RESUMO
RESEARCH OBJECTIVE: Military personnel are at greater risks of head and facial traumas and permanent blindness from orbital compartment syndrome in modern warfare. Rapid treatment must be implemented with a low-risk surgical remedy: lateral canthotomy and cantholysis (LCC). Traditional training of LCC is primarily performed using an animal tissue trainer (ATT); however, limitations to these types of trainers exist. Therefore, our research objectives were focused on highlighting the effectiveness, benefits, and vision-saving potential of learning LCC on a synthetic trainer. METHODS: Participants included 22 second-year medical students and 6 healthcare professionals. A pre-quiz assessed baseline knowledge. Next, an experienced ophthalmologist provided an overview and instruction. Subjects were randomized to either the synthetic trainer or the ATT and then switched to the other model for comparison. After performing LCC procedures on both models, a post-quiz and survey were administered. RESULTS: Participants found the synthetic trainer easier to use than the ATT model (p < 0.01). There was no statistically significant preference (p = 0.23), or preference of practical eye anatomy (p = 0.26) between the trainers. Post-quiz results demonstrated an overall improvement from pre-quiz scores for participants (p < 0.001). CONCLUSIONS: The synthetic trainer is comparable to the traditional swine model for training LCC procedures, and should be considered as a future training platform.
Assuntos
Desenho de Equipamento/normas , Procedimentos Cirúrgicos Oftalmológicos/educação , Simulação de Paciente , Ensino/normas , Animais , Descompressão Cirúrgica/métodos , Modelos Animais de Doenças , Avaliação Educacional/métodos , Humanos , Aparelho Lacrimal/cirurgia , Procedimentos Cirúrgicos Oftalmológicos/métodos , Estudos Prospectivos , Inquéritos e Questionários , SuínosRESUMO
Special Operations Forces (SOF) medical personnel function worldwide in environments where endemic anthrax (caused by Bacillus anthracis infection) may present in one of three forms: cutaneous, pulmonary, or gastrointestinal. This report presents a rare periocular anthrax case from Haiti to emphasize the need for heightened diagnostic suspicion of unusual lesions likely to be encountered in SOF theaters.
Assuntos
Antraz/tratamento farmacológico , Antibacterianos/uso terapêutico , Ceftriaxona/uso terapêutico , Cicatriz/cirurgia , Dermatoses Faciais/tratamento farmacológico , Dermatopatias Bacterianas/tratamento farmacológico , Adolescente , Antraz/complicações , Antraz/diagnóstico , Cicatriz/etiologia , Olho , Dermatoses Faciais/diagnóstico , Músculos Faciais/cirurgia , Feminino , Haiti , Humanos , Dermatopatias Bacterianas/complicações , Dermatopatias Bacterianas/diagnósticoRESUMO
PURPOSE: To evaluate the toxic effects and associated mechanisms in corneal tissue exposed to the vesicating agent, nitrogen mustard (NM), a bifunctional alkylating analog of the chemical warfare agent sulfur mustard. METHODS: Toxic effects and associated mechanisms were examined in maximally affected corneal tissue using corneal cultures and human corneal epithelial (HCE) cells exposed to NM. RESULTS: Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury. CONCLUSIONS: Results from this study provide insight into the molecular targets and pathways that could be involved in NM-induced corneal injuries laying the background for further investigation of these pathways in vesicant-induced ocular injuries, which could be helpful in the development of targeted therapies.