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1 Faculty of Health and Social Care, University of West of England, Bristol BS16 1DD and 2 Department of Medical Physics and Bioengineering, Bristol Haematology and Oncology Centre, Horfield Road, Bristol BS2 8ED, UK
| Abstract |
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| Introduction |
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This is true when considering a cell within the target volume, where that cell will receive a tumouricidal dose from a course of radical radiotherapy, whether or not a malignant change has been induced. But a cell just outside the target volume will receive a less than tumouricidal dose, partly from scatter and partly from "concomitant dose", defined in the "Guidance Notes" [2] as the contribution from radiotherapy localization and verification.
In radiation protection, absorbed dose is used to mean the dose averaged over a tissue or organ [3]. The probability of stochastic effects, primarily the induction of malignancy, also depends on the type and energy of ionizing radiation, taken into account by the application of a radiation weighting factor, wR, to absorbed dose to give equivalent dose in tissue T, HT. The vast majority of radiotherapy applications utilize high energy X-ray photons or electrons of similar linear energy transfer (LET) and are assigned a radiation weighting factor of 1.
The relationship between the probability of stochastic effects and equivalent dose also depends on the tissue or organ irradiated. Tissue weighting factors (wT) defined by the International Commission on Radiological Protection (ICRP) [3] give the relative contribution of an organ or tissue to the total detriment from irradiation of the whole body. The weighted equivalent dose is termed the effective dose, E, where E=
wT.HT. As the sum of the tissue weighting factors wT is normalized to unity, the contribution to effective dose resulting from the exposure of an individual organ can be calculated, albeit as an approximation, because of assumptions and simplifications made as detailed in ICRP publication 60 [3]. Table 1
indicates the relative probabilities of inducing a fatal cancer in column 2 and simplified tissue weighting factors in column 3.
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The risk from leakage and scatter from the treatment beams cannot be reduced once the prescription has been fixed. For a radical course of radiotherapy, the effective dose from such leakage and scatter may well be in the order of a few hundred mSv, with a corresponding risk of cancer induction in the order of 1%. However, there is effectively no control on such radiation-induced cancers they are an unavoidable consequence of the decision to treat with radiation.
On the other hand, there is a degree of choice in the level of concomitant radiation exposure, particularly with regard to the verification process, depending upon the number of times patients are imaged, the size of fields used and the characteristics of the imaging system. Underlying IR(ME)R is the principle that, where there is a choice in the level of radiation exposure, the benefits must outweigh the risks.
In this work, only the contribution of the concomitant exposure to the effective dose was evaluated. This was achieved by using only portal beams and not treatment beams in the treatment planning system, so that the contribution of the treatment beam leakage and scatter was effectively removed.
The effective dose from diagnostic X-ray energy exposures, including simulator fluoroscopy and radiography localization procedures and CT localization may be calculated using readily-available computer programs [4], but there appear to be no similar programs for the calculation of effective dose from megavoltage X-ray photon energies.
Under IR(ME)R [1] the employer is required to establish diagnostic reference levels (DRLs) for routine examinations in diagnostic radiology and nuclear medicine. This is to ensure that the dose is "commensurate with the clinical purpose" by reducing radiation exposure that does not contribute to the medical imaging task [5]. DRLs act as investigation levels to identify unusually high levels, which require review if consistently exceeded.
Several authors have examined the use of portal imaging in radiotherapy with both filmscreen combinations and electronic portal imaging devices (EPIDs), and mention the desire to minimize dose outside the treated volume [68]. However, current evidence also leads to recommendations that portal imaging should be performed frequently or even daily during a course of radiotherapy, especially for conformal techniques with small margins for set-up error [912].
Unfortunately, megavoltage portal images have poor image contrast, leading to difficulties in visualizing bony landmarks to which the treatment volume may be related. Clinically useful portal images often require a double-exposure technique whereby the treatment field is first exposed, followed by a larger field exposure to demonstrate relative anatomy. Many linear accelerators have EPIDs but others do not, requiring the use of filmscreen systems with associated higher exposures to give sufficient optical densities [8, 13]. The use of double-exposure portal imaging, by EPID and filmscreen system, will lead to an increase in the probability of inducing a fatal cancer in sensitive organs outside the treatment volume. The probability that 1 mSv will induce a fatal cancer in an average person is 0.005% [3], or, using the linear model of dose dependence, an effective dose of 200 mSv has 1% chance of inducing a fatal cancer.
It would be correct, of course, to query the process of calculating the risk of inducing a fatal cancer in patients who already have cancer. While the probability of inducing a cancer in a patient will not generally depend upon whether they already have cancer, the induced cancer may not have the chance of being fatal because the patient may first succumb to the original cancer. Nevertheless, patients being treated radically may have a high expectation of cure, and in those patients, the effective dose from portal imaging will indicate the chance that they may die from a radiation induced cancer.
There is no doubt that portal imaging can reduce systematic and random set-up errors [11]. But does the benefit due to verification exposures outside the treatment volume outweigh the risk, as required by IR(ME)R [1]? This paper attempts to quantify the detriment resulting from portal imaging.
| Method |
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CT localization scans for this patient were transferred to a 3D treatment planning system (Helax TMS v 5.1A, MDS Nordion, Sweden) and a planning target volume was grown around the prostate. The bladder, colon and sites of red bone marrow were outlined on each axial CT image. Under magnification, the walls of the bladder and colon were identified and outlined. Red bone marrow was assumed to be present in the medullary cavity of the os coxae, sacrum and upper half of the femora and outlined as such.
The treatment planning system was used to model portal beams for a 6 MV Elekta SL22 linear accelerator (Elekta Oncology Systems Ltd, Crawley, UK) representing local protocol for double-exposure portal imaging: the planned field size plus 4 cm in each dimension for an anteroposterior (AP) and lateral view. Full 3D planning was employed with normalization to the depth of maximum dose, dmax.
For each tissue/organ in Table 1
, a volume of interest (VoI) was generated by outlining the organ, or, at least, that part appearing within the portal field. Any part of the tissue/organ exposed to the treatment beam was excluded from the VoI, because it would not contribute to the effective dose. To see why this was necessary, consider a uniform dose deposited in an organ from a portal field. If half of that organ were also in the treatment beam any cancer cells induced in that half would be sterilized. Then the contribution from the portal field to the effective dose in the organ would be only half of that found by multiplying the dose by wT for the organ (essentially, because the probability of inducing surviving cancer cells would be halved in this case).
The mean dose to the VoI was then calculated using the treatment planning computer to generate a dosevolume histogram (DVH) of the VoI. The contribution of the tissue/organ to the effective dose was determined by multiplying the mean dose to the VoI by the ratio of the VoI to the total volume (Vtotal) of the tissue/organ in the body (giving the mean dose to the complete organ) and also by the relative probability of fatal cancer for the complete organ (see Table 2
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A separate 3D treatment plan was produced for each portal beam with the isocentre in the tumour, but with the dose distribution normalized to dmax, since the effective doses are calculated for each portal beam separately.
The same method was employed to calculate effective doses for large-field portal images of other sites.
| Results |
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Typically, the number of MU required for the larger field for a double exposure portal image is 4 when using an EPID, and 12 using a filmscreen system. This would result in effective doses of 1.4 mSv and 4.1 mSv, respectively, from the AP image.
Approximately 25% of the total bladder volume is outside the treated volume but within the extended portal image field for a typical radical prostate technique. This bladder volume contributes 44% to the total effective dose. If the bladder were fully within the treated volume, as it would be for a radical bladder technique, there would be no contribution from the bladder to effective dose. This would give a total effective dose of 0.19 mSv per MU.
| Discussion |
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Verification protocols differ between centres and may depend on availability of linear accelerators with EPIDs. Verification frequency may range from once at the start of treatment to every treatment session. Taking the multicentre RT01 prostate cancer trial [16] as an example, treatment verification of all treatment fields during phase 1 is required daily during week 1, using an EPID, and then weekly. Even for the low dose arm of the trial (64 Gy), this would result in at least 30 verification images giving a total effective dose of about 40 mSv if a double exposure EPID technique is used, based on the representative effective doses given in Table 3
. This would be in addition to an effective dose of the order of 10 mSv from CT localization [17] giving a total effective dose approaching 50 mSv.
Given a 1% chance of inducing a fatal cancer with an effective dose of 200 mSv, 50 mSv to each of the 800 patients recruited into the RT01 trial could be translated into an additional two fatal cancers within that population. IR(ME)R 2000 [1] requires all concerned to reduce unnecessary exposure of patients to radiation. This implies reviewing the use of filmscreen systems alongside the use of EPIDs, and particularly amorphous silicon (aSi) detectors.
Studies involving the implementation into clinical use of active matrix flat panel imagers (AMFPI), using aSi photodiode arrays indicate increased image quality alongside the potential to reduce effective dose [18, 19].
However, EPIDs are not always utilized routinely due to their perceived poor image quality when compared with film. Nevertheless, Kruse et al [20] compared a scanning liquid ion chamber (SLIC) with the more recent aSi AMFPI and ready-pack verification film. Results showed no statistical differences between film and SLIC in terms of clarity of anatomical landmarks, and increased clarity for aSi. Set-up errors were identified more accurately with both EPIDs compared with the film. This might not have been the case if a different film had been used, with its increased image quality [18] but this must be balanced against increased effective dose where extended fields are employed.
In addition, the visual inspection and measurement of anatomical landmarks from film has been shown to be subjective and unreliable [21], a further indication for the routine use of EPIDs and image matching software.
| Conclusion |
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The cumulative effective dose from concomitant exposures may then be recorded and monitored for individual patients, allowing an informed justification of such exposures to be made, in accordance with IR(ME)R [1]. An "action level" of, say, 100 mSv could be set, where the chance of inducing a fatal cancer would be in the order of 0.5% in addition to the natural lifetime risk of approximately 25% [5].
| Acknowledgments |
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Received for publication March 27, 2003. Revision received October 28, 2003. Accepted for publication December 3, 2003.
| References |
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