Analysis of neuro-theatre utilisation and reasons for cancellation to improve efficiency and productivity.

In neurosurgery, much emphasis has recently been placed on theatre cancellation and time utilization as a key hospital management performance indicator. We sought to evaluate our unit's theatre throughput efficiency and identify the causes of elective surgery cancellations. We retrospectively audited all scheduled elective neurosurgical procedures over a period of nine months. Mean theatre utilization time was 47.0%. The common causes of cancellations were lack of theatre time (32%), non-availability of beds in recovery room (18.6%), and insufficient preoperative patient preparation (5.5%). Inefficiencies were noted in turnover of patients and inaccurate prediction of operative time. Our theatre utilization time is consistent with available literature; however, cancellations of elective surgery waste valuable operative time and resources. The study concludes that a multi-dimensional approach must be taken to improve theatre utilization and reduce cancellation rates. A pre-assessment clinic has been introduced in order to reduce cancellation rates.

The role of insulin receptor substrate 2 in hypothalamic and beta cell function.

Insulin receptor substrate 2 (Irs2) plays complex roles in energy homeostasis. We generated mice lacking Irs2 in beta cells and a population of hypothalamic neurons (RIPCreIrs2KO), in all neurons (NesCreIrs2KO), and in proopiomelanocortin neurons (POMCCreIrs2KO) to determine the role of Irs2 in the CNS and beta cell. RIPCreIrs2KO mice displayed impaired glucose tolerance and reduced beta cell mass. Overt diabetes did not ensue, because beta cells escaping Cre-mediated recombination progressively populated islets. RIPCreIrs2KO and NesCreIrs2KO mice displayed hyperphagia, obesity, and increased body length, which suggests altered melanocortin action. POMCCreIrs2KO mice did not display this phenotype. RIPCreIrs2KO and NesCreIrs2KO mice retained leptin sensitivity, which suggests that CNS Irs2 pathways are not required for leptin action. NesCreIrs2KO and POMCCreIrs2KO mice did not display reduced beta cell mass, but NesCreIrs2KO mice displayed mild abnormalities of glucose homeostasis. RIPCre neurons did not express POMC or neuropeptide Y. Insulin and a melanocortin agonist depolarized RIPCre neurons, whereas leptin was ineffective. Insulin hyperpolarized and leptin depolarized POMC neurons. Our findings demonstrate a critical role for IRS2 in beta cell and hypothalamic function and provide insights into the role of RIPCre neurons, a distinct hypothalamic neuronal population, in growth and energy homeostasis.