RESUMO
BACKGROUND: Preclinical simulator training has the potential to decrease endoscopic procedure time and patient discomfort. This study aims to characterize the learning curve of endoscopic novices in a part-task simulator and propose a threshold score for advancement to initial clinical cases. METHODS: Twenty novices with no prior endoscopic experience underwent repeated endoscopic simulator sessions using the part-task simulator. Simulator scores were collected; their inverse was averaged and fit to an exponential curve. The incremental improvement after each session was calculated. Plateau was defined as the session after which incremental improvement in simulator score model was less than 5%. Additionally, all participants filled out questionnaires regarding simulator experience after sessions 1, 5, 10, 15, and 20. A visual analog scale and NASA task load index were used to assess levels of comfort and demand. RESULTS: Twenty novices underwent 400 simulator sessions. Mean simulator scores at sessions 1, 5, 10, 15, and 20 were 78.5 ± 5.95, 176.5 ± 17.7, 275.55 ± 23.56, 347 ± 26.49, and 441.11 ± 38.14. The best fit exponential model was [time/score] = 26.1 × [session #]-0.615; r 2 = 0.99. This corresponded to an incremental improvement in score of 35% after the first session, 22% after the second, 16% after the third and so on. Incremental improvement dropped below 5% after the 12th session corresponding to the predicted score of 265. Simulator training was related to higher comfort maneuvering an endoscope and increased readiness for supervised clinical endoscopy, both plateauing between sessions 10 and 15. Mental demand, physical demand, and frustration levels decreased with increased simulator training. CONCLUSION: Preclinical training using an endoscopic part-task simulator appears to increase comfort level and decrease mental and physical demand associated with endoscopy. Based on a rigorous model, we recommend that novices complete a minimum of 12 training sessions and obtain a simulator score of at least 265 to be best prepared for clinical endoscopy.
Assuntos
Competência Clínica/normas , Endoscopia/educação , Treinamento por Simulação , Adulto , Simulação por Computador , Avaliação Educacional , Endoscopia/normas , Feminino , Humanos , Curva de Aprendizado , Masculino , Treinamento por Simulação/normas , Análise e Desempenho de TarefasRESUMO
BACKGROUND: The Gastroenterology Core Curriculum and American Society of Gastrointestinal Endoscopy provide guidelines for endoscopic training. Program adherence to these recommendations is unclear. This study aims to assess endoscopic training experience during fellowship. DESIGN: Questionnaire study. SETTING: The questionnaire was circulated to US fellowship programs, with the assistance of the American Gastroenterological Association. PARTICIPANTS: Graduating third-year fellows. RESULTS: Seventy-three fellows returned the questionnaire. Nearly all fellows met the required numbers for esophagoduodenoscopy (98%) and colonoscopy (100%), with fewer meeting requirements for PEG (73%) and non-variceal hemorrhage (75%). The majority of fellows did not meet minimum numbers for variceal banding (40%), esophageal dilation (43%), capsule endoscopy (42%). Fellows rated training in cognitive aspects of endoscopy as 3.86 [1 (inadequate), 5 (excellent)] and reported greatest emphasis on interpreting endoscopic findings and least on virtual colonography. Quality indicators of endoscopy received little emphasis (rating of 3.04; p = 0.00001), with adenoma detection rate being least emphasized. Fifty-six percent of fellows reported having routine endoscopy conferences. Half of the programs have endoscopic simulators, with 15% of fellows being required to use simulation. Following direct hands-on experience, fellows rated external endoscopy courses (64%) as the next most useful experience. CONCLUSIONS: Many fellows do not meet required numbers for several endoscopic procedures, and quality indicators receive little emphasis during training. Most programs do not provide simulation training or hold regular endoscopy conferences. Fellowship programs should perform internal audits and make feasible adjustments. Furthermore, it may be time for professional societies to revisit training guidelines.
Assuntos
Educação de Pós-Graduação em Medicina/normas , Endoscopia Gastrointestinal/educação , Bolsas de Estudo , Gastroenterologia/educação , Fidelidade a Diretrizes/normas , Adulto , Varizes Esofágicas e Gástricas , Feminino , Guias como Assunto , Humanos , Masculino , Inquéritos e QuestionáriosAssuntos
Anticoagulantes/efeitos adversos , Doenças do Ceco/diagnóstico , Doenças do Colo/diagnóstico , Colonoscopia , Hemorragia Gastrointestinal/diagnóstico , Hematoma/diagnóstico , Heparina de Baixo Peso Molecular/efeitos adversos , Trombose Venosa/prevenção & controle , Idoso , Anticoagulantes/administração & dosagem , Doenças do Ceco/induzido quimicamente , Doenças do Colo/induzido quimicamente , Colonoscopia/efeitos adversos , Hemorragia Gastrointestinal/induzido quimicamente , Hematoma/induzido quimicamente , Heparina de Baixo Peso Molecular/administração & dosagem , Humanos , Injeções Subcutâneas , Masculino , Valor Preditivo dos TestesRESUMO
Hepatocyte death results in a sterile inflammatory response that amplifies the initial insult and increases overall tissue injury. One important example of this type of injury is acetaminophen-induced liver injury, in which the initial toxic injury is followed by innate immune activation. Using mice deficient in Tlr9 and the inflammasome components Nalp3 (NACHT, LRR, and pyrin domain-containing protein 3), ASC (apoptosis-associated speck-like protein containing a CARD), and caspase-1, we have identified a nonredundant role for Tlr9 and the Nalp3 inflammasome in acetaminophen-induced liver injury. We have shown that acetaminophen treatment results in hepatocyte death and that free DNA released from apoptotic hepatocytes activates Tlr9. This triggers a signaling cascade that increases transcription of the genes encoding pro-IL-1beta and pro-IL-18 in sinusoidal endothelial cells. By activating caspase-1, the enzyme responsible for generating mature IL-1beta and IL-18 from pro-IL-1beta and pro-IL-18, respectively, the Nalp3 inflammasome plays a crucial role in the second step of proinflammatory cytokine activation following acetaminophen-induced liver injury. Tlr9 antagonists and aspirin reduced mortality from acetaminophen hepatotoxicity. The protective effect of aspirin on acetaminophen-induced liver injury was due to downregulation of proinflammatory cytokines, rather than inhibition of platelet degranulation or COX-1 inhibition. In summary, we have identified a 2-signal requirement (Tlr9 and the Nalp3 inflammasome) for acetaminophen-induced hepatotoxicity and some potential therapeutic approaches.