RESUMO
BACKGROUND: Enhanced recovery after surgery (ERAS) protocols have been propagated in general surgery since the mid-1990s due to medical and health economic advantages for patients as well as hospitals. A comprehensive implementation in Germany is not yet established, although the demographic change requires more than ever concepts for the safe treatment of multimorbid frail patients. The aim of this review is to present modern ERAS concepts, to discuss an extension to prehabilitation measures for frail patients and to present aspects of structural feasibility. MATERIAL AND METHOD: A selective literature search in the PubMed database was performed and national as well as international guidelines up to the cut-off date of 1 July 2022 were considered. RESULTS: From an anesthesiological point of view, preoperative optimization, individual anesthesia management and postoperative analgesia are prioritized. The implementation of ERAS protocols requires a high degree of interdisciplinarity and needs in addition to medical know-how, appropriate information systems and structures. Modern ERAS concepts can reduce hospital costs and improve patient outcome. CONCLUSION: The implementation of ERAS protocols is beneficial for patients as well as economically and should be further promoted. In addition, the benefit of an extension of ERAS concepts, e.g. in older multimorbid patients, should be further scientifically analyzed.
Assuntos
Recuperação Pós-Cirúrgica Melhorada , Satisfação do Paciente , Humanos , Idoso , Assistência Perioperatória/métodos , Cuidados Pós-Operatórios/métodos , Terapia CombinadaRESUMO
Neuroblastoma is a malignant childhood cancer arising from the embryonic sympathoadrenal lineage of the neural crest. Retinoic acid (RA) is included in the multimodal therapy of patients with high-risk neuroblastoma to eliminate minimal residual disease. However, the formation of RA-resistant cells substantially lowers 5-year overall survival rates. To examine mechanisms that lead to treatment failure, we chose human SH-SY5Y cells, which are known to tolerate incubation with RA by activating the survival kinases Akt and extracellular signal-regulated kinase 1/2. Characterization of downstream pathways showed that both kinases increased the phosphorylation of the ubiquitin ligase mouse double minute homolog 2 (Mdm2) and thereby enhanced p53 degradation. When p53 signaling was sustained by blocking complex formation with Mdm2 or enhancing c-Jun N-terminal kinase (JNK) activation, cell viability was significantly reduced. In addition, Akt-mediated phosphorylation of the cell-cycle regulator p21 stimulated complex formation with caspase-3, which also contributed to cell protection. Thus, treatment with RA augmented survival signaling and attenuated basal apoptotic pathways in SH-SY5Y cells, which increased cell viability.