Background: The knotting or in vivo entrapment of epidural catheters is an uncommon butchallenging issue for anesthesiologists. This study aimed to identify the possible causes behindentrapped epidural catheters and the effective methods for their removal. Methods: A systematic review of relevant case reports and series was conducted using thepatient/population, intervention, comparison and outcome framework and keywords suchas “epidural,” “catheter,” “knotting,” “stuck,” “entrapped,” and “entrapment.” The PreferredReporting Items for Systematic Reviews and Meta-Analyses statement was followed, andthe review protocol was registered with International Prospective Register for Systematic Reviews(CRD42021291266). Results: The analysis included 59 cases with a mean depth of catheter insertion from theskin of 11.825 cm and an average duration of 8.17 h for the detection of non-functioningcatheters. In 27 cases (45.8%), a radiological knot was found, with an average length of2.59 cm from the tip. The chi-squared test revealed a significant difference between the initialand final positions of catheter insertion (P = 0.049). Conclusions Deep insertion was the primary cause of epidural catheter entrapment. To removethe entrapped catheters, the lateral decubitus position should be attempted first, followedby the position used during insertion. Based on these findings, recommendations forthe prevention and removal of entrapped catheters have been formulated.

Alzheimer’s disease (AD) is a multifactorial, rapidly progressing neurodegenerative disorder. As the exact cause of the disease is still unclear, the drug development is very challenging. This review encompasses the commonly used AD models involving various chemicals, heavy metals and endogenous substances induced models and the transgenic models. It also provides insight into the reliable emerging models of AD that may overcome the shortcomings associated with available models. Chemicals like streptozotocin, scopolamine, colchicine and okadaic acid render the animal susceptible to neuroinflammation and oxidative stress induced neurodegeneration along with amyloid-β deposition and tau hyperphosphorylation. Similarly, endogenous substances like acrolein and amyloid-β 1–42 are efficient in inducing the major pathologies of AD. Heavy metals like aluminum and fluoride and mixture of these have been reported to induce neurotoxicity therefore are used as animal models for AD. Transgenic models developed as a result of knock-in or knock-out of certain genes associated with AD including PDAPP, APP23, Tg2576, APP/PS1, 3 × Tg and 5 × FAD have also been incorporated in this study. Further, emerging and advanced pathomimetic models of AD are provided particular interest here which will add on to the current knowledge of animal models and may aid in the drug development process and deepen our understanding related to AD pathogenesis. These newly discovered models include oAβ25-35 model, transgenic model expressing 82-kDa ChAT, oDGal mouse and APP knock-in rat.This study may aid in the selection of suitable model for development of novel potent therapeutics and for exploring detailed pathogenic mechanism of AD.