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Diagnostic imaging has evolved from the single technique of radiography discussed in the first edition of Caffey's Pediatric X-Ray Diagnosis in 1945 to a specialty with many modalities and techniques. Many of these modalities use ionizing radiation, and some, such as computed tomography (CT) and nuclear imaging, entail relatively high doses of radiation. Therefore the imaging community (and our medical colleagues) must jointly adhere to two of the principles of radiation protection for our patients: justification (i.e., the examination is warranted) and optimization (i.e., the appropriate technique is used). For example, in computed or direct digital radiographic examinations, image processing can accommodate overexposures. The image can be adjusted to appear as if it were obtained using standard techniques, whereas with screen film technology, the film image would be recognized as overexposed (dark) ( Fig. 1.1 ). Without accountability for displaying dose metrics (such as the exposure index available with digital radiography), it is difficult or impossible to account for patient exposures in clinical practice. Additionally, uninformed and potentially irresponsible justification of medical imaging occurs when persons are unfamiliar with the methods of estimating an effective radiation dose during CT examinations in children. Increasing accountability is expected from the medical community with regard to the use of imaging modalities that expose children (as well as adults) to ionizing radiation. As such, a basic understanding of radiation biology, including bioeffects, radiation doses of various types of imaging examinations, and risks of radiation, is essential for the pediatric imager. A glossary of terms and dose descriptors is found in the addendum at the end of this chapter.
Approximately 4 billion imaging examinations using ionizing radiation (i.e., radiography, fluoroscopy/angiography, CT, and nuclear imaging) are performed annually worldwide. In the United States, medical imaging currently accounts for a significant percentage of the annual radiation exposure to the population. Natural or background sources account for about 50% of the annual radiation exposure in the United States, and diagnostic medical radiation accounts for most of the remainder, an approximately sixfold increase during the past 30 years ( Figs. 1.2A and B ). CT alone accounts for nearly 25% of all radiation exposure to the US population. Many reasons exist for the increased use of diagnostic medical radiation, and much use of such radiation is based on sound medical decision making. However, other factors determine use as well, including defensive medicine.
Hall has written an excellent review of radiobiology for the radiologist. The biologic effects of radiation result primarily from damage to deoxyribonucleic acid (DNA). The x-ray particle, the photon, gives up its energy to produce a fast recoil electron, which may damage DNA directly but which also can interact with a molecule of water to produce a free radical ( Fig. 1.3 ). A free radical is a highly reactive atom or molecule with an unpaired electron in the outer shell:
where the asterisk indicates a free radical.
Two-thirds of x-ray damage occurs via OH radicals, suggesting that someday this component of radiation damage might be reduced through the use of chemical radioprotectants. The topic of radioprotectants was recently well reviewed.
The biologic effects of radiation result primarily from damage to double-stranded DNA as opposed to single-strand injury (see Fig. 1.3 ). Single-strand breaks of DNA are readily repaired and are presumed to have a negligible effect. Breaks in both DNA strands that are opposite or separated by a few base pairs are much more difficult to repair. These double-strand breaks can cause important biologic effects, including genetic mutations, carcinogenesis, and cell death. Dicentric and fragmented breaks typically result in cell death, whereas nonlethal translocation repairs may cause impaired cellular function, including development of an oncogene.
The biochemical and physiologic damage produced by radiation generally occurs within hours or days, but the impact of these changes, such as the induction of cancer, can take decades to manifest. This carcinogenic process has several steps. Aberrations in chromosomes (e.g., deletions, translocations, or aneuploidy) are produced by DNA damage. Because these damaged cells survive, they become “stable aberrations” (some with neoplastic transformation), the first step to radiation-induced carcinogenesis. The second step is cellular immortality; that is, most cancer cells are descendants of a single cell that originally underwent neoplastic transformation. The third step is tumorgenicity. The radiation exposure induces a cellular genomic instability that is transmitted to progeny, which Little described as “a persistent enhancement in the rate of which genetic changes arise in the descendants of the irradiated cells after many generations of replication…[this process] has been termed a nontargeted effect of radiation as genomic damage occurs in the cells that in themselves receive no direct radiation exposure.”
Most childhood tumors occur sporadically, but in 10% to 15% of the cases, a strong family association and genetic basis for radiation sensitivity are present. Persons with certain diseases are uniquely sensitive to radiation-induced cancers, although the exact mechanism is unclear ( Box 1.1 ).
Ataxia-telangiectasia
Basal cell nevoid syndrome
Cockayne syndrome
Down syndrome
Fanconi anemia
Gardner syndrome
Nijmegan breakage syndrome
Usher syndrome
The two types of biologic effects from radiation are tissue effects (also called deterministic effects ) and stochastic (random) effects. Tissue bioeffects are characterized by a threshold dose, and the severity of the effect is dose dependent. For example, cataracts occur above a threshold recent data suggest is near 500 mGy. Table 1.1 shows some of the doses for deterministic effects. In general, such effects from diagnostic imaging doses are extremely rare. Exceptions with head perfusion CT scanning in adults have been reported. Deterministic effects such as skin ulcers and burns should never occur from diagnostic imaging, but they are occasionally seen with relatively lengthy interventional procedures.
Skin Injury | Approximate Threshold |
---|---|
S kin | |
Transient erythema | 200 rad (2 Gy) |
Dry desquamation | 1000 rad (10 Gy) |
Moist desquamation | 1500 rad (15 Gy) |
Temporary epilation | 200 rad (2 Gy) |
Permanent epilation | 700 rad (7 Gy) |
Late effects on tissue | More variable |
Stochastic effects are more of a concern because they have the potential to occur at any dose, and the severity of the effect is independent of the dose. No threshold exists with stochastic effects, but the probability of an effect (e.g., cancer) increases with increasing doses.
From a public health perspective, all ionizing radiation, including that from medical imaging, is considered to be potentially harmful because we assume that no threshold exists below which radiation is safe (i.e., no harmful effects will occur). This “linear no threshold” model is applied to low-level radiation exposure.
The effects of radiation are greatest on rapidly developing tissues and organs—in fetuses, infants, and young children. In pregnancy, the major biologic effects of fetal demise, growth restriction, organ malformations, and cognitive deficits are seen only with doses far in excess of routine diagnostic imaging. The risk of developing cancer from exposure of a fetus to radiation is uncertain; potential effects could be seen with uterine doses that occur as a result of relatively high direct exposures (e.g., a pelvis CT scan for possible appendicitis). No data in humans indicate that genetic effects result from diagnostic levels of radiation.
Compared with middle-aged adults, children are from 2 to 15 times more sensitive to radiation-induced carcinogenesis. However, Shuryak et al. recently noted that the cancer induction risk (greater at younger ages) must be balanced with the radiation-induced promotion of premalignant damage (greater in middle age), which may differ for certain types of cancer. Thus cancer risks may be higher in the adult population than traditionally believed.
Low-dose effects have been described by Pierce and Preston, who studied the data from atomic bomb survivors reported by the Radiation Effects Research Foundation. Among persons who had received dosages of 0.005 to 0.2 sievert (500 mrad to 20 rad), 35,000 people survived, and 5000 cases of cancer developed. The authors made the following conclusions: first, the solid cancer risk persists for more than 50 years. Second, there is a 10% increase over the expected cancer rate. Low-dose relative risk factors are shown in Fig. 1.4 .
The overall increased risk of excess cancer for the entire population suggested by the International Commission on Radiological Protection is 5% per sievert for low doses and low-dose rate. This value is an average value; for adults in late middle age, the excess risk decreases to only 1% per sievert, whereas for children, the excess risk may be as high as 16% per sievert for girls and 12% per sievert for boys. The female dose is higher because of the greater incidence of breast and thyroid cancers ( Fig. 1.5 ). Radiation risks from diagnostic imaging low-level radiation were reviewed recently. Two excellent reviews also recently were published by Linet et al. ( e-Table 1.2 ). We have cautious uncertainty regarding cancer risk and low-level radiation. As Hricak et al. state, “In brief, there is reasonable, though not definitive, epidemiologic evidence that organ doses in the range from 5 to 125 mSv result in a very small but statistically significant nonzero increase in cancer risk.”
Study | Upper Age Limit (y) | Type/No. of Cases | Type/No. of Controls | Method of Exposure to Assessment | Type of Exposure | Exposure Prevalence in Controls | Estimated Relative Risk |
---|---|---|---|---|---|---|---|
L eukemia | |||||||
Stewart et al., UK (1953–1955) | 10 | Deceased (619) | Population (619) | Interview, medical records | Diagnostic | 12.9 | 1.2 |
Therapeutic | 0.2 | 5.0 | |||||
Polhemus & Koch, US (1950–1957) | NS | Incident (251) | Hospital (251) | Questionnaire | Diagnostic | 41.4 | 2.1 * |
Fluoroscopic | 3.2 | 3.5 * | |||||
Therapeutic | 3.6 | 3.7 * | |||||
Ager et al., US (1965) | 4 | Deceased (109) | Siblings (102) | Interview, medical records | Any | 16.7 | 1.3 |
Neighborhood (110) | 18.2 | 1.1 | |||||
Graham et al., US (1966) | 14 | Incident (319) | Population (884) | Medical records | Any | 36.0 | 1.2 |
>1 site | 7.6 | 2.1 | |||||
Shu et al., China (1974–1986) | 14 | Incident, prevalent (309) | Population (618) | Interview | Any | 27.3 | 0.9 |
Fajardo-Gutierrez et al., Mexico (1993) | 14 | Incident, prevalent (79) | Population, hospital (148) | Interview | Any | 27.0 | 1.1 |
A cute L ymphocytic L eukemia | |||||||
Shu, China (1974–1986) | 14 | Incident, prevalent (172) | Population (618) | Interview | Any | 27.3 | 0.9 |
Magnani et al., Italy (1981–1984) | NS | Incident, prevalent (142) | Hospital (307) | Interview | Diagnostic | 45.9 | 0.7 |
Shu et al., China (1986–1991) | 14 | Incident (166) | Population (166) | Interview | Any | — | 1.6 |
Shu, US (1989–1993) | 15 | Incident (1842) | Population (1986) | Interview | Diagnostic | 39 | 1.1 |
Infante-Rivard, Canada (1980–1998) | 14 | Incident (701) | Population (701) | Interview | Diagnostic, 1 | 19.1 | 1.1 |
Diagnostic, ≥2 | 18.8 | 1.5 * | |||||
A cute M yeloid L eukemia | |||||||
Shu et al., China (1974–1986) | 14 | Incident, prevalent (92) | Population (618) | Interview | Any | 27.3 | 1.0 |
L ymphoma | |||||||
Shu et al., China (1981–1991) | 14 | Incident (87) | Population (166) | Interview | Any | — | 1.6 * |
B rain T umors | |||||||
Howe et al., Canada (1977–1983) | 19 | Incident (74) | Population (138) | Interview | Chest diagnostic | 8.0 | 2.1 |
Skull diagnostic | 4.3 | 6.7 * | |||||
McCredie et al., Australia (1985–1989) | 14 | Incident (82) | Population (164) | Interview | Dental | 9.1 | 0.4 |
Skull diagnostic | 2.4 | 2.3 | |||||
Shu et al., China (1981–1991) | 14 | Incident (107) | Population (107) | Interview | Any | — | 1.5 |
Schuz et al., Germany (1993–1997) | 15 | Incident (466) | Population (2458) | Interview | Any | 4.3 | 0.8 |
A strocytoma | |||||||
Kuijten et al., US (1980–1986) | 14 | Incident (163) | RDD (163) | Interview | Head or neck | NS | 1.0 |
Dental | NS | 0.9 | |||||
Bunin et al., US/Canada (1986–1989) | 5 | Incident (155) | RDD (155) | Interview | Head, neck, or dental | 13.5 | 1.2 |
Dental | 9.0 | 1.0 | |||||
Head | 3.2 | 1.1 | |||||
P eripheral N euroepithelioma | |||||||
Bunin et al., US/Canada (1986–1989) | 5 | Incident (166) | RDD (166) | Interview | Head, neck, or dental | 12.0 | 1.1 |
Dental | 8.4 | 0.5 | |||||
Head | 4.2 | 0.9 | |||||
N euroblastoma | |||||||
Greenberg et al., US (1972–1981) | 14 | Incident (104) | Hospital (208) | Medical records | Chest | 33.2 | 0.3 * |
Wilms (105) | 11.7 | 2.0 | |||||
Cranial | 6.2 | 0.3 | |||||
1.3 | 1.6 | ||||||
Abdominal | 6.7 | 0.4 | |||||
3.9 | 0.8 | ||||||
O steosarcoma | |||||||
Gelberg et al., US (1997) | 24 | Incident (130) | Population (130) | Interview | Medical | NS | 1.0 |
E wing S arcoma | |||||||
Daigle et al., US (1975–1981) | 20 | Incident, prevalent (98) | RDD (98) | Interview | Any | NS | 1.0 |
Incident, prevalent (95) | Siblings (95) | NS | 1.0 | ||||
Winn et al., US (1983–1985) | 22 | Incident (204) | RDD (204) | Interview | Diagnostic | 37.7 | 1.6 * |
Dental | 50.0 | 1.2 | |||||
A ll S ites | |||||||
Stewart et al., UK (1953–1955) | 10 | Deceased (1299) | Populaton (1299) | Interview, medical records | Diagnostic | 13.6 | 1.0 |
Therapeutic | 0.2 | 2.7 | |||||
Hartley et al., UK (1980–1983) | 14 | Incident (535) | General practitioner (1068) | Interview, medical records | Neonatal | 0.3 | 2.0 |
Incident (465) | Hospital (928) | Diagnostic | 1.0 | 1.1 | |||
Shu et al., China (1994) | 14 | Incident (642) | Population (642) | Interview | Any | — | 1.3 * |
When discussing radiation dose, it is important to state clearly whether entrance dose, skin dose, exit dose, or organ (absorbed) dose is considered. For example, a vast difference can exist between skin dose and gonadal dose for the same incident radiation. (The terms for dose and quantitative comparisons are provided in the glossary, and dose metrics are provided in Box 1.2 .) “Effective dose” is one measure of radiation that is widely used in discussions of medical radiation. It is commonly used because it is relatively easily derived and allows gross comparisons of dose estimations between examinations of different regions as well as different modalities. However, the application of effective dose in medical imaging can be problematic.
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