RAD425 Measurement of Radiation Dose & Biological Effects PDF

**[Measurement of radiation dose]** 1. Describe units of measurement for radiation dose 2. List approximate radiation doses for common imaging examinations and compare them with non-imaging events 3. Describe methods used to measure radiation doses for imaging examinations **Absorbed...

**[Measurement of radiation dose]** 1. Describe units of measurement for radiation dose 2. List approximate radiation doses for common imaging examinations and compare them with non-imaging events 3. Describe methods used to measure radiation doses for imaging examinations **Absorbed dose:** **Defined as energy imparted to organ or tissue per unit mass.** Average absorbed dose to that tissue. Unit: gray (Gy) **Equivalent dose:** **Defined as absorbed dose to organ or tissue weighted for type of radiation.** Unit: sievert (Sv) H~T~ = Σ~R~ w~R~. D~T,R~ w~R~ = 1 for diagnostic X-rays, Beta and Gamma Radiation. w~R~ = 20 for alpha particles w~R~ = 5-20 (for neutrons -- energy dependent) **Effective dose:** **Defined as absorbed dose to organ or tissue weighted for type of radiation AND type of tissue.** Unit: sievert (Sv) E = Σ~T~ w~T~. H~T~ where H~T~ = equivalent dose to tissue T, w~T~ = tissue weighting factor for T The effective dose is: - Based on scientific evidence on the effects of radiation - Directly related to risk to 'average person' irradiated -- more relevant to populations Risk depends on: - Amount of energy absorbed per unit mass - Type of radiation - The radiosensitivity of the site where radiation is absorbed **Excess risk from radiation:** Risk of inducing a fatal cancer -- 1 in 20,000 per mSv (5% per sievert) Radiation risk to children is higher because: - Longer life span for cancers to develop -- more time for radiation damage to manifest - Developing tissues may be more radiosensitive -- cells in children and foetuses divide rapidly, providing more opportunity for radiation to disrupt the process and cause cell damage. Radiation risk to the elderly is lower. **Patient dosimetry:** - Estimation of dose to patient -- want an effective dose measured in millisieverts, mSv - Estimation of risk -- based on critical organ doses - Dose comparison -- e.g. different hospital or modalities -- dose area product DAP or dose length product DLP Dose calculation methods in DR: - Entrance surface dose (ESD) -- simplest - Dose area product (DAP) -- planar X-ray dose metric - Dose length product (DLP) -- CT dose metric **Entrance surface doses (ESD):** - A measurement of absorbed dose -- AIR KERMA - Units: Grays (Gy or J/Kg), commonly cited as mGy - Can be directly measured at patient's skin using a TLD - Calculated from known tube output and other known factors **Dose area product (DAP):** - Measures the product of absorbed dose in air and X-ray field area. - Units Gy.cm\^2 -- mGy.cm\^2 - Independent of FSD (fraction incident beam absorbed) - Measured directly using a DAP metre, a flat area parallel plate IC mounted to the tube port. **Dose length product (DLP):** - Units Gy.cm, commonly cited as mGy.cm - Directly calculated from CTDI vole and scan length -- CTDIL computed tomography dose index Monte Carlo Simulations: - Mathematical modelling of a limited range of photons. - Frequently used in nuclear medicine dosimetry. Considering: - Half-life - Radionuclide emission data - Biological clearance - Also used in radiotherapy for beam modelling Dose and risk: - Effective dose has limitation - Weighting factors are tailored to a population - Not necessarily ideal for individual patient risk - Useful for dose comparisons across modalities **What is a diagnostic reference level?** The DRL is used in medical imaging to indicate whether, in routine conditions, the dose to the patient or the number of radiopharmaceuticals administered in a specific radiological procedure is unusually high or low for that specific procedure **National Diagnostic Reference level:** In the UKR NDRLS are based on the body region being examined and the clinical requirement for the examination. **Local Diagnostics Reference Level:** LDRLs should generally be lower than NDRLS -- if the data set is large enough these can be used over NDRLs -- can be updated more frequently, easier to implement and reflect local needs. **Patient dose reduction:** ALARP -- As Low As Reasonably Practicable Limitation: - Time - Shielding - Distance Justification: - Benefit outweighs the risk of harm Optimisation: - Minimise the dose for diagnostic imaging Practicalities: - Use appropriate kV -- allows optimised mAs and reduces unnecessary dose to tissue. - Check field size -- avoid unnecessary repeats, avoid over exposure and reduce scatter dose - Patient positioning -- best image is when patient is closest to the detector as it allows optimised factor and reduces skin dose e.g. PA chest is less dose than AP chest due to breast exposure. - Appropriate system use/ training - Reduce patient thickness where possible e.g. mammogram compression - Increase focus to skin distance -- best image when patient is closest to detector, allows optimised factors and reduces skin dose. - Increase tube filtration, reduces quantity of low energy X-rays, reduces unnecessary skin dose. - System sensitivity -- more efficient use X-rays, allows lower mAs **Foetal exposure:** Foetal radiation risk -- risk is related to stage of foetal development and quantity of radiation exposure. Radiation related risks are most significant during organogenesis. Radiation induced malformations **(deterministic risk)** -- threshold of typically 100mGy and usually associated with CNS problems. 1 Gy can result in severe learning difficulties and microcephaly. Radiation induced cancer (**stochastic risk** -- chance risk) -- cell modified rather than killed, throughout most of the pregnancy foetus is assumed to be at the same level of risk of carcinogenic effect of radiation as children -- for an individual exposed in utero to 1 mGy, the absolute risk of cancer at ages 0-15 is about 1 excess case per 13,000 **Informed consent:** - The pregnant patient has a right to know the magnitude of the risk -- risk is negligible = \1mGy a more detailed explanation should be given. - Crosses the placenta and can pose foetal risk, foetal thyroid accumulate iodine after ten week -- high foetal thyroid dose can result in permanent **hypo**thyroidism -- if pregnancy is discovered within 12hr of I-131 administration prompt oral administration of stable potassium iodine to the mother can reduce foetal thyroid dose. **Occupational exposure** **IRR17 -- protects staff and public** 20mSv in one year is the maximum exposure we can be exposed to. Dose monitoring: Dose quantity is defined by ICRU Passive: results are not instant 0 commonly used routinely for staff monitoring e.g. TLD, OSL and film Real-time: instant monitoring -- used for less routine monitoring -- EPD Passive dose monitoring, TLDs: Thermo-luminescent dosimeter: - Radiation absorbed - Electrons stimulated to a higher energy state - The dosimeter is heated - Electrons drop out of a higher energy state, releasing energy as light photons - Light is proportional to the dose Real-time dose monitoring, EPD: - Electronic personal dosimeter - Solid state detector - Incident radiation creates electron-hole pairs - Instant read out - No. holes is proportional to incident radiation energy Types of dose monitoring: - Whole body - Eye -- interventional staff groups - Skin and extremity -- nuclear med and interventional Limitations: - Doesn't measure effective or organ dose **Nuclear Medicine Exposure:** Dose is dependent on activity administered and the chosen radiopharmaceutical -- there is library of doses for radiopharmaceuticals and radionuclides. - Patient dose is reduced by administering lower activity - Staff dose reduced by minimising time, maximising distance and wearing PPE Typical doses: - Bone scan (600 MBq Tc-99m phosphonate): 2.9 mSv - PET scan (400 MBq F-18 FDG): 7.6 mSv (without CT) - Renal scan (80 MBq Tc-99m DMSA): 0.7 mSv - Glomerular filtration rate (kidney function) non-imaging test (10 MBq Tc-99m DTPA): 0.05 mSv **[Biological effects of radiation]** 1. Describe the mechanisms by which radiation damages living tissue\ 2. Describe the health risks of radiation in human populations\ 3. Describe the evidence base underpinning radiation risk to health.\ 4. Compare the risk of radiation dose to the risk of deterministic and stochastic effects\ 5. Describe the effect of patient demographics on radiation-induced risk e.g. age, sex, size Radiation can cause cancer -- a latency period of 10-40 years. Units of measurement: - Gray (Gy) -- average **absorbed dose** to organ/tissue (J//Kg - Sievert (Sv) -- **Equivalent dose** is absorbed dose to organ or tissue weight for type of radiation - Sievert (Sv) -- **Effective dose** is absorbed dose to organ or tissue weight for type of radiation and type of tissue **Ionising radiation in tissue:** - Deposition of energy from ionising radiation is localised on the atomic scale. - The energy released locally in each ionisation event is more than enough to break atomic bonds. - Typical energy released when one atom is ionised is about 35 eV - Ionisation events comprise small clusters of ion pairs because the secondary electrons that are liberated in the initial ionisation process often have enough energy to ionise other atoms. Ionising radiation damages biological molecules through two types of interaction: - **Direct** - The release of energy from an ionisation event (\~35 eV) is sufficient to break molecular bonds\ \*\*The energy of a covalent bond in a strand of a DNA molecule is 4 eV.\*\*\ \*\*The energy of hydrogen bonds which bind the strands of DNA together is 0.4 eV.\*\* - **Indirect** - Damage may also be induced by the interaction of free radicals produced by the ionisation. Eighty percent of tissue is made up of water. When water molecules ionise H+ ions and OH free radicals are formed. **Cell Damage:** Free radical reactions cause damage to proteins, enzymes, DNA etc. Damage cells/DNA may be repaired perfectly but the cell can also: - Die -- deterministic - Mutate -- which can become cancerous, this is **stochastic**. **Tissue reactions (deterministic effects):** - Cell death can lead to tissue reactions - Most organs are unaffected by the loss of a few cells, however, if enough are lost there will be a loss of tissue function - At small doses the probability of harm is zero - Above the threshold dose the probability of harm is 100% - Above the threshold dose severity of harm is proportional to dose -- latency period is short (days to weeks) Examples of deterministic effects from radiation: - Hair loss - Nausea - Skin effects - Ulcerations - Erythema - Cataracts - Paralysis +-----------------------+-----------------------+-----------------------+ | **Dose absorbed to | **Critical system** | **Time to death** | | organ system** | | | | | | **(days)** | | **(Gy)** | | | +-----------------------+-----------------------+-----------------------+ | 3 - 5 | Bone marrow | 30 - 60 | +-----------------------+-----------------------+-----------------------+ | 5 - 15 | GI tract | 7 - 20 | +-----------------------+-----------------------+-----------------------+ | 5 - 15 | Lung / kidney | 60-150 | +-----------------------+-----------------------+-----------------------+ | \> 15 | CNS | \< 5 | +-----------------------+-----------------------+-----------------------+ **Tissue Effects: there is sensitivity variation among patients** - **Erythema --** reddening of skin due to blood vessel dilation -- burns and ulcerations - **Depilation** - **Sterility** - temporary (0.1 Gy) permanent (F 3 Gy and M 6 Gy) - **Cataracts --** 0.5 Gy **Deterministic effects on embryo/foetus:** No significant hark below 100 mGy Malformations of organ development may occur above this threshold; sensitivity depends on gestational age -- severe intellectual disability = 300 mGy -- most sensitive period is 8-15 weeks. **Linear Quadratic model of cell survival** describes the relationship between cell survival and delivered dose. Can be used in radiotherapy with differential cell killing of tumour vs healthy tissues -- radiotherapy is a fractionated process to give healthy tissue a recovery period. **Biological Damage:** **Stochastic effects** are caused by: - Prevention or delay of cell division - Modification of normal cell -- neoplasmic transformation - Modifications to germinal cells of reproductive tissues which are then passed on to daughter cells - This may occur immediately or after a LATENCY PERIOD **Summary:** **Deterministic effects/ tissue effects:** Kills cells leading to organ damage -- **there is a threshold radiation level for occurrence and severity increases with radiation dose not chance/probability.** **Stochastic effects:** - Cellular damage that doesn't repair properly, mutations can lead to cancer -- **no threshold dose, probability increases with radiation dose not severity.** Linear no threshold model -- mainly concerned with cancer induction **Censer and Heritable effects:** If an irradiated cell is damaged but not killed, then its function may be changed -- a modified reproductive cell may lead to damage in future generations -- a modified somatic cell may lead to carcinogenesis. **Carcinogenesis:** If an irradiated SOMATIC cell is modified, it can lead to cancer (somatic cells are anything but gametes) -- STOCHASTIC EFFECT - Probability of cancer induction is proportional to dose - Severity unrelated to dose - No minimum threshold - Variable latent period is 5-40 years - Risk factor is 1 Sv = 5% risk **Genetic effects:** A modified GAMETE cell or precursor may lead to the effects of radiation being expressed in children of exposed persons -- little evidence of this occurring in humans as it is masked by the natural incidence of disabilities. Risk factors: 1Sv = 0.4% risk. **Estimating Risk:** Estimated by ICRP -- report 103 2007 defines the effective dose and gives the 5% per Sv risk which applies to typical people. Effective dose can be attributed to risk of lifetime cancer induction. We can use the dosimetric quantity of effective dose to management of radiation protection to weigh up and compare techniques -- Age, sex and organs involved should be considered before exposing. **Background radiation:** Sources of exposure include - Terrestrial radiation - Radon gas -- significant contributor -- radon gas seeps from the ground into gaps in building, poor ventilation can increase exposure. - Cosmic radiation -- high energy articles from the sun and outside solar system, vary within the atmosphere. - Intakes of radionuclides - Medical exposures - Nuclear industry and weapons We consume radionuclide -- radioactivity can be taken up by plants and animals which we ingest as well as some present in the atmosphere which we inhale -- C14 from plants, Rb87 from plants and animals -- 100g of Brazil nuts gives an effective dose of 0.01 mSv = 1 chest X-ray. [Revision] 1. Describe units of measurement for radiation dose Sievert and Gray Sievert measures the biological effects of radiation -- gray x weighting factor -- used for dose assessments Gray measures the absorbed dose of radiation -- joules per Kg 2\. List approximate radiation doses for common imaging examinations and compare them with non-imaging events CXR = half a day of background radiation 3\. Describe methods used to measure radiation doses for imaging examinations Measured using the effective dose, measured in mSv. We can use DRL, NDRL and LDRLs to measure radiation doses as well as the Monte Carlo transport code. 1. Describe the mechanisms by which radiation damages living tissue Stochastic and Deterministic effects Stochastic effects = likelihood of developing cancer due DNA damage Deterministic effects = above threshold dose effects are 100% - Hair loss - Nausea - Skin effects - Ulcerations - Erythema - Cataracts - Paralysis 4\. Compare the risk of radiation dose to the risk of deterministic and stochastic effects Increasing radiation dose directly increases the severity of deterministic effects; it increases the likelihood of stochastic effects but does not affect the severity. 5\. Describe the effect of patient demographics on radiation-induced risk e.g. age, sex, size Younger patients are at greater risk of stochastic effects due to the latency period of 10-40 years for cancer. Their tissues are also more radiosensitive. Older patients are at less risk as their cells are not dividing as frequently, making their tissues less radiosensitive, and they will likely die before the latency period for cancer to catch them. Larger patients are at greater risk for deterministic effects because greater doses of radiation need to be used, meaning that the localised tissues interacting with the radiation will be more severely harmed.