Safety Series 2
Safety Series 2
Safety Series 2
RADIATION INJURIES
SAFETY REPORTS SERIES No. 2
© IAEA, 1998
Although great care has been taken to maintain the accuracy of information contained
in this publication, neither the IAEA nor its Member States assume any responsibility for
consequences which may arise from its use.
The mention of names of specific companies or products (whether or not indicated as
registered) does not imply any intention to infringe proprietary rights, nor should it be
construed as an endorsement or recommendation on the part of the IAEA.
CONTENTS
1. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.1. Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2. Objective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
1.3. Scope . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
1.4. Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
3. EXTERNAL EXPOSURE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
4.1. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
4.2. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
4.2.1. Decontamination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
4.2.2. Decorporation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
5.1. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
5.2. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
6. CONSULTING SYSTEM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
7. RECORD KEEPING . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
REFERENCES .............................................. 32
1.1. BACKGROUND
1
Nonetheless, two of the men were so seriously injured that their legs had to be partly
or completely amputated. The most highly exposed worker died six months later,
death being attributed to residual lung damage and other injuries [4].
The International Atomic Energy Agency has provided detailed reports on these
accidents in various publications [3–6]. The report on the accident at Tammiku,
Estonia, is currently being prepared for publication by the Agency.
1.2. OBJECTIVE
1.3. SCOPE
This report provides information in tabulated form on clinical criteria for dose
assessment. Additionally, it discusses the appropriate dose–effect relationship in
cases of external radiation involving either total body or local exposures, as well as
internal contamination. It is not within the scope of this report to provide details of
conventional treatment procedures. However, indications as to when to perform spe-
cific therapies are provided. The underlying principles of radiobiology and radiation
pathology are not discussed.
1.4. STRUCTURE
Section 2 covers the different types and modes of accidental exposure and their
medical management including triage, which is an important step to establish priori-
ties for medical treatment and hospitalization. Sections 3 and 4 deal with the medical
management following external exposure and internal contamination, reviewing diag-
nosis and treatment. Section 5 provides a classification of combined radiation injuries
and their treatment. Section 6 offers information on a consulting system from which
advice and assistance can be obtained in the event of a radiation accident, and
Section 7 gives instructions on how to collect data relating to patient care.
Annex I contains a set of record form samples for data collection. Annex II gives a
description of the diagnosis and treatment used at Goiânia.
2
2. TYPES OF ACCIDENTAL EXPOSURE AND THEIR
MEDICAL MANAGEMENT
The facilities in which X rays and radionuclides are either produced or used, the
types of radiation source, and the levels of activity have to be identified in order to
3
TABLE I. COMMON RADIATION SOURCES, FACILITIES AND EXPOSURE
MODES
External
Group Source and/or facility Contamination Mixed
exposure
4
TABLE II. RADIOLOGICAL AND NUCLEAR ACCIDENTS RESULTING IN
RADIATION INJURY
Possible number of
Area of application Source, radionuclide Part of body exposed
persons injured
Industry
Sterilization Co-60, Cs-137 Whole body, hands 1–3
Radiography Ir-192, Cs-137 Hands, other parts 1–10
Gauging Ir-192, Cs-137 Hands, other parts 1–2
Medicine
Diagnostics X ray generators Hands, face 1–10
Therapy Co-60, Cs-137 Whole body, hands 1–10
and accelerators and other parts (more in extremely
rare cases)
— direct radiation from the source or facility and from any radioactive material
released;
— inhalation of airborne material (volatiles, aerosols, particulates);
— direct radiation from ground or surface deposition;
— contamination of skin and clothing.
5
For these exposure routes it has been shown that direct radiation from the
source is the strongest contributor to the doses received [7, 8]. In particular, accidents
associated with γ radiography are likely to have significant radiological conse-
quences. In nuclear accidents the radioactive plume may act as a main source of exter-
nal radiation, while radioactive airborne material, especially radioactive isotopes of
iodine, may significantly contribute to the internal dose of the thyroid gland.
6
TABLE III. GUIDE FOR THE MANAGEMENT OF RADIATION INJURIES
BASED ON EARLY SYMPTOMS
induced injuries and the type and level of medical care needed. Three main categories
of exposed persons can be distinguished.
The first category includes those individuals, whether overexposed or suspect-
ed of overexposure, that display signs of conventional injuries such as trauma,
wounds, burns and/or chemical contamination. These individuals should be managed
as in any medical emergency. In addition, they should undergo specific testing with-
out delay (blood cell counts, blood sampling for cytogenetic studies and HLA typ-
ing), in order to assess the severity of the exposure and to provide the basis for treat-
ment initiation. If a sufficient number of first aid personnel are available, then specif-
ic testing on-site should be implemented as soon as feasible.
The second category includes individuals who are likely to have been exposed
externally or who have external or internal contamination, or who are suspected of
having been exposed at such dose levels that they may require a certain degree of
medical management. For this category, preplanned actions are required. These
7
victims should be regrouped in a treatment centre where a secondary triage into three
subcategories should be carried out. These subcategories include: persons whose
whole body has been exposed; those whose body has been locally exposed; and those
who have been contaminated with radionuclides. Simultaneously, the availability of
medical facilities at regional and/or national level should be determined. In the days
immediately following the exposure, most victims can be handled by physicians, to
ensure that examinations and follow-up are carried out properly. These basic exami-
nations should be listed on a special protocol drawn up by the medical centre respon-
sible for handling the accident. In a second phase, a further classification into cate-
gories of severity will be based on clinical and biological findings.
The last category comprises individuals who are likely to have received only
low doses and are free from any other injury. These individuals should be registered
and monitored as outpatients for a few days.
The severity of the injury depends on the dose level incurred, the dose rate, the
radiosensitivity of the tissues involved, the area of the body exposed and the extent of
exposure suffered by the organ system. The severity of the injury is greater when the
whole body is exposed; partial body exposure to the same dose has less impact on
health. An absorbed radiation dose of about 3.5 Gy is generally expected to result in
the death of 50% of the exposed population group within two months if there is no
medical treatment. This LD50/60 value can be increased to about 5.0–6.0 Gy with ade-
quate supportive treatment. Table IV presents the main diagnostic methods used in
cases of whole body exposure.
Minimum exposure
Procedure Finding Time of onset
(Gy)
Clinical Nausea, vomiting Within 48 h ~1
observations Erythema Within hours to days ~3
Epilation Within 2–3 weeks ~3
Laboratory
examinations
Blood count Absolute lymphocyte Within 24–72 h ~0.5
countb < 1 G/L
8
The severity of the exposure will usually be assessed in an iterative manner:
(a) A very early classification will be based on clinical symptoms such as nausea,
vomiting, diarrhoea, erythema and fever. These signs, as well as the time of their
appearance, their frequency and their severity, should be carefully recorded. This
permits the classification of victims into two categories according to whether the
absorbed dose is greater or less than 2 Gy.
(b) Confirmation and more precise classification will be based on haematological
counts, including, in particular, tests to observe the decline of lymphocytes
within the first two days, allowing a more detailed classification within the
category where the dose exceeded 2 Gy.
(c) Further confirmation will be effected in hospital, on the basis of the evolution
of clinical and laboratory findings, and of more specific means of analysis such
as haematological examinations, and biological (cytogenetic) and physical
dosimetry.
To meet the requirements of this assessment (a–c), planning a medical response
and training the necessary medical personnel are of prime importance. Planning effi-
ciency depends mainly upon the incorporation of a catastrophic event medical
response action into the medical plan, with regular drills to test the performance of
the medical response team. The medical management of large groups of victims in the
wake of large scale accidents will depend upon local and national capabilities and
available resources. The need for specialized units and/or personnel may require
international collaboration.
3. EXTERNAL EXPOSURE
9
If a source were located relatively close to the body and there were some
shielding, partial or local exposure would result. The closer the source to the body,
the smaller the area exposed.
The duration of the exposure, or dose rate, is also important. If the same dose
were delivered within a shorter time (higher dose rate) a more severe radiation effect
would be observed.
Local radiation injury (LRI) is much more frequent than WBE and hence
described in detail in the specialized literature [10]. LRI caused by high doses of radi-
ation (>8–10 Gy) produces signs and symptoms similar to a thermal burn except for
the striking delay in the onset of clinical changes, from several days to a week or
longer. The severity of LRI depends not only on the dose and type of radiation, but also
on the location and size of the area exposed. Although not usually life threatening, its
delayed effects can result in serious impairment.
10
TABLE VI. CLINICAL SIGNS OF LRI TO THE HAND FOLLOWING LOW
ENERGY RADIATION EXPOSURE
Period of onset of clinical signs Time and Estimated
in the acute phase evolution of Delayed dose
Primary Secondary Erosion, late phase effects effects range
Blisters Necrosis (d) (Gy)
erythema erythema ulceration
11
found in only a small number of cultured lymphocytes at a local exposure with a dose
range of 5–10 Gy [14] and provides qualitative rather than quantitative information.
Two diagnostic procedures can be used to assess the severity of local over-
exposures: thermal and radioisotopic methods. Both are most reliable when the
irradiated area can be compared with a corresponding unirradiated one.
Thermography can be used to identify any injury and to determine its extent. It
is a useful and sensitive technique for detecting local radiation injuries, especially in
the early and latent phases when clinical symptoms are not evident [15]. Additionally,
both contact thermography and infrared telethermovision are useful. Although the
latter technique is possibly superior in the diagnosis of a partial body irradiation, prin-
cipally when the extremities are affected, it is also significantly more expensive. A
radioisotopic method can be used to record the vascular circulation in an organ or part
of the body when 99Tcm pertechnate is injected intravenously, the distribution being
monitored with a scintillation camera [16].
Thermography and the radioisotopic method are complementary. They do
not permit an exact assessment of the dose, but can assist in assessing the clinical
severity of the injury. Promising new techniques, such as hair cortical cell counting,
are being studied, as indicators of radiation exposure to parts of the human
body [17].
3.2.3. Treatment
12
are clinically evident, the operation should be undertaken as soon as possible, after
the necessity of the procedure has been explained to the patient. Indications for ampu-
tation include very severe lesions with destruction of underlying tissues, including
vascular damage, intractable pain and lack of infection control. Table VII illustrates
the clinical aspects and the diagnostic and therapeutic options available for acute local
radiation injuries and their chronic evolution [18].
3.3.1. Diagnosis
Diagnosis of ARS is based on clinical and laboratory data. The prodromal phase
may occur within hours after exposure and is characterized by anorexia, nausea and
vomiting (Table VIII). In this phase of ARS, laboratory evidence of haematopoietic
damage can already be observed after an exposure of about 0.5 Gy (Table IX). There
is usually a remission in the symptoms, allowed by a relatively asymptomatic latent
phase that lasts one to three weeks, depending upon the dose incurred (Table X). The
latent phase is followed by the critical phase (Table XI).
The circulating lymphocytes are one of the most radiosensitive cell lines,
and a fall in the absolute lymphocyte count is the best and most useful laboratory
test to determine the level of radiation exposure in the early phase of observation
(Tables IX–XI). Immunological dysfunction appears within 48 h. Gastrointestinal
symptoms are observed at doses in excess of 10–15 Gy, and sometimes even with a
lower dose, overlapping the bone marrow syndrome. Accelerated prodromal and
shortened latent phases may be followed by diarrhoea. Neurovascular syndrome
occurs after exposures exceeding 20 Gy and is characterized by the immediate onset
of severe prodromal signs, leading to vasomotor collapse and death within one to
two days.
Among the assays for biological dosimetry, the chromosomal aberration analy-
sis from cultured circulating lymphocytes is the most widely accepted and reliable
one. The dose–response relationships are well established in many laboratories
around the world [14, 19–21]. The sensitivity of the technique depends on the dose
and radiation qualities. The lower limit of detection of a dose by using this
cytogenetic method is approximately 0.2 Gy of γ rays or X rays and approximately
10–20 mGy of fission spectrum neutrons [22–24].
There are limitations for using this technique in cases of partial body irradia-
tion [25, 26]. The presence of chromosomal aberrations might indicate the radiation
injury but does not permit a precise dose assessment. In addition, doses from internal
radiation sources cannot always be assessed, owing to the varying distributions of
different radionuclides.
13
TABLE VII. CLINICAL AND DIAGNOSTIC ASPECTS, AND THERAPEUTIC OPTIONS FOR LOCAL RADIATION INJURIES:
14
ACUTE PHASE
History
Dose estimation
{ Physical dosimetry
Accident reconstruction
Biological dosimetry
{
Peripheral blood counts
Sperm counts Vascular
Irradiation Routine examinations Slit lamp examination of eyes thermography
Serial colour photographs
{
Vascular scintigraphy
CAT scan
Specialized studies MRI
Thermography
end of ↓ 1st day end of ↓ 1st week end of ↓ 1st month
PRODROMAL PHASE LATENT PHASE ACUTE PHASE
Pain
Heat sensation
Itching
Symptoms Itching Minor (itching, pain), if any
Paresthesia
Tenderness
Clinical Hyperalgia
picture Erythema
Oedema
Signs Transient erythema Minor epilation, if any
Blistering
Moist desquamation
Pain relief
Non-steroidal anti-inflammatory
Avoidance of trauma drugs (NSAIDs)
Analgesics Local antibiotics
Treatment Symptomatic Hydration emulsion Vasodilators
(sweet almond oil) Healing drugs
Anti-adherent platelet drugs
Epidermal growth factors
Debridement
TABLE VII. (cont.) CLINICAL AND DIAGNOSTIC ASPECTS, AND THERAPEUTIC OPTIONS FOR LOCAL RADIATION
INJURIES: CHRONIC PHASE (continued time-scale)
Injury Pain
Reopening Altered tactile and thermal sensitivities
Pain
Vasculitis (possible) Paresthesia
Pain Skin dryness
Late erythema
Oedema Atrophy, telangiectasia, pigmentary changes, keratoses,
Ulceration
Ulcer epilation or problems with hair, deformity (ankilosis),
Necrosis
Necrosis (spontaneous healing impossible) functional incapacity
3.3.2. Treatment
17
18
Diarrhoea None None Rare Appears on days 6–9 Appears on days 4–5
Epilation None Moderate, beginning Moderate or complete Complete earlier Complete earlier
on day 15 or later on days 11–21 than day 11 than day 10
Clinical manifestations Fatigue, Fever, infections, High fever, infections High fever, diarrhoea, High fever,
weakness bleeding, weakness, bleeding, epilation vomiting, dizziness diarrhoea,
epilation and disorientation, unconsciousness
hypotension
Medical response Prophylactic Special prophylactic Special prophylactic Special treatment from Symptomatic only
treatment from days treatment from days the first day; isolation
14–20; isolation from 7–10; isolation from from the beginning
days 10–20 the beginning
a In very severe cases, with a dose >50 Gy, death precedes cytopenia.
19
20
TABLE XII. PRINCIPAL THERAPEUTIC MEASURES FOR ACUTE RADIATION SYNDROME ACCORDING TO DEGREE
OF SEVERITY
HLA-identical
Symptomatic
allogene BMT
therapy only
(first week)
Note: BMT: bone marrow transplantation; G-CSF: granulocyte-colony stimulating factor; GM-CSF: granulocyte macrophage-colony stimulating
factor; IL-3: interleukin.
administering prophylactic antibiotics and transfusing blood products (platelets and
erythrocytes). Platelet and erythrocyte transfusions are used prophylactically when
the platelet count is less than 20 G/L (1 G/L = 109 cells/L) and the haemo-
globin is less than 100 g/L. The use of prophylactic antibiotics and the administration
of blood products are decided after isolation in an antiseptic ward and careful clini-
cal observation for symptoms of fever, bleeding, oropharyngeal ulceration, and neu-
rological and vascular changes. Microbiological monitoring provides guidelines for
an efficient treatment of infection. Blood culture should be performed whenever the
fever is higher than 38°C (98.6°F).
Symptomatic and supportive treatment is also necessary. This may include the
use of tranquilizers and drugs to relieve pain, supportive fluids and adequate nutrition.
Intravenous routes should be employed as needed to supply fluid, electrolyte and
nutrition. Barriers to prevent hospital infection are desirable, as is the use of sterile
food. Raw vegetables and raw fruits should be avoided.
Because the care is directed towards preventing the consequences of agranulo-
cytosis and loss of immune competence, help from a haematologist/oncologist is
desirable.
21
3.3.4. Use of haematopoietic growth factors
22
This information is essential for the adequate evaluation, assessment and med-
ical management of a contaminated individual.
4.1. DIAGNOSIS
Room setting An isolated room or a room away from the general emergency
area should be used. Air circulation should be prevented and a
tub or table with a drainage system provided. Other useful
items include containers for waste water and any contaminated
materials, and plastic bags.
23
radioisotopes on the surface of, and within, the organism. In the event of
simple contamination, with one or several radionuclides, there will be no clinical
manifestations initially.
4.2. TREATMENT
4.2.1. Decontamination
24
TABLE XV. DECONTAMINATION PROCEDURES
Procedural priority Remove all clothing and place in plastic bags. Carry out life
saving measures first. Identify contaminated areas, mark
clearly and cover until decontamination takes place. Start with
decontamination of the wound, when present, and move on to
the most contaminated area.
Local contamination Cover uncontaminated area with plastic sheet and tape edges.
Soak the contaminated area, gently scrub with soap, and rinse
thoroughly. Repeat the cycle and observe changes in activity.
One cycle should not last longer than about 2–3 min. Avoid
vigorous scrubbing. A stable isotope solution may facilitate the
process.
Extensive contamination Shower for those not seriously injured. Bathing on the
operating table or stretcher for the seriously injured. Soak–
scrub–rinse cycle should also be observed.
Prophylactic measures Cover areas still contaminated with plastic sheet and tape
edges. Gloves can be used for hands. Repeat washing after
allowing the skin to rest.
25
blotted dry. Immersing the patient in a bath or complete showering as an initial mea-
sure is not recommended because such steps often spread contamination to clean
areas. Note that fingertips, hair, nostrils and ear canals are regions in which
decontamination is more difficult.
Clipping nails facilitates the process, and cutting or shaving hair may be
considered when shampooing does not sufficiently remove the contaminant.
Sweating of extremities by covering with plastic or rubber gloves overnight may be
helpful. Surgical debridement may be necessary to remove embedded matter from
highly contaminated wounds.
Caution is needed to avoid excessive vigour in decontamination. Patients very
rarely, if ever, suffer deleterious effects from contamination except from very high
exposures to skin, such as those occurring at Chernobyl in 1986 and in the accident
in Goiânia in 1987. The goal of decontamination is to prevent development of
late stage deleterious effects and at the same time avoid damage from efforts of
decontamination and decorporation.
4.2.2. Decorporation
The procedures recommended for the treatment of persons with acute, inter-
nally deposited radionuclides are intended to reduce the absorbed radiation dose and
hence the risk of possible future health effects (Table XVI). These aims can be
accomplished by reducing absorption, thereby preventing incorporation and internal
deposition within organs, and promoting elimination or excretion of absorbed
nuclides, which is more effective when started at the earliest opportunity. Reduction
of gastrointestinal absorption can be performed through application of stomach
lavage, mild emetics, purgatives to accelerate the removal of radioisotopes, activated
charcoal, Prussian blue (against caesium), aluminium containing antacids (against
strontium) and barium sulphate to absorb the radioactive materials.
26
Specific decorporation procedures can be used depending on the type and meta-
bolic pathway of the contaminating radionuclides. These include blocking, diluting
and displacement agents. For radioiodine, which concentrates mostly in the thyroid,
the blocking of the gland with stable iodine (e.g. potassium iodide) will prevent the
uptake of radioiodine. The effectiveness of this treatment is strongly time dependent.
Administration of the thyroid blocking dose of a stable iodine compound 4 h after the
radioiodine intake will result in only a 50% decrease of the thyroid dose. Thyroid
blocking on the day following radioiodine inhalation is ineffective. The daily single
dose of potassium iodide should be given as rapidly as possible following an acci-
dental radioiodine intake, depending on the age of the patient as follows: 10–20 mg
to infants (those not breast fed); 20–50 mg to children of 1–10 years of age;
50–100 mg to children of 11–18 years of age; and 100–300 mg to adults. This
treatment may be continued over a few days, according to the risk of ingestion of 131I
contaminated food, such as cow’s milk and leafy vegetables or fresh fruit [44–47].
In the case of tritium intake, a large amount of fluids (water, tea) should be
administered as a dilutant over a period of one week. At the same time, diuretics may
also be given [48].
Mobilizing (displacement) agents are compounds that increase a natural
turnover process, thereby enhancing the elimination of radionuclides from body tis-
sues. These agents are more effective if they are administered soon after exposure.
However, some are still effective if they are administered within weeks. Chelating
agents such as diethyltriamidepentaacetate (DTPA) (in the form of aerosols in the
case of inhalation), desferrioxamine, etc., can be used systematically or locally, either
by application to the skin or when performing lung lavage. This last procedure should
be performed only if large amounts of contaminant have been identified and then only
performed by very well trained specialists.
27
5.1. CLASSIFICATION
According to the combination of the radiation dose with other factors, CRIs can
be classified as follows:
(a) Thermal CRI: external and/or internal irradiation with thermal burns.
(b) Mechanical CRI: external and/or internal irradiation with wound or fracture, or
with haemorrhage.
(c) Chemical CRI: external and/or internal irradiation with chemical burns or
chemical intoxication.
5.2. TREATMENT
The medical handling of conventional trauma and life saving activities have the
highest priority. Treatment has to be individualized according to the nature and grade
of the combined injuries. Since a radiation injury is characterized by a latent period,
all important treatments of the non-radiation component of CRI should be carried out
during the first two or three weeks. Later efforts will be necessary for the treatment
of bone marrow and skin radiation injuries.
6. CONSULTING SYSTEM
WHO Headquarters
WHO,
CH-1211 Geneva 27, Switzerland
Fax: +41 22 791 0746
Tel: +41 22 791 3763
28
WHO Collaborating Centres and Liaison Institutions
29
India Bhabha Atomic Research Centre,
400085 Mumbai
Fax: +9122 556 0750
Tel: +9122 551 1677
30
United States of America Radiation Emergency Assistance, REAC/TS,
Oak Ridge, TN 37831-0117
Fax: +1 615 576 9522
Tel: +1 615 576 3450
IAEA Headquarters
IAEA,
Wagramer Strasse 5, P.O. Box 100, A-1400 Vienna, Austria
Fax: +431 20607
+431 2060 29309 (for emergency service during office hours)
+431 239270 (for 24 h emergency service)
Tel: +431 2060
7. RECORD KEEPING
Detailed record keeping is essential, not only for patient care and subsequent
dosimetric and medical follow-up, but also for medical and legal considerations.
Record keeping is the responsibility of the respective employer or governmental
authority.
The assistance of the radiation protection officer of the facility where an acci-
dent has occurred is essential for the collection of data and for consultations with the
physicians and governmental authorities involved. The officer will be in a position to
provide information on the type of accident, sources and kinds of radioactivity, and
dosimetry of the affected subjects and the environment. The following approaches
might be suggested:
(a) Use of a still camera (preferably colour) as serial, frequent and dated photos are
of great value;
(b) Use of a video camera and tape recorder for the preservation of patient inter-
views and narrative, and for a reconstruction of events;
(c) Computerization of all data.
Annex I provides examples of record forms for the collection of data. Careful
use of these forms, together with the use of the technical devices listed above, will be
of great value in the often lengthy clinical treatment of the injured.
31
REFERENCES
32
[17] HAMILTON, C., POTTEN, C., “Hair cortical cell counts as an indicator of radiation dose
and sensitivity in humans”, Proc. Int. Congr. on Radiation Research, Würzburg, 1995
(abstract).
[18] OLIVEIRA, A.R., “Clinical features of internal radiation exposure and main principles
of medical handling”, paper presented at Interregional Training Course on Management
of Radiological Accidents, Rio de Janeiro, 1995.
[19] ISHIHARA, T., SASAKI, M.S., Radiation Induced Chromosome Damage in Man,
Alan R. Liss, New York (1983).
[20] LLOYD, D.C., EDWARDS, A.A., MOQUET, J.E., FINNON, P., Doses in radiation
accidents investigated by chromosome aberration analysis. XX. Review of cases
investigated 1991–1993, Rep. NRPB-R-268, National Radiation Protection Board,
Didcot, UK (1994).
[21] NATARAJAN, A.T., et al., Goiânia radiation accident: Results of initial dose estimation
and follow-up studies, Prog. Clin. Biol. Res. 372 (1994) 145–154.
[22] BENDER, M.A., Cytogenetics research in radiation biology, Stem Cells 13 Suppl. 1
(1995) 172–181.
[23] RAMALHO, A., CURADO, M.P., NATARAJAN, A.T., Lifespan of human
lymphocytes estimated during a six year cytogenetic follow-up of individuals
accidentally exposed in the 1987 radiological accident in Brazil, Mutat. Res. 331
(1995) 47–54.
[24] DARROUDI, F., NATARAJAN, A.T., “Premature chromosome condensation: A novel
method for biological dosimetry”, High Levels of Natural Radiation (Proc. Int. Conf.
Ramsar, 1990) (SOHRABI, M., AHMED, J.U., DURRANI, S.A., Eds), IAEA, Vienna
(1993) 479–485.
[25] WELLS, J., SIEBER, V.K., HOPEWELL, J.W., HALL, S.C., Biological dosimetry of
non-uniform radiation exposure, CEGB Res. (1989) 17–22.
[26] FONG, I., et al., Chromosome aberrations induced in human lymphocytes after partial
body irradiation, Radiat. Res. 144 (1995) 97–101.
[27] LIVINGSTONE, G.K., FOSTER, A.E., ELSON, H.R., Effect of in vivo exposure to
iodine-131 on the frequency and persistence of micronuclei in human lymphocytes, J.
Toxicol. Environ. Health 40 (1993) 367–376.
[28] FENECH, M., The cytokinesis-block micronucleus technique: A detailed description of
the method and its application to genotoxicity studies in human populations, Mutat. Res.
285 (1993) 35–44.
[29] KÖTELES, G.J., BOJTOR, I., Radiation induced micronucleus frequency alterations in
lymphocytes from individuals of an urban population, Centr. Eur. J. Occup. Environ.
Med. 1 (1995) 187–198.
[30] SZIRMAI, S., BÉRCES, J., KÖTELES, G.J., Computerized image analysis for deter-
mination of micronucleus frequency, Environ. Health Perspect. 101 (1992) 57–60.
[31] INTERNATIONAL ATOMIC ENERGY AGENCY, Medical Handling of Accidentally
Exposed Individuals, Safety Series No. 88, IAEA, Vienna (1988).
[32] GUSKOVA, A.K., BARABANOVA, A.V., DRUTMAN, R.D., MOISEEV, A.A., The
Manual of Medical Handling of Radiation Accidents, Energoatomizdat, Moscow (1989).
[33] BROWNE, D., WEISS, J.F., MACVITTIE, T.J., PILLAI, M.V. (Eds), Treatment of
Radiation Injuries, Plenum Press, New York (1990).
33
[34] RICKS, R.C., FRY, S.A. (Eds), The Medical Basis for Radiation Accident Preparedness.
II. Clinical Experience and Follow-up since 1979, Elsevier, London and New York
(1990).
[35] NENOT, J.C., THIERRY, D., “Clinical approaches to treatment of radiation-induced
haematopoietic injury”, Radiation Toxicology — Bone Marrow and Leukaemia
(HENDRY, J.H., LORD, B.J., Eds), Taylor and Francis, London (1995) 195–243.
[36] METTLER, F.A., Jr., KELSEY, C.A., RICKS, R.C., Medical Management of Radiation
Accidents, CRC Press, Boca Raton, FL (1990).
[37] INTERNATIONAL ATOMIC ENERGY AGENCY, The Radiological Accident in
Soreq, IAEA, Vienna (1993).
[38] GROOPMAR, J.E., Colony-stimulating factors: Present status and future applications,
Hematology 26 Suppl. 30 (1988).
[39] TESTA, N.G., GALE, R.P. (Eds), Hematopoiesis: Long Term Effects of Chemotherapy
and Radiation, Marcel Dekker, New York (1988).
[40] APPLEBAUM, F.R., Clinical use of hematopoietic growth factors, Semin. Hematol. 26
Suppl. 7 (1989).
[41] INTERNATIONAL ATOMIC ENERGY AGENCY, The Radiological Accident at the
Irradiation Facility in Nesvizh, IAEA, Vienna (1996).
[42] LIESCHKE, G.J., BURGESS, A.W., Granulocyte colony-stimulating factor and granu-
locyte-macrophage colony-stimulating factor (Parts I and II), N. Engl. J. Med. 327
(1992) 28–35, 99–106.
[43] BARANOV, A., “Bone marrow transplantation in patients exposed to the Chernobyl
accident”, Medical Aspects of the Accident at the Chernobyl Nuclear Power Plant
(ROMANENKO, A.E., Ed.), Zdorovya, Kiev (1988) 155–161.
[44] IL’IN, L.A. (Ed.), Radioiodine as a Radiation Safety Problem, Atomizdat, Moscow
(1972).
[45] TURAI, I., TOIVONEN, M., Radiohygiene of Fission Isotopes of Iodine, Rep.
STL-A42, Institute of Radiation Protection, Helsinki (1983).
[46] WORLD HEALTH ORGANIZATION, Guidelines for Iodine Prophylaxis Following
Nuclear Accidents, WHO Regional Office, Copenhagen (1989).
[47] WALT, H., LAUSMANN, D., CONRADY, J., SEHER, C., Schutz der Schilddrüse vor
radioaktivem Jod, Kaliumjodid-Prophylaxe bei nuklearem Unfall, Rep. 386, Staatliches
Amt für Atomsicherheit und Strahlenschutz, Berlin (1990).
[48] INTERNATIONAL ATOMIC ENERGY AGENCY, Assessment and Treatment of
External and Internal Radionuclide Contamination, IAEA-TECDOC-869, Vienna
(1996).
34
Annex I
1. Identification of informant
Date Signature
35
Sample Identity Tag for Accidental Exposure (front and rear view)
IDENTITY TAG
IDENTITY TAG
(FIRST AID POST)
Name (FIRST AID POST)
Dept-
Name
Dept. Contamination Y/N
Site of contamination
Contamination Y/N
Site ofInjury
contamination Y/N
InjurySite of injury Y/N
Site of injury
Overexposure Y/N
Overexposure Y/N
Preliminary actions taken
Preliminary actions taken
Treatment
First aid
Treatment
Decontamination
First aid
Note: The contamination level should be expressed in disintegrations per minute/100 cm2 or
over the affected area if less than 100 cm2. Both α and β contamination levels should be indi-
cated. If β–γ contamination levels are high, they may be given in mGy/h measured with a
Geiger–Müller probe with an open window. An estimate of the total contamination should be
given wherever possible. Both the initial level of contamination and the level of contamination
at the time the patient is referred to the personnel decontamination centre/site hospital should
be provided.
36
Sample Medical Information Form
Full name
(BLOCK LETTERS)
Age Sex
Full name
(BLOCK LETTERS)
Designation
Affiliation
Date Time
4. EXPOSURE CONDITIONS
end of exposure
Duration
37
4.1. DOSIMETRY INFORMATION
5. FIRST SYMPTOMS
Wound
Trauma
Burn
Date of examination
38
Weakness Yes No
Headache Yes No
Nausea Yes No
Temperature
Pulse
Blood pressure
Oedema Yes No
Erythema Yes No
Other
Undressing Yes No
Decontamination Yes No
39
DTPA administration Yes No
Blood samples
Date Time
Date Time
Urine samples
(If applicable, for radioactivity measurement) Yes No
8. PHYSICIAN’S CONCLUSIONS
Date Signature
40
Annex II
The Goiânia radiological accident was caused by the removal of a 137Cs source,
formerly used in a radiotherapy unit, from an abandoned clinic in Goiânia, Brazil.
The caesium source, with an activity of 50.9 TBq (1375 Ci), was in the form of
powder, compacted into a steel capsule within the shielding container of the unit.
Persons who handled the capsule were exposed to γ radiation attenuated by the steel.
Those who handled the caesium powder directly were contaminated internally and
externally, and exposed to a mixed β and γ radiation field.
The exact duration of each exposure could not be established as the patients
were exposed to the source several times each day in different ways. The source–
subject geometry was extremely variable and for many patients there was external
contamination due to direct contact with the body surface. Part of the caesium
powder was removed and rubbed on patients’ bodies. The body irradiation was of a
heterogeneous character and the corporal distribution of localized radiation induced
lesions concentrated mainly on the extremities, especially the palms of hands and
the fingers.
41
II–2. EARLY MEDICAL RESPONSE
A specialized medical team from Rio de Janeiro arrived in Goiânia ten hours
after the severity of the accident was established and began preliminary examinations
and treatment at the Olympic Stadium. Clinical and laboratory evaluations (blood
counts) were performed, as well as external decontamination, when necessary, with
warm water and neutral soap. The medical team promptly adapted a ward in the
Goiânia General Hospital to receive the patients and set up a control point to avoid
spreading the contamination. The ward was divided into controlled, supervised and
clean areas. To assess the severity of each patient’s condition the procedures adopted
included collection of clinical and accident histories and of haematological data, as
well as monitoring body surfaces to determine the presence of external and/or
internal contamination.
It was apparent that the accidental exposure of the majority of the victims had
a heterogeneous and protracted character. The patients had received significant whole
body and localized irradiation and suffered internal and external contamination. It
was clear from the outset that precise dose estimation, a very important parameter for
treatment and prognosis, would be a major problem.
The main purpose of triage was the identification and referral of the most seri-
ously injured individuals to the appropriate medical unit in Rio de Janeiro.
Additionally, it was helpful in identifying those victims who should be
hospitalized immediately in the Goiânia General Hospital.
42
II–3. CLINICAL OBSERVATIONS
Local symptoms appeared a few hours after contact between the source and the
skin surface. Pain, sensation of local heat, burning and itching, as well as changes in
sensitivity, were the most frequent complaints. Some patients reported the simulta-
neous appearance of transient erythema in the affected regions.
After a period of latency, ranging from a few days to two weeks, a second wave
of localized disturbances erupted, characterizing the ‘critical phase’, which was
represented by stronger pain and oedema, always preceded by secondary
erythema, resembling a classical thermal burn. Soon thereafter, blisters or bullae
developed, coinciding in general with the swollen region. This phase of bullous
epithelitis lasted approximately two weeks. In some cases the bullae were so tense
and painful that drainage was required to relieve the symptomatology and allow
movement of the extremity.
43
The resection of dead tissues disclosed a raw and extremely painful dermis,
with a swollen aspect and sparse evidence of epithelialization. This phase was fol-
lowed by a fairly slow regeneration process, characterized by tissue granulation
beginning at the outer edges of the injury and progressing towards the middle, a
process requiring months to complete. Generally, the scar tissue was thin, translucent
and very sensitive to touch.
The final aspect of the injury was generally poor, owing mainly to its retractile
appearance. Some patients received such intense local irradiation that recovery was
never achieved. In such cases, the dermis was covered with a relatively thin layer of
fibrin, lightly fixed to the underlying dermis. The necrotic aspect of the injury was
observed in at least four patients. Seven patients developed more severe local radia-
tion induced injuries, resulting in areas of superficial necrosis caused by attenuated
(shielded) γ rays plus β emissions of caesium and in deeper necrotic injuries of a dark-
er tone, both requiring surgery. In these cases, a clear reduction in the evolutionary
phase was noticed.
44
Patients were given total blood transfusions or red packed cells in order to
maintain the level of haemoglobin within safe limits. Platelet transfusions were per-
formed to keep these elements at a level above 20 G/L or whenever bleeding occurred
in patients with a platelet count of less than 60 G/L.
GM-CSF was used for treating eight individuals with bone marrow suppres-
sion. After administration of GM-CSF (doses of 500 µg/m2 of body surface per day),
four patients responded well to the therapy with a clear myeloproliferative recovery,
reflected in the peripheral blood by a rapid and acute rise in the number of neu-
trophils. One patient died of infectious complications, although showing overt signs
of bone marrow recovery. The other patients who died, two females and one young
male, showed marked bone marrow involvement and multiple organ failure. No rela-
tion was established between GM-CSF administration and the behaviour of platelets
and haemoglobin.
45
To reduce skin dryness, hands and fingers were immersed in boric acid solu-
tion. With some patients, in order to avoid excessive administration of narcotics, iced
water was sprinkled on the areas surrounding the lesion, which provided pain relief.
Creams and ointments with healing and anti-inflammatory properties were applied
freely on the raw surfaces of the injuries. Attempts to increase blood flow to the bed
of the injury were made by using a peripheral vasodilator and a drug intended to
improve the flow properties of blood, by decreasing its viscosity, with action at
microcirculation level (Pentoxifylline). When blisters and bullae ruptured the exposed
surfaces were protected with non-adherent dressings coated with neomycin. Although
the majority of lesions presented bacterial colonization, in only a few instances
did infection develop during hospitalization.
All patients with deep ulceration or necrosis on hands, feet and thighs under-
went repair surgery. The success of the surgery depended essentially on the location
and depth of the lesion, as well as the viability and integrity of the tissue over which
the grafted tissue was applied.
Extensive lesions involving thick, fatty or muscular regions required removal of
all necrotic and infected tissues until reaching an area of good blood supply. Only
then could the bed of the wound be covered with a good quality split skin graft. In
two cases, lesions on the palms of the hand required ample debridement, practically
to the level of the flexor muscles and tendons, followed by coverage of the ulcer bed
with an abdominal flap. Surgical treatment of finger lesions consisted of resection of
the damage followed by coverage with a skin graft. In one case it was necessary to
perform microsurgery, transferring a segment of tissue with the intact vascular pedi-
cle to be anastomosed to the finger vessels. In two patients, the development of necro-
sis and mummification of fingers necessitated amputation as soon as the irreversibil-
ity of the damage was confirmed on clinical and laboratory grounds. Finally, in a
patient with a severe injury of the lateral aspect of the right thigh, excision was per-
formed followed by coverage of the wound bed with a skin graft of the contralateral
limb one year after exposure. An attempt to use a dermoexpansor to increase the skin
surface, which would assist closure of the wound, failed. Unfortunately, dehiscence
and infection occurred during expansion, demanding interruption of the procedure.
A total of 46 individuals were treated with Prussian blue in doses varying from
1 to 10 g. The drug was given orally two, three, six or ten times a day, depending on
the total dose, with a minimum of 2 h between doses. With the administration of
Prussian blue, the expected pattern of caesium elimination changed and removal via
the faeces became predominant, owing to the efficiency of Prussian blue in binding
caesium ions in the lumen of the gut, thereby interrupting its enteric cycle and pre-
venting subsequent reabsorption. With the use of the drug, caesium half-lives in
46
adults were reduced to one third of the normal value, which is consistent with the
reduction of half-lives obtained in previous studies.
(a) Repeated baths in warm water with neutral soap, which reduced the contami-
nation levels substantially.
(b) Use of acetic acid for increasing the solubility of caesium and thus facilitating
its removal.
(c) Applications of titanium dioxide associated with hydrated lanolin, in cases
where a great amount of radioactive material was present on palms and soles.
Owing to its mildly abrasive action, titanium dioxide, after repeated applications,
was able to remove considerable quantities of caesium from non-superficial
skin layers.
(d) Additional mechanical methods for decontamination, such as callus abraders,
rigid bristle nylon brushes and pumice stone, were used for patients with severe
sole contamination.
(e) Later, after all the above described means were exhausted, use was made of an
ion exchange resin, substituting caesium for potassium. The resin was placed
inside gloves and plastic overshoes, where hands or feet would remain in
contact with it for at least 20 min. As a consequence, a 50% removal of
residual caesium was achieved.
47
residual stem cells existed and that a factor able to stimulate their proliferation and
differentiation might play an important role in recomposing the natural defence
mechanisms of the irradiated patients.
Regarding local radiation injuries, it became evident that conventional treat-
ment did not greatly modify the clinical evolution of severe radiation injuries.
Unfortunately, the detailed extent of radiation damage can be accurately established
only a few months after exposure, when it is possible to choose a more definitive ther-
apy. The two problems challenging physicians are determining the extent of the dam-
age and deciding which tissues will inevitably be destroyed, and choosing the most
suitable moment to perform surgery. Data provided by MRI, computerized tomogra-
phy, vascular scintigraphy, and histochemical and immunocytochemical studies of
biopsy material, as well as topographic dosimetry, including in-depth distribution of
the doses, and clinical evolution should all be taken into consideration.
Prussian blue proved to be an excellent antidote in cases of caesium contami-
nation, even when administered several days after contamination. The optimum dose
suggested is 3 g/d, administered at regular intervals, i.e. in doses of 1 g (two capsules)
every 8 h, in order to maintain its gastrointestinal availability throughout the day. The
drug can be used over long periods of time, for months if necessary. Definitive
suspension of the drug is indicated when no more caesium is detected in the excreta.
BIBLIOGRAPHY
— Medical Handling of Accidentally Exposed Individuals, Safety Series No. 88, IAEA, Vienna
(1988).
48
CONTRIBUTORS TO DRAFTING AND REVIEW
Consultants Meetings
Vienna, Austria: 23–27 May 1993, 1–4 April 1996
49