto e não exposto. Resultados: O estudo inicio o primeiro de agosto de 2011 e finalizou o 25 de junho de 2013. Não se apresentou associação entre a explosão no estudo e o fracasso anatômico, RR=4.0 [IC 95% RR = 0.47-34.35]. Além disso, não houve associação entre o fracasso anatômico e perfuração timpânica ≥50%, localização anterior da perfuração timpânica e inflamação/infecção ao momento do procedimento cirúrgico [IC 95% RR incluiu o valor 1]. Os pacientes do grupo exposto tiveram um RR=1.76 de fracasso funcional [IC 95% RR=1.19-2.59]. Conclusões: O resultado anatômico da timpanoplastia tipo I é equiparável entre os pacientes com perfuração timpânica secundaria ao trauma por onda explosiva quanto a aqueles com perfurações timpânicas por otites crônica. Embora, foi observado um pior resultado funcional entre os pacientes vítimas de trauma por onda explosiva.
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Adulto , Perda Auditiva Provocada por Ruído , Miringoplastia , Otite Média , Perfuração da Membrana Timpânica , TimpanoplastiaRESUMO
Radiological imaging is often used for the preoperative localization of foreign body following blast injury, but their utility in case of migration during intra‑operative period is limited. Transesophageal echocardiography (TEE) has been used for intra‑operative localization and removal of intra‑cardiac foreign body; however, reports for localization of extracardiac migrating foreign body are few. Preoperative radiological imaging, in a victim of factory blast‑injury, suggested foreign body in the posterior mediastinum. However, the intra‑operative TEE showed it in the left atrium, which later migrated into the left ventricle necessitating a change in surgical approach for its removal.
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Adulto , Traumatismos por Explosões/cirurgia , Traumatismos por Explosões/diagnóstico por imagem , Ecocardiografia Transesofagiana/métodos , Migração de Corpo Estranho/cirurgia , Migração de Corpo Estranho/diagnóstico por imagem , Átrios do Coração/diagnóstico por imagem , Ventrículos do Coração/cirurgia , Ventrículos do Coração/diagnóstico por imagem , Humanos , Masculino , Monitorização Intraoperatória/métodosRESUMO
Objective To study the effects of vagus nerve stimulation (VNS) on brain tissue tumor necrosis factor-α (TNF-o),interleukin-1β (IL-1β) and IL-10 levels in serum and brain tissues after blast brain injury in rabbits.Methods Twenty New Zealand white male rabbits were randomly divided into sham-operated group (n=6),traumatic brain injury (TBI) group (n=10),TBI+VNS group (n=8).Rabbit brain blast injury models of TBI group and TBI+VNS group were established; and the right cervical vagus nerves of the rabbits in TBI+VNS group were stimulated (10 V,5 HZ,5 ms,20 min).The TNF-α,IL-1β and IL-10 changes in the serum (6 h after injury) and brain tissues (24 h after injury) and the water content in the injured brain tissues were observed and recorded.Results The TNF-α and IL-1β levels in the serum and brain tissues,the water content in the brain tissues of the TBI group were significantly higher than those in the sham-operated group and TBI+VNS group (P<0.05); the IL-10 level in the TBI+VNS group was significantly higher than that in the sham-operated group and TBI group (P<0.05).Conclusion VNS can reduce the brain edema degree by increasing the IL-10 level and decreasing the TNF-α and IL-1 β levels,which plays a key role in brain protection effect after brain blast injury in rabbits.
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A 44-year-old man was cutting an outer plate of a ship, at a depth of 25 m below sea level. Following a sudden explosion, he was discovered unconscious and was carried to the surface by other divers. There was no evidence of vital signs upon arrival at the hospital. Postmortem computed tomography, which was performed prior to autopsy, revealed massive pneumocephalus in the brain, pneumohemothorax, diffuse lung contusions with multiple traumatic lung cysts, air-fluid level in the cardiac chamber of the chest, and pneumoperitoneum in the abdomen. Postmortem external examination showed a circular abrasion on the jaw, diffuse subcutaneous emphysema, and contusion in the right upper arm. An internal examination revealed intravascular air bubbles in all four chambers of the heart, and diffuse pulmonary trauma including contusion, laceration, and multiple traumatic cysts. Blast injury to the chest, and air embolism due to the underwater explosion were established as the underlying cause of death.
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Adulto , Humanos , Abdome , Braço , Autopsia , Traumatismos por Explosões , Encéfalo , Causas de Morte , Contusões , Mergulho , Embolia Aérea , Explosões , Coração , Arcada Osseodentária , Lacerações , Pulmão , Pneumocefalia , Pneumoperitônio , Navios , Enfisema Subcutâneo , Tórax , Sinais VitaisRESUMO
En el medio militar el personal se ve sometido a los más altos niveles de ruido; se considera que las detonaciones de las armas de fuego superan en intensidad a todos los ruidos industriales. Este trabajo pretende abordar los factores de riesgo y vulnerabilidad asociados a la exposición al ruido en el ambiente militar, los aspectos más actuales relacionados con la lesión auditiva inducida por ruido y su protección. Se realizó una revisión de los artículos más representativos mediante la base de datos Medline e Hinari, se empleó para la búsqueda y creación de la bibliografía el gestor personal de referencias bibliográficas Procite, referencias al tema en revistas, tesis y referencias en Internet mediante el buscador Google. Los resultados reafirman la vulnerabilidad del personal militar a padecer algún tipo de lesión del aparato auditivo inducida por ruido, originado por los niveles de ruido elevado que se producen en el medio militar, la necesidad de enfocar de forma multidisciplinaria este tipo de lesiones y la importancia de implementar sistemas de protección auditiva eficientes, con el fin de elevar la calidad de vida de los expuestos a ruido y evitar que se produzca la discapacidad auditiva, considerando que la mejor opción es su prevención.
Extremely high noise levels are characteristic of the military environment. Firearm detonations are considered to exceed the intensity of any industrial noise. The paper approaches the risk factors and vulnerabilities associated with exposure to noise in the military environment, as well as the most recent notions about noise-induced hearing injury and hearing protection. A review was conducted of the most representative papers on the topic using databases Medline and Hinari. Bibliography lists were searched for and created using Procite personal bibliographic reference manager. Google search engine was used to find references to the topic in journals, theses and Internet references. Results confirm the vulnerability of military personnel to suffer from noise-induced hearing injuries resulting from the high noise levels occurring in the military environment, the need to approach such injuries in a multidisciplinary manner, and the importance of implementing efficient hearing protection systems, with a view to improving the quality of life of persons exposed to noise and preventing hearing impairment, based on the certainty that prevention is always the best option.
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Blast injuries are increasing worldwide from combat and explosions in heavy industry. Primary blast injury is direct injury due to the high pressure effects and pressure differentials of the blast wave itself. Alternating overpressure and underpressure imposed upon tissues of heterogenous densities, particularly air-filled organs. The ear is the first affected organ to primary blast injury because it is the body's most sensitive pressure transducer. Otologic blast injury and tympanic membrane perforation have traditionally been used as a predictor, or biomarker, of occult serious primary blast injury. Hearing loss and tinnitus are the most common ear symptoms. This review details the otologic consequences of blast exposure.
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Traumatismos por Explosões , Orelha , Explosões , Audição , Perda Auditiva , Metalurgia , Zumbido , Transdutores de Pressão , Perfuração da Membrana TimpânicaRESUMO
The main objective of this study is to provide an overview of the basic mechanisms of blast induced hearing loss and review pharmacological treatments or interventions that can reduce or inhibit blast induced hearing loss. The mechanisms of blast induced hearing loss have been studied in experimental animal models mimicking features of damage or injury seen in human. Blast induced hearing loss is characterized by perforation and rupture of the tympanic membrane, ossicular damage, basilar membrane damage, inner and outer hair cell loss, rupture of round window, changes in chemical components of cochlear fluid, vasospasm, ischemia, oxidative stress, excitotoxicity, hematoma, and hemorrhage in both animals and humans. These histopathological consequences of blast exposure can induce hearing loss, tinnitus, dizziness, and headache. The pharmacological approaches to block or inhibit some of the auditory pathological consequences caused by blast exposure have been developed with antioxidant drugs such as 2,4-disulfonyl alpha-phenyl tertiary butyl nitrone (HXY-059, now called HPN-07) and N-acetylcysteine (NAC). A combination of antioxidant drugs (HPN-07 and NAC) was administered to reduce blast induced cochlear damage and hearing loss. The combination of the antioxidant drugs can prevent or treat blast induced hearing loss by reducing damage to the mechanical and neural component of the auditory system. Although information of the underlying mechanisms and treatment of blast induced hearing loss are provided, further and deep research should be achieved due to the limited and controversial knowledge.
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Animais , Humanos , Acetilcisteína , Membrana Basilar , Traumatismos por Explosões , Tontura , Cabelo , Cefaleia , Audição , Perda Auditiva , Hematoma , Hemorragia , Isquemia , Modelos Animais , Estresse Oxidativo , Ruptura , Zumbido , Membrana TimpânicaRESUMO
The main objective of this study is to provide an overview of the basic mechanisms of blast induced hearing loss and review pharmacological treatments or interventions that can reduce or inhibit blast induced hearing loss. The mechanisms of blast induced hearing loss have been studied in experimental animal models mimicking features of damage or injury seen in human. Blast induced hearing loss is characterized by perforation and rupture of the tympanic membrane, ossicular damage, basilar membrane damage, inner and outer hair cell loss, rupture of round window, changes in chemical components of cochlear fluid, vasospasm, ischemia, oxidative stress, excitotoxicity, hematoma, and hemorrhage in both animals and humans. These histopathological consequences of blast exposure can induce hearing loss, tinnitus, dizziness, and headache. The pharmacological approaches to block or inhibit some of the auditory pathological consequences caused by blast exposure have been developed with antioxidant drugs such as 2,4-disulfonyl alpha-phenyl tertiary butyl nitrone (HXY-059, now called HPN-07) and N-acetylcysteine (NAC). A combination of antioxidant drugs (HPN-07 and NAC) was administered to reduce blast induced cochlear damage and hearing loss. The combination of the antioxidant drugs can prevent or treat blast induced hearing loss by reducing damage to the mechanical and neural component of the auditory system. Although information of the underlying mechanisms and treatment of blast induced hearing loss are provided, further and deep research should be achieved due to the limited and controversial knowledge.
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Animais , Humanos , Acetilcisteína , Membrana Basilar , Traumatismos por Explosões , Tontura , Cabelo , Cefaleia , Audição , Perda Auditiva , Hematoma , Hemorragia , Isquemia , Modelos Animais , Estresse Oxidativo , Ruptura , Zumbido , Membrana TimpânicaRESUMO
Objective To evaluate the role of magnetic resonance spectroscopy (MRS) and diffusion-weighted MRI (DWI) in detecting regional cerebral metabolic changes and changes of water molecular motion in rabbits after explosive brain injury at different time points of injury after being treated with hyperbaric oxygen therapy. Methods Ninety New Zealand white rabbits were divided into control group, trauma group and hyperbaric oxygen treatment group. The injured models in the later 2 groups were established using 600 mg TNT equivalent of paper detonators in the rabbit brain at the top of 6.5 cm vertical distance. Rabbits in the trauma group and hyperbaric oxygen treatment group were sub-divided into 1, 3, 7, 14 and 21 d treatment groups, respectively. The survival of these rabbits was observed at these time points. Hyperbaric oxygen treatments lasting for 1, 3, 7, 14 and 21 d were given to each hyperbaric oxygen treatment sub-groups, respectively. Performance under MRS was detected and dynamic changes of N-acetylaspartate (NAA)/creatine (Cr) ratio and NAA/choline(Cho)+Cr value were observed with MRS. DWI was employed to detect the dynamic changes of apparent diffusion coefficient (ADC) values. Results The NAA/Cr ratio in the trauma group markedly decreased right after the injury and slightly rose 7 d after the injury. Compared with that in the trauma group, the NAA/Cr ratio in the hyperbaric oxygen treatment group was significantly increased (P<0.05). The NAA/Cho+Cr value in the trauma group was markedly decreased right after the injury, while that in the hyperbaric oxygen treatment group was obviously increased as compared with that in the trauma group (P<0.05). ADC values in the region of interest of the trauma group was decreased after 1 d of treatment and gradually increased after 3 d of treatment; the ADC values in the hyperbaric oxygen treatment group was obviously higher than those in the trauma group (P<0.05). Conclusion Hyperbaric oxygen might improve the prognosis by improving local metabolism of neurons, inhibiting brain edema, and enhancing local gliosis repair;, ultra-early intervention (within one week of injury) may be much favorable for animals/patients after explosive brain injury.
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PURPOSE: Recently, the incidence of blast injury has been on the increase worldwide. The purpose of this study was to evaluate and analyze blast injuries in South Korea. METHODS: This was a retrospective multi-center study of blast injuries in three tertiary military centers. The medical records of patients with blast injuries from January 2003 to December 2007 were reviewed. The injury severity was evaluated according to the Injury Severity Score (ISS), the Revised Trauma Score (RTS), and the Trauma Score and the Injury Severity Score (TRISS). RESULTS: This study revealed epidemiological data of blast injury in the three tertiary military hospital. A total of 94 cases of blast injury had occurred. Various body regions were involved. The most frequently injured site was the upper extremity (52.1%). The mechanisms for the blast injuries were primary (41.5%), secondary (74.5%), tertiary (7.4%), and quaternary (29.8%). The mean injury-to-hospital arrival time was 3.2+/-1.7 hour. The rate of admission was 88.3%, and the rate of ICU admission was 32.5%. Thirty-six (36) cases required an emergency operation. Most were performed by an Orthopedist (55.6%), an Ophthalmologist (19.4%), or a general surgeon (13.9%). The mortality rate from blast injury was 4.3%. CONCLUSION: This was the first paper to present data on the type of injury, the site of injury, the cause of death, and the mortality from blast injury in South Korea. Chest injury, brain injury, tertiary injury mechanisms, ISS> or = 16, and a Maximal Abbreviated Injury Scale Score (ABI)> or =4 were significantly associated with death.
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Humanos , Escala Resumida de Ferimentos , Traumatismos por Explosões , Regiões do Corpo , Bombas (Dispositivos Explosivos) , Lesões Encefálicas , Causas de Morte , Emergências , Hospitais Militares , Incidência , Escala de Gravidade do Ferimento , Coreia (Geográfico) , Prontuários Médicos , Militares , República da Coreia , Estudos Retrospectivos , Traumatismos Torácicos , Extremidade SuperiorRESUMO
Objective To investigate the changes of surfactant associated protein A (ST-A) concentration inBALF and its relatiomhips with pulmonary injury after blast injury and blast injury combined with hypoxia. MethodTotally 131 Wistar rats (purchased from animal center of research Institute of Surgery, Daping Hospital, ThirdMilitary Medical University) were randomly divided into four groups: blast injury group ( BI group), blast injurycombined with hypoxia group Ⅰ (BAg Ⅰ group), blast injury combined with hypoxia group Ⅱ (BA Ⅱ group) andnormal control group. After blast injury was made by KST - Ⅰ bio-shock tube, rats of BA Ⅰ and BA Ⅱ groups wereput into hypoxia cabins immediately, where gas mixtures of 12.5% and 10.0% oxygeon were given, respectively.Rats were sacrificed at 1, 3 and 6 hours after injury for gross anatomic examination, light and electron microscopeobservation and lung water determination. The level of SP-A in BALF was detected by Western blot. The data wereprocessed by t test or Chi-square test. Results The respiration increased with shortness of breath and dysphoria inrats of BA Ⅰ and BA Ⅱ groups, and obvious cyanosis on the lips and nose in rats of BA Ⅱ group after blast injury.The lung water in rats of all injury groups was significantly higher than that in normal control group (P<0.05).Gross anatomy changes were mainly pulmonary bleeding and edema. Under light microscope, incrassation of alveo-lar wall, bleeding in alveolar and mesenchyme edema were found. Whereas under electron microscope, breakageof alveolar wall and decrease of lamellar bodies in type Ⅱ cell were observed. All these changes were most obviousin BA Ⅱ group followed by BA Ⅰ and BI groups in severity decling order, with mortality rate of 37.5%, 11.1%and 2.1% respectively at 6 hours (P<0.01). The SP-A level in BALF decreased significantly (P<0.01) andhad a good negative relationship with the lung water after injury (r=0.796, P<0.001 ). Conclusions Blastinjury combined with hypoxia significantly deteriorates the lung injury. More severe and longer hypoxia may resultin more severe lung injury and higher mortality rate. A decrease in SP-A value in BALF shows a good negative re-lationship with the pulmonary edema. The SP-A can be a good indicator for lung injury severity after blast injuryand blast injury combined with hypoxia.