A model for preemptive maintenance of medical linear accelerators-predictive maintenance.

BACKGROUND: Unscheduled accelerator downtime can negatively impact the quality of life of patients during their struggle against cancer. Currently digital data accumulated in the accelerator system is not being exploited in a systematic manner to assist in more efficient deployment of service engineering resources. The purpose of this study is to develop an effective process for detecting unexpected deviations in accelerator system operating parameters and/or performance that predicts component failure or system dysfunction and allows maintenance to be performed prior to the actuation of interlocks. METHODS: The proposed predictive maintenance (PdM) model is as follows: 1) deliver a daily quality assurance (QA) treatment; 2) automatically transfer and interrogate the resulting log files; 3) once baselines are established, subject daily operating and performance values to statistical process control (SPC) analysis; 4) determine if any alarms have been triggered; and 5) alert facility and system service engineers. A robust volumetric modulated arc QA treatment is delivered to establish mean operating values and perform continuous sampling and monitoring using SPC methodology. Chart limits are calculated using a hybrid technique that includes the use of the standard SPC 3σ limits and an empirical factor based on the parameter/system specification. RESULTS: There are 7 accelerators currently under active surveillance. Currently 45 parameters plus each MLC leaf (120) are analyzed using Individual and Moving Range (I/MR) charts. The initial warning and alarm rule is as follows: warning (2 out of 3 consecutive values ≥ 2σ hybrid) and alarm (2 out of 3 consecutive values or 3 out of 5 consecutive values ≥ 3σ hybrid). A customized graphical user interface provides a means to review the SPC charts for each parameter and a visual color code to alert the reviewer of parameter status. Forty-five synthetic errors/changes were introduced to test the effectiveness of our initial chart limits. Forty-three of the forty-five errors (95.6 %) were detected in either the I or MR chart for each of the subsystems monitored. CONCLUSION: Our PdM model shows promise in providing a means for reducing unscheduled downtime. Long term monitoring will be required to establish the effectiveness of the model.

A combination of high dose rate (10X FFF/2400 MU/min/10 MV X-rays) and total low dose (0.5 Gy) induces a higher rate of apoptosis in melanoma cells in vitro and superior preservation of normal melanocytes.

The aim of this study was to determine the apoptotic effects, toxicity, and radiosensitization of total low dose irradiation delivered at a high dose rate in vitro to melanoma cells, normal human epidermal melanocytes (HEM), or normal human dermal fibroblasts (HDF) and to study the effect of mitochondrial inhibition in combination with radiation to enhance apoptosis in melanoma cells. Cells irradiated using 10X flattening filter-free (FFF) 10 MV X-rays at a dose rate of 400 or 2400 MU/min and a total dose of 0.25-8 Gy were analyzed by cell/colony counting, MitoTracker, MTT, and DNA-damage assays, as well as by quantitative real-time reverse transcriptase PCR in the presence or absence of mitochondrial respiration inhibitors. A dose rate of 2400 MU/min killed on average five-fold more melanoma cells than a dose rate 400 MU/min at a total dose of 0.5 Gy and preserved 80% survival of HEM and 90% survival of HDF. Increased apoptosis at the 2400 MU/min dose rate is mediated by greater DNA damage, reduced cell proliferation, upregulation of apoptotic genes, and downregulation of cell cycle genes. HEM and HDF were relatively unharmed at 2400 MU/min. Radiation induced upregulation of mitochondrial respiration in both normal and cancer cells, and blocking the respiration with inhibitors enhanced apoptosis only in melanoma cells. A high dose rate with a low total dose (2400 MU/min, 0.5 Gy/10X FFF 10 MV X-rays) enhances radiosensitivity of melanoma cells while reducing radiotoxicity toward HEM and HDF. Selective cytotoxicity of melanoma cells is increased by blocking mitochondrial respiration.

Suppression of dark current radiation in step-and-shoot intensity modulated radiation therapy by the initial pulse-forming network.

The effect of the initial pulse forming network (IPFN) on the suppression of dark current is investigated for a Siemens Primus accelerator. The dark current produces a spurious radiation, which is referred to as dark current radiation (DCR) in this study. In the step-and-shoot delivery of an intensity modulated radiation therapy (IMRT), the DCR could be of some concern for whole body dose along with leakage radiation through collimator jaws or multileaf collimator. By adjusting the IPFN-to-PFN ratio to >0.8, the DCR can be measured with an ion chamber during the "PAUSE" state of the accelerator in the IMRT mode. For 15 MV x rays, the magnitude of the DCR is approximately equal to 0.7% of the dose at dmax for a 10 x 10 cm2 field. The DCR has a similar central axis depth dose as a 15 MV beam as determined from a water phantom scan. When the IPFN-to-PFN ratio is lowered to <0.8, no DCR is detected. For low energy x rays (6 MV), no DCR is detected regardless of the IPFN-to-PFN ratio. Although the DCR is studied only for the Siemens Primus model accelerator, the same precaution applies to other models of modern accelerators from other vendors. Due to the large number of field segments used in a step-and-shoot IMRT, it is imperative therefore, that dark current evaluation be part of machine commissioning and annual calibration for high-energy photon beams. Should DCR be detected, the medical physicist should work with a service engineer to rectify the problem. In view of DCR and whole body dose, low-energy photon beams are advisable for IMRT.