Accounting for costs, QALYs, and capacity constraints: using discrete-event simulation to evaluate alternative service delivery and organizational scenarios for hospital-based glaucoma services.

BACKGROUND: Decision-analytic models are routinely used as a framework for cost-effectiveness analyses of health care services and technologies; however, these models mostly ignore resource constraints. In this study, we use a discrete-event simulation model to inform a cost-effectiveness analysis of alternative options for the organization and delivery of clinical services in the ophthalmology department of a public hospital. The model is novel, given that it represents both disease outcomes and resource constraints in a routine clinical setting. METHODS: A 5-year discrete-event simulation model representing glaucoma patient services at the Royal Adelaide Hospital (RAH) was implemented and calibrated to patient-level data. The data were sourced from routinely collected waiting and appointment lists, patient record data, and the published literature. Patient-level costs and quality-adjusted life years were estimated for a range of alternative scenarios, including combinations of alternate follow-up times, booking cycles, and treatment pathways. RESULTS: The model shows that a) extending booking cycle length from 4 to 6 months, b) extending follow-up visit times by 2 to 3 months, and c) using laser in preference to medication are more cost-effective than current practice at the RAH eye clinic. CONCLUSIONS: The current simulation model provides a useful tool for informing improvements in the organization and delivery of glaucoma services at a local level (e.g., within a hospital), on the basis of expected effects on costs and health outcomes while accounting for current capacity constraints. Our model may be adapted to represent glaucoma services at other hospitals, whereas the general modeling approach could be applied to many other clinical service areas.

Contribution of active membrane processes to conducted hyperpolarization in arterioles of hamster cheek pouch.

OBJECTIVE: Conduction of vasodilation triggered by acetylcholine (ACh) in arteriolar networks reflects hyperpolarization and its spread from cell to cell along the vessel wall. The amplitude and distance of the vasomotor response appear greater than can be explained by simple passive decay of the electrical signal. The authors tested the hypothesis that the conduction of hyperpolarization involves active membrane processes as the signal travels along the arteriolar wall. METHODS: Intracellular recordings of membrane potential were made from either the smooth muscle or endothelial cell layer of arterioles of the hamster cheek pouch in vivo. Acetylcholine was delivered onto an arteriole using microiontophoresis at defined distances from the recording site, and transient hyperpolarizations were recorded. The area enclosed by the transients (voltage x time integral below baseline) was measured and compared to the area expected if the hyperpolarization was spreading passively. RESULTS: In 11 of 15 recordings from smooth muscle and 5 of 7 from endothelium, areas of the transients were larger than expected for purely passive spread of the electrical signal. CONCLUSIONS: Conduction of hyperpolarization is enhanced by active membrane processes as the signal travels along the arteriolar wall. Signal augmentation will promote blood flow to tissue regions from which hyperpolarization of arterioles originates.