101
HUMAN RASEATION INJURY
as a PuacRadiation
tienof TypeofExposure,Dose
and Time Afecr Exposure
651 Bece of Superficial, Peastreting sad Ie
Radistion injuries can be divided into three
general classes:
a. The syndromes of whole body radiation
injury which are produced by penetrating ionizing radiation, and which are dose dependent.
b. Superficial rediation burns produced by
seft radiations (beta and low energy X- of
gamena radiations).
a a aeee ee ee
ec. Radiation injery produced by the depoaition of radionuclides within the body. The
chnical picture varies with the site and amount
of depositica.
Each of the above is associated with an early
phase in which acute symptome and signe may
be observed, and a late phase in which chronic
changes or manifestations such as cancer may
be observed. Also, the degree of injury is proportioned to dose. Particularly in (Class a,
total-body irradiation, the disease entity seen
ia highly dependent on dose.
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The Syadromes From Tota! Body Penetrating Radéetions
The dose-dependent syndromes resulting
from total-body exposure in the mammal have
been described in detail (10-13) and need only
be summarized here. After large closes (ap-
proximately 6,000 r or more*) the centraéd nervous system ryndvurne (CNS) is produced
(10).
Death may occur unde; the beam after
some hours, and is preceded by hyperexcita-
bility, ataxia, respiratory distress, and intermittent stupor. Doses capable of producing
thix syndrome are always uniformly fatal. If
an occasional anima! survives thin CNS he has
yet to expemence the gastrotalesatinal «ynd rime
(GOS), (10, 12) whieh when produced by doses
im exceam of 1500 ¢ is always fatal wrhin 3-0
days.** The GIS is so named because of the
marked nausea, vomiting, diarrhes, saad denwdation of the small bowel mecosa. The (IS is
a aniformly fatal syndreme in moet laboratory
animals. If the short duration GIS of a few
hours does not produce the 3-4 day death, the
survivors of this syndrome have yet te expert
ence the sequelae of bone marron depression
which has been termed the Acmopoietic syndrome (HS). The HS is not necessarily fatal.
It in the clinical pictere that is seen in the
lethal range for all mammals and in general
the LD, values reported represent the LD,, for
the sequela of hemopoietic depression—grant-
locytopenia and depressed defenses aguinst infection, thrombopenia, and anemia with the possible resulting infections, diffuse purpura, and
hypoxia due to anemia, any of which may be
fatal. More detailed descriptions of the path-
ogenesis of these phenomena have been published (10-16).
The above picture ofradiation syndromes is
based on animal experimentation: however,
human experience (6, 17-22) has indicated that
n probably corresponds quite closely to the
general mammalian response outlined sbove
with the exception of some differences in time
of occurrence.
Nagasaki (21, 22) nor would one expect it to
be observed since doses to produce this syn-
drome were well within the area of total di struction. The (:1S with deaths in the Ist
week are well documented clinically and patholomcally as are deaths from the HS (6, 15,
JI, 22). However, in the case of man, deaths
from infection were most prevalent in the 2d
to +h weeks (maximum incidence during jd
week) and from hemorrhagic phenomena in the
‘do to 6th weeks (maximum incidence in 4th
week). Inthe Japanese, after the bombing of
Hiroshima and Nayanzaki, deaths from radis
tien injury were occurcing as late as the Tth
°*There are tecwes ued strain variations
§=6The 1-4
day deathe are cast prevalent in dug. rats sed nee
Salt
*~eertes Vartetioa.
The (‘NS apparently was not
observed by the Japanese at Hiroshima and
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