Observed rates of surgical instrument errors point to visualization tasks as being a critically vulnerable point in sterile processing and a significant cause of lost chargeable OR minutes.

BACKGROUND: The reporting of surgical instrument errors historically relies on cumbersome, non-automated, human-dependent, data entry into a computer database that is not integrated into the electronic medical record. The limitations of these reporting systems make it difficult to accurately estimate the negative impact of surgical instrument errors on operating room efficiencies. We set out to determine the impact of surgical instrument errors on a two-hospital healthcare campus using independent observers trained in the identification of Surgical Instrument Errors. METHODS: This study was conducted in the 7 pediatric ORs at an academic healthcare campus. Direct observations were conducted over the summer of 2021 in the 7 pediatric ORs by 24 trained student observers during elective OR days. Surgical service line, error type, case type (inpatient or outpatient), and associated length of delay were recorded. RESULTS: There were 236 observed errors affecting 147 individual surgical cases. The three most common errors were Missing+ (n = 160), Broken/poorly functioning instruments (n = 44), and Tray+ (n = 13). Errors arising from failures in visualization (i.e. inspection, identification, function) accounted for 88.6% of all errors (Missing+/Broken/Bioburden). Significantly more inpatient cases (42.73%) had errors than outpatient cases (22.32%) (p = 0.0129). For cases in which data was collected on whether an error caused a delay (103), over 50% of both IP and OP cases experienced a delay. The average length of delays per case was 10.16 min. The annual lost charges in dollars for surgical instrument associated delays in chargeable minutes was estimated to be between $6,751,058.06 and $9,421,590.11. CONCLUSIONS: These data indicate that elimination of surgical instrument errors should be a major target of waste reduction. Most observed errors (88.6%) have to do with failures in the visualization required to identify, determine functionality, detect the presence of bioburden, and assemble instruments into the correct trays. To reduce these errors and associated waste, technological advances in instrument identification, inspection, and assembly will need to be made and applied to the process of sterile processing.

Insulin potentiates essential amino acids effects on mechanistic target of rapamycin complex 1 signaling in MAC-T cells.

Different models of lactation offer conflicting evidence as to whether insulin signaling is required for AA to stimulate mechanistic target of rapamycin complex 1 (mTORC1) activity. We hypothesized that insulin potentiates essential AA stimulation of mTORC1 activity in the MAC-T mammary epithelial cell line. Here, our objective was to assess mTORC1 signaling activity in response to insulin and individual or grouped essential AA. Insulin and essential AA concentrations in the treatment medium ranged from normo- to supraphysiological, with insulin at 0, 1, 10, or 100 nmol/L and essential AA at approximately 0, 0.01, 0.05, 0.1, 1, or 3× reference plasma levels. Effects and interaction of insulin and total essential AA were tested in a 3 × 5 factorial design (n = 3 replicates/treatment); insulin and the individual AA Leu, Met, Ile, and Arg were likewise tested in 3 × 4 factorials (n = 4). As the remaining individual AA His, Lys, Phe, Thr, Trp, and Val were expected to not affect mTORC1, these were tested only at the highest insulin level, 100 nmol/L (n = 4). For all of these, linear and quadratic effects of total and individual AA were evaluated. Essential AA were subsequently grouped by their positive (Leu, Met, Ile, Arg, and Thr; TOR-AA) or absent-to-negative effects (His, Lys, Phe, Trp, and Val; NTOR-AA), and tested for interaction in a 2 × 2 factorial design (n = 4), with each AA at its respective 1× plasma level, and insulin held at 100 nmol/L. All experiments consisted of 1 h treatment incubation, followed by Western blotting of cell lysates to measure phosphorylation and abundance of the mTORC1 pathway proteins Akt (Ser473); ribosomal protein S6 kinase p70 (S6K1, Thr389); eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1, Ser65); and ribosomal protein S6 (S6, Ser240/244). The Akt phosphorylation was overall increased by insulin, with a possible negative interaction with both total essential AA and the individual AA Leu. Total essential AA also increased S6K1 and 4E-BP1 phosphorylation in an insulin-dependent manner. The individual AA Leu, Met, Ile, and Arg increased S6K1 phosphorylation in an insulin-dependent manner. Similarly, Met and Arg increased 4E-BP1 phosphorylation in an insulin-dependent manner. Histidine, Lys, Trp, and Val did not affect S6K1 phosphorylation. However, S6K1 phosphorylation was linearly increased by Thr and quadratically decreased by Phe. Relative to the phosphorylation of S6K1 when cells were incubated with no essential AA, the NTOR-AA group had no effect, whereas the TOR-AA increased phosphorylation to the same degree observed with all 10 essential AA. Overall, we have found that insulin is required for essential AA to stimulate mTORC1 activity in MAC-T cells. In addition, the AA responsible for the bulk of mTORC1 activation in MAC-T are limited to Leu, Met, Ile, Arg, and Thr.