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Quentin Pellenc Vascular and Endovascular Surgery Unit, Clinique de Genolier, Swiss
Medical Network, Genolier, Switzerland
Department of Vascular and Endovascular Surgery, La Cote Healthcare Group, Morges,
Lausanne, Switzerland
M. Pichlmaier Department of Cardiac Surgery, Ludwig-Maximillian University Hospital,
Munich, Germany
A.L.Pouncey Imperial Vascular Unit, London, UK
Calin-Gheorghe Precup Department of Vascular and Endovascular Surgery, University
Hospital of Lyon, Lyon, France
AnastasiosPsyllas Rhein Main Vascular Center, Department of Vascular and Endovascular
Surgery, Asklepios Clinics Langen, Wiesbaden and Seligenstadt, Langen, Germany
Celia Riga Imperial Vascular Unit, Imperial College Healthcare NHS Trust, St Mary’s
Hospital, London, UK
MarieJoseevan Rijn Erasmus Medical Center, Rotterdam, The Netherlands
TarunSabharwal Guy’s and St. Thomas Hospital, NHS Foundation Trust, London, UK
KalyanSajja Life Hospital, Guntur, India
S.A.Salazar Florida International University Herbert Wertheim College of Medicine, Miami,
FL, USA
List of Contributors
Karim M. Salem Division of Vascular Surgery, Department of Surgery, University of
Pittsburgh Medical Center, Pittsburgh, PA, USA
Division of Vascular Surgery, Department of Surgery, Rutgers New Jersey Medical School,
Newark, NJ, USA
Athanasios Saratzis Department of Cardiovascular Sciences, University of Leicester,
Leicester, UK
MohamedHosnySayed Guy’s and St Thomas’ NHS Foundation Trust, London, UK
Cairo University Hospitals, Cairo, Egypt
VittorioMariaSegramora Vascular Surgery Department, Fondazione IRCCS San Gerardo,
Monza, Italy
Dana B. Semaan Division of Vascular Surgery, University of Pittsburgh Medical Center
(UPMC), Heart and Vascular Institute, Pittsburgh, PA, USA
George S. Sfyroeras Vascular Surgery Department, Attikon University Hospital, Athens,
Greece
J.Shea Imperial Vascular Unit, London, UK
AustinShinagawa Division of Vascular and Interventional Radiology, Kaiser Permanente,
Los Angeles, CA, USA
CalebSolivio California University of Science and Medicine, Colton, CA, USA
KonstantinosSpanos Vascular Surgery Department, Faculty of Medicine, Larissa University
Hospital, School of Health Sciences, University of Thessaly, Larissa, Greece
P.Spath
Department of Vascular Surgery, Ludwig-Maximillian University Hospital, Munich,
Germany
StavrosSpiliopoulos 2nd Department of Radiology, National and Kapodistrian University,
“ATTIKON” University General Hospital, Athens, Greece
List of Contributors
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xxvii
NatalieSridharan University of Pittsburgh Medical Center, Pittsburgh, PA, USA
TrilochanSrivastava SMS Medical College and Hospital, Jaipur, India
J.Stana Department of Vascular Surgery, Ludwig-Maximillian University Hospital, Munich,
Germany
Gemmi Sufali Vascular Surgery Unit, University Hospital, IRCCS Policlinico S. Orsola,
University of Bologna—DIMEC, Bologna, Italy
A.Svetlikov Division of Faculty Surgery, Cardiovascular Surgery Department, North Western
Scientic Clinical Center of Federal Medical Biological Agency of Russia, St. Petersburg State
University, St. Petersburg, Russia
GerganaT.Taneva Rhein Main Vascular Center, Department of Vascular and Endovascular
Surgery, Asklepios Clinics Langen, Wiesbaden and Seligenstadt, Langen, Germany
Apostolos K. Tassiopoulos Division of Vascular and Endovascular Surgery, Stony Brook
Medicine, New York, USA
EmmanuelTeiger Cardiology Department, Hôpitaux Universitaires Henri Mondor, Créteil,
France
IakovosTheodoulou Guy’s and St Thomas’ NHS Foundation Trust, London, UK
Barts NHS Health Trust, The Royal Hospital, London, UK
NarayananThulasidasan Interventional Radiology, Guys and St Thomas’ NHS Foundation
Trust, London, UK
Guy’s & St Thomas’ NHS Foundation Trust- Interventional Radiology Department, London,
UK
Department of Vascular Surgery, Ramsay Group, Champigny sur Marne, France
ValerioTolva Vascular Surgery Department, Fondazione “De Gasperis”, Grande Ospedale
Metropolitano Niguarda, Milan, Italy
Konstantinos Toutouzas First Department of Cardiology, Medical School, National and
Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece
Georgios Trantalis First Department of Cardiology, Medical School, National and
Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece
Santi Trimarchi Section of Vascular Surgery, Cardio Thoracic Vascular Department,
Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
N. Tsilimparis Department of Vascular Surgery, Ludwig-Maximillian University Hospital,
Munich, Germany
CostasTsious First Department of Cardiology, Medical School, National and Kapodistrian
University of Athens, Hippokration Hospital, Athens, Greece
T.Turlejski Department of Radiology, John Radcliffe Hospital, Oxford, UK
VasileiosTzilalis 401 General Military Hospital, Athens, Greece
RamanUberoi Department of Interventional Radiology, Oxford University Hospitals NHS
Foundation Trust, Oxford, UK
GeogyVatakencherry Division of Vascular and Interventional Radiology, Kaiser Permanente,
Los Angeles, CA, USA
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ManolisVavuranakis Third Department of Cardiology, National and Kapodistrian University
of Athens, Sotiria Hospital, Medical School, Athens, Greece
PaoloVerlato School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy
Vascular Surgery Department, Fondazione IRCCS San Gerardo, Monza, Italy
DemetriosV.Vlahakos National and Kapodistrian University of Athens, School of Medicine,
Athens, Greece
LenaL.Vodovotz University of Pittsburgh Medical School, Pittsburgh, PA, USA
PanagiotisVolteas Division of Vascular and Endovascular Surgery, Stony Brook Medicine,
Stony Brook, NY, USA
Vascular and Endovascular Surgery, Stony Brook Medicine, New York, USA
Gregory Walker Division of Neurology, Department of Medicine, Royal Columbian
Hospital, New Westminster, BC, Canada
AngieWhite The Whiteley Clinic, Guildford, UK
MarkS.Whiteley The Whiteley Clinic, Guildford, UK
IosifXenogiannis Second Department of Cardiology, Attikon University Hospital, National
and Kapodistrian University of Athens Medical School, Athens, Greece
BowenXie University of Pittsburgh Medical Center, Pittsburgh, PA, USA
List of Contributors
Theodore H. Yuo Division of Vascular Surgery, University of Pittsburgh Medical Center
(UPMC), Heart and Vascular Institute, Pittsburgh, PA, USA
Part I
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Introduction in Endovascular Techniques
Biological Effects ofIonizing Radiations
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SotiriosEconomides
1
Introduction
The rst biological effects of ionizing radiation were reported
soon after their discovery. A lot of data on the health effects
that might be caused by the exposure to ionizing radiation
have been collected from occupationally exposed workers
(e.g., radiologists, technologists, miners, etc.) as well as
from the survivors of the atomic bombs in Hiroshima and
Nagasaki.
The process associated with the appearance of the biological effects is triggered by the energy deposited by the
ionizing radiations during their interactions with matter. Part
of this energy may appear as heat which is biologically
harmless. However, there is a part of this energy which will
be absorbed by the cell, leading to direct and indirect biological effects.
Direct effects are associated with the killing of signicant
number of cells by ionizing radiation that may lead to biological effects which appear weeks or months effects after
irradiation (deterministic effects). On the other hand, indirect
effects of ionizing radiation may be caused by modications
in the genetic material of cells and appear several years after
their irradiation.
To assess the biological effects due to the exposure to ionizing radiation, the doses received by an individual are considered cumulatively (i.e., each dose received is added to the
previous ones). Moreover, this should be taken into account
in the design of systems of radiation protection and the
establishment of dose limits and constraints for the exposed
workers and the public.
S. Economides (*)
Greek Atomic Energy Commission (EEAE), Athens, Greece
e-mail: sotiris.economides@eeae.gr
Direct andIndirect Eects ofIonizing
Radiation
The appearance of biological effects to living organisms due
to the exposure to ionizing radiations is the result of the damage that may be induced to cells and more specically to
their DNA.This damage is associated to either direct or indirect effects.
The direct effects concern mainly the damage caused to
atoms or molecules (i.e., proteins, RNA, DNA) when the
cells are directly hit by ionizing radiation. This damage may
be associated to single or multiple breaks to the chromosomal strands of the DNA [1]. While most of the damage to
single-stranded DNA may be repaired, lesions to doublestranded DNA may lead to cell death due to deletions, mutations, and chromosomal alterations.
The indirect effects of ionizing radiation are caused by
free radicals which are produced through the radiolysis of
cell water and can cause chemical modications to their
DNA, [1, 2]. These DNA lesions are capable to generate oxidized DNA forms which activate an inammatory cascade
[3].
Moreover, cells in temporal or spatial distance from a cell
damaged by ionizing radiation may present delayed effects
such as the bystander effect and the genomic instability.
The bystander effect concerns the spread of the effect
caused by the ionizing radiation through the communication
of the damaged cells with their neighboring cells [1]. This
effect can be attributed either to gap junctional intercellular
communication or release of soluble factors from the affected
cells [4, 5].
The genomic instability is associated to delayed effects
(e.g., reproductive death) that may appear to the descendants
of cells which have been affected by ionizing radiation.
Irradiated cells damaged but not killed by the ionizing radiation may exhibit an increased mutation rate in their descendants, several generations after the initial exposure to
ionizing radiation [1, 6, 7].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_1
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S. Economides
Repair Mechanisms
The repair characteristics concerning the damages caused to
the DNA (i.e., simple, and multiple strand breaks) are
strongly associated to the biological effects which may
appear due to exposure to ionizing radiation [8, 9]. In addition, the response of the DNA strongly depends on the radiation dose induced the damage and the associated dose rate, as
well as on the quality (energy) of the radiation. In this
respect, simple DNA strand breaks can be corrected by the
cell’s repair mechanisms while double breaks are difcult to
correct and may lead to mutations or the death of the cell.
Apoptosis is one additional cell “repair” mechanism
which reduces the occurrence of surviving cells which may
carry mutations. It can be considered as a form of pro-
grammed cell death that occurs in multicellular organisms
after certain cell changes (e.g., blebbing, cell shrinkage,
nuclear fragmentation, chromatin condensation, DNA fragmentation, etc.) [8, 10].
Assessment ofRadiation Risks
The assessment of the risks associated with the appearance
of biological effects induced by ionizing radiations should be
based on certain quantities such as:
Table 1.1 Radiation weighting factors (wR) values for the calculation
of equivalent dose HT [8]
Radiation type Radiation weighting factor (wR)
Photons 1
Electrons 1
Protons 2
Alpha particles 20
Neutrons Continuous function of neutron energy
Table 1.2 Tissue weighting factors (wT) values for the calculation of
effective dose E [8]
Tissue weighting
Tissue
Bone marrow, colon, lungs, stomach, breast,
remainder tissues
Gonads 0.08
Bladder, esophagus, liver, thyroid 0.04
Bone surface, brain, salivary glands, skin 0.01
factor (wT)
0.12
or tissue, weighted by an appropriate RBE value for this
organ or tissue should be used [11–13]. The RBE values
depend on
– the type and energy of ionizing radiation,
– the dose and dose rate of the exposure, and,
– the tissue or organ irradiated.
– Absorbed dose (D): Is the mean energy deposited in a
tissue or organ volume. It is well dened at any point in
matter and measurable. The radiation damage induced to
tissues or organs depends on the absorbed dose which is
expressed in Grays (Gy).
– Equivalent dose (HT): Is dened as the product of the
corresponding radiation weighting factor (wR) for a radia-
tion R with the absorbed dose. Radiation weighting factor
(wR) values (Table1.1) are associated with the Relative
Biological Effectiveness (RBE) of the different types of
ionizing radiations as well as on biophysical consider-
ations and judgements [8].
– Effective dose (E): Is equal to the product of the corre-
sponding tissue weighting factor value wT (Table1.2) and
the equivalent dose HT for a certain type of radiation. E is
measured in Sieverts (Sv) and used to assess the potential
of an exposure to cause biological effects considering the
type of radiation and the radiosensitivity of different tis-
sues and organs.
To assess the likelihood for tissue reactions due to exposure to ionizing radiation, the absorbed dose (D) to an organ
For the assessment of external exposures at workplaces
usually the effective dose (E) values are used. It is indirectly
estimated by measuring personal dose equivalent at 10mm
below a specied point of the body (Hp (10)), assuming uniform whole-body irradiation [8].
The use of effective dose to assess patients’ exposure is
not suggested, as often only parts of an organ or the human
body are irradiated during medical exposures, and the age
distribution of patients differs from that of the general
public.
To optimize radiological protection (mainly occupational
exposure) collective dose quantities could be used. These
quantities consider the exposure of a group of individuals for
a certain period or during an operation in designated radiation areas. Collective effective dose, S (Sv) is the sum of all
individual effective doses over a certain period or during an
operation under consideration. Its estimation assumes a linear dose effect relationship for stochastic effects without a
threshold (i.e., LNT model). On this basis it is possible to
regard effective doses as additive [8].
1 Biological Eects ofIonizing Radiations
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5
Deterministic Eects
As deterministic are considered those biological effects of
ionizing radiation the severity of which increases proportionally with the dose received above a threshold value (Fig.1.1).
Examples of deterministic effects are skin injuries, hair loss,
cataract, etc. For interventional radiology procedures, skin is
the tissue of main concern as it receives the highest radiation
doses during uoroscopically guided procedures.
Deterministic effects can result from the impairment of
the integrity and function of organs and tissues due to the
exposure to high ionizing radiation doses. These doses may
cause the death of a signicant number of cells, sufcient to
result in tissue reactions.
The response of tissues and organs to ionizing radiation
strongly depends on their structure. In a few cases, the loss of
cells after irradiation is mediated by apoptosis, while in others, it is caused by reproductive failure of regenerative stem
cells.
Most non-proliferating mature cells do not die from irradiation, but from natural senescence. This is one of the main
reasons for the existence of a threshold dose for deterministic effects to appear. This threshold dose differs among different individuals, organs or tissues and is subject to
biological variation (i.e., cellular radiosensitivity, function of
differentiated cells, cellular composition, cell renewal capacity, etc.) [8].
Early tissue reactions may appear hours or a few weeks
after the exposure to ionizing radiation. They can be of
inammatory type such as erythema, and subsequent reactions due to cell loss (e.g., mucositis, and desquamatory
reactions in epithelial tissues). More prone to early reactions
Table 1.3 Range of doses (exposure to acute low LET uniform wholebody radiation) associated with the appearance of specic deterministic
effects and death [8]
Absorbed dose
(Gy) Syndrome
3–5 (LD
5–15 Damage to the
5–15 Damage to the lungs and
>15 Damage to nervous
a
The LD50/60 is the dose necessary to kill 50% of the exposed popula-
tion in 60days
)aDamage to bone marrow 30–60
50/60
gastrointestinal tract
kidney
system
Time of death after
exposure (days)
7–20
60–150
<5, dose-dependent
are tissues with rapidly proliferating cell systems (e.g.,
hematopoietic tissue, cells lining the gastrointestinal tract,
the basal cell layer in the skin, male germ cells, etc.) [8].
Late tissue reactions may appear several months or even
years after the exposure to radiation. They may be associated
to damages to blood vessels or connective tissue elements
that are essential for the function of organs and tissues. Late
reactions can be either “generic” if they occur due to the
damage caused to the target tissue (e.g., vascular occlusions)
[8] or “consequential” if they occur because of early reactions (e.g., dermal necrosis, intestinal strictures, etc.) [13].
For exposures at dose rates lower than around 0.1Gy/h
there is repair of cellular damage while for high LET irradiations the injury is less repairable. Furthermore, some cells
seem to be hypersensitive to doses less than 0.5Gy, but not
at higher doses [14].
At doses more than about 5 Gy, additional effects may
occur, including severe gastrointestinal (stem cell and endothelial capillary cell) damage which, when combined with
hemopoietic damage, causes death in 1–2weeks (Table1.3).
At even higher doses toward 50Gy and above, there is acute
damage in the nervous and cardiovascular systems resulting
in death after a few days [15].
Fig. 1.1 Probability of occurrence and severity for deterministic
effects as a function of dose
Stochastic Eects
Exposing cells, even to very low doses of ionizing radiation,
may lead to the damage of their genetic material. Killing of a
small number of cells due to this exposure, in most cases,
have no further impact. However, the induction of genetic
modications or transformations to a single cell leading to
malignancy, may have serious consequences (i.e., development of radiation induced cancer many years later, heritable
disease in future generations and developmental effects
under certain conditions) [8].
The above effects are called stochastic and may appear
even at very low radiation doses. As they are associated with
a likelihood of occurrence, there is no threshold dose for
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Fig. 1.2 Probability of occurrence and severity of stochastic effects as
a function of dose
their appearance. The risk of stochastic effects increases in
the range of low doses linearly with dose while their severity
is not affected [8, 15]. In addition, their severity does not
increase with an increase in the received dose (Fig.1.2).
For low radiation doses and/or dose rates, the risk for stochastic effects is substantially lower, as there is a greater
likelihood for the induced damage to be repaired. However,
there is still a risk of long-term effects (e.g., cancer) that may
appear years or even decades later. This risk is higher for
children and adolescents, due to their increased radiosensitivity compared to adults.
S. Economides
Epidemiological studies on populations exposed to ionizing radiation, such as atomic bomb survivors or radiotherapy patients, indicate that a signicant increase in the risk of
cancer at doses above 100mSv. Additionally, recent studies
on individuals who underwent medical exposures during
childhood have indicated that the risk of cancer may increase
even at doses in the range of 50–100mSv.
For doses lower than about 100mSv an increase in dose
will be proportional to the likelihood of incurring cancer.
The associated detriment adjusted nominal risk coefcients
for cancer are 5.5 × 10−2Sv−1 for the whole population and
4.1 × 10−2Sv−1 for adult workers [8].
Hereditary Eects
When ionizing radiation hits germ cells, it may damage their
genetic material and result in malformations, metabolic disorders, immune deciencies etc. in the descendants of
exposed individuals that may appear after many
generations.
The detriment adjusted probability coefcients for heritable effects up to the second generation are 0.2 × 10−2Sv−1
for the whole population and 0.1 × 10−2Sv−1 for adult workers [8]. So far, no association between radiation exposure
and the occurrence of hereditary damage has been observed
in humans.
The International Commission on Radiological Protection
(ICRP) assumes that an acute dose of 1 gray (Gy) to parental
gonads leads to one additional severe disease caused by
radiation- induced mutations in 500 births. This genetic risk
may last for up to two generations [8].
Risk ofCancer
Ionizing radiation can induce most, but not all cancer types.
The latency period for the appearance of cancer after irradiation is approximately a decade, but shorter (2–5years) for
leukemia and thyroid cancer. The phases of tumors’ develop-
ment due to cell mutations after their exposure to ionizing
radiation are as follows [8, 15–17]:
(a) Tumor initiation: Entry of a normal cell into pre-
neoplastic state that can lead to cancer.
(b) Tumor promotion: Growth and development of a pre-
neoplastic clone of initiated cells.
(c) Malignant conversion: Change from a pre-neoplastic
state to one where cancer development is likely.
(d) Tumor progression: Cells gain properties that allow
more rapid development and acquire of invasive
characteristics.
Other Diseases Caused by Ionizing Radiation
The results of the analysis of data from the Japanese atomic
bomb survivors and cancer patients who underwent radiotherapy indicate that there is statistical evidence that noncancer effects (i.e., heart disease, stroke, digestive disorders,
and respiratory disease) can be induced by exposures at
effective doses of the order of 1Sv. These effects seem to be
directly associated with the level of the absorbed dose.
Radiotherapy to the heart at high doses (>10Gy) increases
the risk of radiation-related heart diseases (e.g., pericarditis,
valvular disease, cardiomyopathy, etc.) after a minimal
latency period of 1–2years (although acute pericarditis may
develop as soon as some weeks after). Furthermore, there is
a dose–response relationship in late cardiovascular disease
mortality, including both heart disease and stroke after at
least a decade. Such an effect could neither been conrmed
nor excluded at doses lower than 0.5Gy [17–19].
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Eects ofIonizing Radiation totheEmbryo/
Fetus
The embryo is sensitive to ionizing radiation during the preimplantation period of embryonic developments. However,
for doses of a few tens of mGy the probability of lethal
effects of ionizing radiation are very low as well as of health
risks after birth [20, 21].
Regarding the appearance of malformations due to the
exposure of the embryo/fetus to ionizing radiation they are
gestational age-dependent, with the period of maximum
radiosensitivity to be that of major organogenesis and for
doses higher than about 100mGy.
More specically:
1st–2nd week post conception: During this phase, the
number of cells of the fertilized egg is small. Therefore,
exposure of the fetus to high doses of ionizing radiation may
cause its failed implantation in the uterine lining or death. In
this case, the pregnancy will not be perceived.
If the pregnancy continues, it is considered that the child
to be born will not be harmed due to its irradiation, without,
however, the radiation consequences being completely ruled
out. In any case, this is considered as a low-risk phase.
3rd–8th week post conception: During this phase of
organogenesis, there is a likelihood of malformations for
doses to the fetus higher than 100 mSv. This likelihood
increases during the proliferation of fetal cells and the differentiation of the developing organs. The probability of end
results is 0.015% per 1mSv.
8th–15th week post conception: It seems that there is a dose
threshold of at least 300mGy for the induction of severe mental retardation due to exposure of fetus to ionizing radiation in
this most radiosensitive period. The impact on IQ of low doses
(few tens of mGy) to the fetus is insignicant in most cases.
According to epidemiological studies, the risk for cancer
after the fetal/embryo exposure to ionizing radiation is similar to the risk after an exposure in early childhood [8].
However, recent evidence on in utero exposure indicates that
the lifetime risks of solid cancers (but not leukemia) are considerably lower than those for exposure in childhood, i.e., at
most, about three times that of the population as a whole [22].
References
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11. National Council on Radiation Protection and Measurements
(NCRP). The relative biological effectiveness of radiations of different quality. Report No. 104. 1990.
12. ICRP.Relative biological effectiveness (RBE), quality factor (Q),
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org/10.18356/49c437f9- en.
16. National Council on Radiation Protection and Measurements
(NCRP). Evaluation of the linear-non threshold dose-response
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jnci/djn045.
Principles andGuidelines forRadiation
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Protection
A.Hertault
2
Why Is Radiation Protection Essential?
Physics Principles andImage Formation
X-rays are electromagnetic waves consisting of photons
propagating in a straight line in vacuum. They are charged
in energy, expressed in electron volts (eV). On the spectrum
of electromagnetic waves, X-rays have a wavelength
between 0.03 and 10 nm, meaning they are between the
ultraviolet and gamma rays. X-rays used in the medical eld
carry an energy between 10 and 150 keV.For comparison,
the energy transmitted by visible light is only around 2eV
[1].
When an X-ray beam crosses matter, several phenomena
are possible [2] (Fig.2.1):
– No interaction: the X-ray beam passes through the matter
without losing energy.
– Scattering: the X-ray beam is redirected in another direc-
tion. This can be done without loss of energy, or by transferring a part of its energy, resulting in an ionization
phenomenon at the atomic level. This last mechanism is
called the “Compton effect”.
– Absorption: the whole energy of the beam is absorbed,
with ionization of the matter. This mechanism is called
the “photoelectric effect”.
Within an X-ray generator, electrons are accelerated and
crushed against an anode. This produces 99% of heat
(explaining the overheating phenomena encountered with
imaging devices, and the need for cooling systems) and the
remaining 1% are photons that will form the X-ray beam [3].
At the exit of the generator, the X-ray beam is homogeneous.
As it passes through the patient, the beam will lose part of its
energy by the mechanisms of diffusion and absorption
A. Hertault (*)
Hopital Privé de Villeneuve d’Ascq, Lille, France
explained above [4]. When it reaches the detector, the beam
has become inhomogeneous, and will form the radiological
image as we know it (Fig.2.2).
In practice, obtaining an X-ray image is inseparable from
an ionization of the tissues, which will be at the origin of the
biological toxicity of X-rays. In addition, the patient will
become a secondary source of radiation due to the scattering
phenomenon, which will expose nearby health care
workers.
Biologic Risks Associated toX-Ray Exposure
Exposure to X-rays will cause damage to biological tissues
by a direct mechanism of alteration of molecules or DNA,
but also indirectly by ionization of water molecules into free
radicals such as hydrogen peroxide. Biological effects related
to X-ray exposure can be divided into two main categories.
On the one hand, the deterministic effects, and on the other
hand, the stochastic effects.
Deterministic Eects
Deterministic effects are related to cell death following
X-ray exposure. They are threshold-dependent and appear
only after being exposed to a certain dose. Their occurrence
can therefore be predicted. Their severity is correlated to the
intensity of the exposure, which means that their severity can
also be predicted. Their appearance is delayed from a few
weeks to a few months after exposure. The main manifestation of deterministic effects found in medicine is radiation
dermatitis. This is a skin burn that can be found at the point
of contact between the X-ray beam and the patient’s skin
(most often on the patient’s back). This complication must be
systematically sought in the weeks following an exposure if
the dose delivered to the skin was greater than 2Gy. In more
severe exposures (>5Gy), a chronic wound with necrosis of
the dermis may be found and may require reconstructive surgery [5].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
G. Geroulakos et al. (eds.), Mastering Endovascular Techniques, https://doi.org/10.1007/978-3-031-42735-0_2
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