DISASTER MEDICINE

DEFINITION AND CLASSIFICATION OF DISASTERS

Disaster medicine is an interdisciplinary scientific field encompassing matters of

medical response in cases of disaster. It is a branch of civil healthcare, with its own
specific scope and objectives.
The objectives of disaster medicine are to prevent or mitigate the impact of a
disaster, to provide treatment and medical evacuation of victims and deal with sanitary
and hygiene problems caused by the disaster.
Subject Field of Disaster Medicine:
1. Basic knowledge of the physical nature and characteristic patterns of
natural and man-made (anthropogenic) disasters.
2. Characteristics of mass casualty disasters and their specific features in
different emergency situations.
3. Prevention, diagnostics and treatment of affecter persons in different
emergency situations.
4. Organisation of medical response in emergency situations.
Main Objectives of Disaster Medicine
1. To study the nature and the characteristics of different disaster impact on
the population.
2. To develop effective models of medical response in cases of disasters.
3. To conduct theoretical and practical training of medical and other non-
medical staff involved in providing emergency assistance in cases of disaster.
4. To conduct scientific studies, to perform analyses, to develop
methodology, documentation, literature and instructions.
I. Definition and terms
Catastrophe /disaster/ - there are a number of different definitions of the term
catastrophe /disaster/:
 According to WHO, a disaster is a natural phenomenon or human activity
which poses or causes threat to human life and health, to a level which is beyond the
capacity of the community to deal with without outside assistance. /A disaster is an
occurrence disrupting the normal conditions of existence and causing a level of
suffering that exceeds the capacity of adjustment of the affected community/.
 In Civil Protection terminology, a disaster is a sudden occurrence which
has severe adverse consequences, such as human casualty, injuries, disruption of
social structures and functions, which cause losses on such a scale that the stricken
community need immediate, large-scale rescue assistance.
Considering all available definitions of catastrophe /disaster/, the following
summarized version of a definition can be drawn:
Catastrophes are violent natural phenomena or human actions, identifiable by
the following characteristic elements:
 suddenness of the event;
 extreme general and medical severity of the situation thus created,
posing threat to human life and health;
 sharp discrepancy between the available capacity and resources and
those necessary to deal with the consequences of such an event;
 necessity of emergent rescue operations.

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 Disaster situation – a situation of disrupted social structures and functions,
severely challenging healthcare services, which strikes one or more areas, as a result
of disasters of different type.
State of emergency – a state in which extraordinary measures are taken in
order to avert a disaster, which is declared in the disaster area.
Accident – a smaller-scale adverse event which causes demands on the
community which are within the capacity of the usual emergency organisations.
Vulnerable places – places where hazardous substances are stored, used,
processed or produced.
Hazardous substances – highly toxic, pathogenic, radioactive, fire susceptible
and explosive substances and substrates.
II. Disaster Assessment Criteria
The criteria applied to distinguish between catastrophes and accidents fall into
two categories: quantitative and qualitative criteria.
The qualitative criteria include the main catastrophe indicators described above.
The main qualitative criterion is the sharp discrepancy between the available capacity
and resources and those necessary to deal with the consequences of the event.
The quantitative criteria include:
 number of people affected and killed;
 number of acute infections cases;
 the ratio between the damage inflicted and the statistical data about
morbidity and mortality in the region.
These qualitative criteria are of relative character due to existing inequality in
the capacity and resources of different regions to deal with the consequences of a
disaster without outside assistance.
According to the WHO terminology, a catastrophe is an adverse event, which
inflicts damage to 10 or more people, causes injuries to 10-25 people and illness to
15-50 people.
For the correct estimation of the number of medical staff and resources
necessary, disasters are divided into the following categories:
 Small scale mass casualty event – not less than 25 casualties, 10 of
whom are in need of hospital care;
 Medium scale mass casualty event – more than 100 casualties, 50 of
whom are in need of hospital care;
 Large scale mass casualty event – more than 1000 casualties.
III. Classification of disasters
Disasters caused by elements of nature:
 meteorological – storms; hurricanes; tornados; cyclones; extreme heat,
extreme cold, ice cover, etc.;
 topological – floods; avalanches; mudslides/landslides, etc.;
 tectonic – earthquakes; volcanic eruptions;
 cosmic - meteor / asteroid crashes, etc.
Anthropological / Man-made disasters:
 Huge impact industrial accidents- release of chemical, radioactive
materials, etc.;
 Socio-economic:
 Economic;
 Social – famine; terrorism; social unrest; alcohol/drug addiction,
etc.;
 Armed conflicts /wars/:
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  using conventional weapons;
 using weapons of mass destruction;
 Transportation accidents – road / railroad accidents; aviation and marine
accidents;
 Other man-made disasters – disasters which do not fall into one of the
above mentioned categories, such as tunnel, shaft tunnel or building collapse;
particularly dangerous and other epidemics; mass poisoning; mass water supply
incidents; major incidents of environmental pollution and destruction, etc.
IV. Disaster Area
Disaster area – the territory directly affected by the adverse impact of a disaster,
together with all people, animals, plants, infrastructural and other physical objects,
existing there.
Types of disaster areas regarding the cause of disaster:
 chemical;
 traumatic;
 biological;
 nuclear;
 radiological;
 mixed-cause disasters
Types of disaster areas regarding the speed of disaster onset:
 Type І – losses are inflicted rapidly and simultaneously or over a short
period of time
 Type ІІ – losses are inflicted over a longer period of time
V. Destruction Causing Factors
Destruction causing factors – phenomena or processes of physical, chemical or
biological nature, causing destruction to people, animals, plants and the environment
as a whole.
Main types of destruction causing factors:
 Thermal – the effect of exposure to extremely high or low temperatures
which cause burns or freezing / frost bites;
 Toxic – the impact of one or more highly-toxic substances causing life-
threatening intoxication;
 Radioactive – the impact of ion radiation causing radioactive damage;
 Mechanical – the impact of physical forces in collision, pressure or
friction, which cause external and internal traumas, wounds, injuries and fractures;
 Biological – the impact of pathogenic micro-organisms and their toxins,
causing severe infectious diseases;
 Psychological and emotional – strong stress reactions which are caused
by the horrifying disaster situation are typical for all disasters.
VI. Medical loss
In disaster situations the population in the disaster area suffer substantial
personal losses, which are collectively called total losses.
 Total losses – all losses among the population caused by the disaster:
dead people, people unaccounted for or injured. They are divided in two
types:
 Irreparable losses – the number of people killed, unaccounted for or dead
in some of the further disaster management and medical response
phases;

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 Medical losses – all people affected in the disaster area, who are in need of first
aid and further medical care.
Characteristics of medical losses – quantity; structure; location of occurrence
and zone distribution on the whole territory affected by the disaster.
Medical losses in disaster situations are characterised by their mass impact,
concomitance and uneven distribution around the disaster area.
Medical losses and their characteristics are the basis for determining the
structure of medical response in different disaster situations.
Types of Medical Losses. The different disaster impact factors cause different
types of medical loss / damage:
 Thermal damage – burns caused by fire / explosions; frost bites caused by
exposure to extreme colds and avalanche submerge, etc.
 Toxic damage – intoxication caused by highly toxic poisonous substances,
typical for large-scale chemical accidents or use of mass destruction chemical
weapons.
 Radioactive damage – acute radiation syndrome, radio-dermatitis, etc.,
caused by nuclear power station accidents or use of mass destruction nuclear
weapons.
 Mechanical damage – external and internal trauma, wounds, injuries and
fractures caused by natural disasters like earthquakes, volcanic eruptions, storms,
hurricanes, tornados, etc. and in man-made disasters such as explosions in industrial
accidents, transportation accidents or terrorist attacks for example.
 Drowning – caused by disastrous floods, marine accidents, etc.
 Infectious diseases – in naturally occurring epidemics; as a result of sharp
deterioration of the hygiene and ecological conditions in a disaster area or when
biological weapons of mass destruction have been used.
 Psychological damage – fear; distress; anxiety; psychological stress, etc.
 Compound damage – they occur when a person is simultaneously exposed
to two or more damaging factors. Such kinds of damage are typical for a great number
disaster situations.
VII. General and Medical Conditions in Disaster Situations
General conditions – refer to the consequences of a disaster for the human
living environment in the disaster area / include collapsed buildings; roads blocked by
debris; disrupted water and electricity supply; destruction to the sewage system, etc.
Medical conditions – refer to quantitative and qualitative characteristics; the
structure and the distribution of medical loss in the disaster area.
Depending on the severity of harm caused, the medical loss in the disaster area
can have the following structure:
 mildly injured – satisfactory general condition, retained mobile and self-care
ability.
 moderate-severely injured – lack of life-threatening injuries but some of them
may suffer long-term or permanent damage.
 severely injured – people with life-threatening injuries or severe disorder of
life-support bodily organs and functions.

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 GENERAL CHARACTERISTICS OF EARTHQUAKES. FORECASTING AND
TYPES OF MEDICAL LOSSES

Earthquakes are one of the most destructive natural disasters. At least 1.3
million deaths occurred during the previous century from earthquakes. On average 16
earthquakes resulting in significant loss of life occur every year. Earthquakes are
produced by the movement of the plates that form the earth's crust. The boundaries
where the plates meet and slide across each other are called faults. If movement of
plates becomes arrested, energy can accumulate along the fault line. When the
accumulated energy exceeds the strength of the rocks along the plate boundary, the
rock may fracture and the plates can move suddenly up to a few meters. This sudden
movement produces vibrations or seismic waves that radiate outward from the focus
of the quake. Surface waves that travel along the earth's crust have the strongest
vibrations and thus produce the greatest damage. Earthquakes tend to recur along
fault lines but may also occur in the middle of a plate.
At the Earth there are 3 seismic belts: Pacific – 75% of the seismic activity
(Chile, Peru, California, Alaska, Japan, Philippines); Alps-Himalayan – 25% (Alps,
Mediterranean lands, Himalayan, China, Indonesia); Mid-Atlantic – 5% of the seismic
activity (Atlantic islands). Bulgaria is a part of Alps-Himalayan belt.
І. Definition
The earthquake is a natural phenomenon arising from sudden shifts in earth
layers, disruption of the crust and deeper layers of the Earth.
There are about 20 plates along the surface of the earth that move continuously
and slowly past each other. When the plates squeeze or stretch, huge rocks form at
their edges and the rocks shift with great force, causing an earthquake. Think of it this
way: Imagine holding a pencil horizontally. If you were to apply a force to both ends of
the pencil by pushing down on them, you would see the pencil bend. After enough
force was applied, the pencil would break in the middle, releasing the stress you have
put on it. The Earth's crust acts in the same
way. As the plates move they put forces on
themselves and each other. When the force
is large enough, the crust is forced to break.
When the break occurs, the stress is
released as energy which moves through the
Earth in the form of waves, which we feel and
call an earthquake.
Earthquakes are the rumblings, shaking or
rolling of the earth's surface. It is usually what happens when two blocks of the earth
suddenly slip past one another, or break apart from each other as a result of tension
caused by prolonged energy build up.
An earthquake is what happens when two
blocks of the earth suddenly slip past one
another. The surface where they slip is called
the fault or fault plane. The location below the
earth’s surface where the earthquake starts
is called the hypocenter, and the location
directly above it on the surface of the earth is
called the epicenter.

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 Earthquakes come in many forms. It can be felt as
a shock under your feet, or may be very powerful
and destructive enough to flatten an entire city.
They can happen anywhere, land or sea. It is
important to understand the earth’s makeup to
help understand earthquakes better.

In this diagram, you will notice that the inner and outer cores of the earth (middle
part) are liquid in nature, containing iron and nickel of extreme temperatures (5,500°C).
The Mantle is semi-molten rock, also
called magma. The outer is the crust,
which is the hard part of the earth that
forms the surface. This outer crust
includes the land on which we live, the
oceans and ocean deeps and
anything within 40km down the earth's
surface. Earthquakes are developed
in the outer crust of the earth.

How do earthquakes form?

Earthquakes develop in the crust of the earth. The crust involves the earth's
surface, submarine levels, down to the ocean floors. The inner part of the earth
contains massive energy. Some of this energy escapes through cracks and other
volcanic activity, but the bulk of it is stored within the earth’s inner part, contained in
the crust.
The earth’s outer crust is held in place like a completed jigsaw puzzle, with
rough edges and lines. The energy stored here causes the pieces to slide, glide, knock
and move around each piece. These pieces best describe what we call ‘Tectonic
plates’.
After a period of time, the built up
energy and movement causes
huge tension in the plates, and
there is massive pressure on the
fault lines. This intense pressure
resulting from energy build up
causes the fault lines give way,
and plates move over, against or
apart from each other.
There is an earthquake at this
point. In the form of seismic
waves the escaping energy
radiates outward from the fault in
all directions. The seismic waves
shake the earth as they move
through it. When the waves
reach the earth’s surface, they shake the ground and anything on it, tearing down
houses and structures.

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 What are the types of earthquakes?
Earthquakes can come in three
main forms, depending on the
plate movements that occur
beneath the earth's surface. They
could occur on a Convergent
Boundary, Divergent Boundary or
a Transform Fault.
1. Convergent boundary: Here, one plate is forced over another plate during
movement creating a thrust fault.
2. Divergent boundary: Here, plates are forced apart each other, usually
forming a Rift Zone. This kind is common in ocean floors where new floors are created.
An example is the Mid Atlantic Ridge.
3. Transform fault: Unlike divergent and convergent, the plates here slip by
each other. This is also called Strike-Slip.
Еarthquake waves.
There are 2 types of earthquakes waves and the difference lies in the way the
seismic waves are transmitted. To understand this better, let us see what a seismic
wave is. These are waves of energy that travel through the earth's layers, and other
elastic layers, often as a result of earthquakes. A wave, by general definition is the
transfer of energy from one place to another without transferring solid, liquid or gas
matter. Examples include light and sound waves.
During an earthquake, the waves released may be “P” or “S” waves depending
on the speed and ways in which they travel.
1. P-Waves (Primary waves): P-waves
are longitudinal in nature. The vibrations
are along the same direction as the
direction of travel. It is also known as
compressional waves. P-waves travel
faster than S-waves.

2. S-Waves (Secondary waves): Here

the waves travel at right angles to the
direction of travel. They are also known
as transverse waves and example
include water waves.

With this in mind, you will notice that if you are close to the point where an
earthquake struck, you will feel both P and S waves close within the same time frame.
If you are further away, you will feel the P-wave first and then the S-wave a bit later.
Both waves can be destructive, but their study helps us to know where the earthquake
struck.
Richter magnitude scale
The Richter magnitude scale (also Richter scale) assigns a magnitude number
to quantify the energy released by an earthquake. The Richter scale, developed in the
1930s, is a base - 10 logarithmic scale, which defines magnitude as the logarithm of
the ratio of the amplitude of the seismic waves to an arbitrary, minor amplitude. As
measured with a seismometer, an earthquake that registers 5.0 on the Richter scale
has a shaking amplitude 10 times greater than an earthquake that registered 4.0, and

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thus corresponds to a release of energy 31.6 times that released by the lesser
earthquake.
Earthquake Magnitude Classes. Earthquakes are also classified in categories
ranging from minor to great, depending on their magnitude.

Class Magnitude

Great 8 or more

Major 7 - 7.9

Strong 6 - 6.9

Moderate 5 - 5.9

Light 4 - 4.9

Minor 3 -3.9

Medvedev–Sponheuer–Karnik scale
The Medvedev–Sponheuer–Karnik scale, also known as the MSK or MSK-64,
is a macroseismic intensity scale used to evaluate the severity of ground shaking on
the basis of observed effects in an area of the earthquake occurrence.
With minor modifications in the mid-1970s and early 1980s, the MSK scale
became widely used in Europe and the USSR. In early 1990s, the European
Seismological Commission (ESC) used many of the principles formulated in the MSK
in the development of the European Macroseismic Scale, which is now a de facto
standard for evaluation of seismic intensity in European countries. MSK-64 is still being
used in India, Israel, Russia, and throughout the Commonwealth of Independent
States.
The Medvedev–Sponheuer–Karnik scale is somewhat similar to the Modified
Mercalli (MM) scale used in the United States. The MSK scale has 12 intensity
degrees.
The intensity is defined for each populated place where the earthquake is
noticed, that means that one earthquake has 1 magnitude and different intensities. The
earthquakes are rarely single. The weaker earth tremors, preceded the basic tremor
are called forshock and the week tremors after the basic – aftershock. Sometimes
months after the basic earthquake, abated aftershocks are noticed.
ІІ. Causes of earthquake:
1. Tectonic.
2. Volcanic.
3. Frustration of caves and galleries.
4. Human activity – ground and underground explosions.
5. Space - a fall of meteorites, comets and more.
III. Effects of earthquakes
The earthquake is one of the most frightening and destructive phenomena of
nature. The earthquakes affect large territories, lead to damages of buildings and
infrastructure of the populated areas, in the earth surface are formed deep clefts and
landslides. Often the earthquakes cause tsunamis (series of waves created when a
body of water, such as an ocean, is rapidly displaced), damages of dams and floods.
The earthquakes cause sometimes damages in industrial enterprises and
development of chemical and radioactive pollution.

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 A. Shaking and ground rupture
B. Landslides and avalanches
C. Fires: Earthquakes can cause fires by damaging electrical power or gas
lines. In the event of water mains rupturing and a loss of pressure, it may also become
difficult to stop the spread of a fire once it has started. For example, more deaths in
the 1906 San Francisco earthquake were caused by fire than by the earthquake itself.
D. Tsunamis
E. Floods: Earthquakes may cause landslips to dam rivers, which
collapse and cause floods.
IV. Risk factors for injury
Ground movement during an earthquake is seldom the direct cause of death or
injury. Most injuries result from collapsing structures, falling masonry, flying glass, and
falling objects, or when people attempt to move during a quake. Structural failure of a
building is generally recognized as the most common cause of death in large
earthquakes. There is generally a higher risk of fatal injury associated with multilevel
commercial and residential buildings, though this is dependent on the construction of
the building. The peak in deaths and injuries occurs during the 24-hour period after an
earthquake, with the highest number of fatalities recorded within minutes after the
quake. Hospitalization for nonfatal injuries also peaks on the day of an earthquake, but
may also have subsequent peaks depending on the presence of secondary disasters
and the strength of aftershocks.
The most common causes of injury and death may vary depending on the
earthquake and the construction of local buildings. Analysis of injury patterns during
the Northridge earthquake in 1994 found that falling building masonry was the most
common cause of injury, followed by being pinned between furniture and objects.
Investigation of the 1988 Armenian earthquake identified building collapse as the most
common cause of injury and death. Data from multiple earthquakes has shown that
exiting from a building is both a risk factor and protective against death.
Earthquake lethality can be magnified by promulgation of secondary disasters.
Ground vibrations can collapse buildings and bridges, disrupt gas and electric service,
and trigger landslides, avalanches, flash floods, fires, and sometimes huge tsunamis.
Tsunamis are a particular risk when earthquakes occur near or beneath the ocean
floor. Immense waves that may reach greater than 15 meters in height and travel at
speeds greater than 960 kilometers per hour can be generated. These waves may
cause significant damage and loss of life in communities near the ocean.
Care should also be taken to avoid injuries from aftershocks. These are smaller
quakes that follow the main seismic event and may cause collapse of previously
weakened or damaged structures. Aftershocks may occur within minutes to weeks
after the main earthquake. Motor vehicle accidents are also a source of earthquake-
related injury and death.
V. Injuries
Major earthquakes create disaster conditions because the resulting structural
collapse causes significant morbidity and mortality. Earthquakes have caused an
estimated 15 million deaths since the beginning of recorded history. Earthquakes have
caused an average of 11,250 deaths per year for the last 40 years accounting for 37%
of all deaths caused by disaster. In addition to the injury and death caused at the time
of the earth movement itself, an earthquake disrupts the community’s capacity to
respond effectively. Transportation, communications, and health care systems are
typically damaged significantly in the hours and days following the event. As a result,
national and international assistance is usually required, since the salvage rate for

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victims buried under a collapsed structure decreases steadily after the first 24 hours
after entrapment, international assistance teams and equipment should be on site
within one or two days. Unfortunately this kind of response time is rarely possible under
present conditions.
Injuries during earthquakes are primarily from blunt trauma. In the 1988 Armenian
earthquake there were 831 fatalities, 533 fractures, 397 crush injuries, and 646 minor
injuries, with greater injury rates noted in females. During the 1994 Northridge
earthquake in California there were 33 related fatalities and 138 hospitalizations.
Analysis of the injury pattern for the Northridge earthquake found specific injury
patterns for fatalities and hospitalized cases. Among fatalities, the head was the most
commonly injured body region, followed by thoracic, abdominal, and lower extremity
injuries. The most common causes of death were asphyxia and body compression
from building collapse. Orthopedic injuries were the most common cause of
hospitalization.
The traumatic toxicology manifests in case of pressure to parts of the body under
heavy objects for long (crush syndrome). In consequence of the mechanical pressure
the distal blood supplying is disturbed because of the pressure, histamine and other
toxins are formed in the tissues. After the release of the sufferers with a rehabilitation
of the circulation of the blood, the toxins rush in body and lead to shock or damage to
the internal organs. For prevention of the shock immediately after the release of the
pressed part, the pressed part has to be bandage tightly with elastic bandage under
the place of the pressure. Take anti-shock measures.
Definition of crush syndrome: syndrome of traumatic rhabdomyolysis causing
myoglobulinuric renal failure, muscle re-perfusion.
• Involvement of muscle mass
• Prolonged compression (4-6 hours)
• Compromised local circulation
• Release of toxins triggering hypovolemic shock and hyperkalemia.
Kidney failure has been identified by the Centers for Disease Control and
Prevention as one of the most urgent public health concerns in Haiti following the 7.0
magnitude earthquake.
VI. Prevention of injuries
The best method of injury prevention during an earthquake is adequate warning.
Unfortunately, earthquakes are not predictable in their magnitude or time of
occurrence. This places a premium on preventative strategies to limit loss of life and
damage to property. The first line of public protection is the institution of building codes
that ensure construction will withstand potential earthquake strengths expected for the
region. Local governments should ensure that the local population is educated through
media campaigns to identify earthquake hazards within the home. The local
government, emergency services, and public utility companies should have disaster
plans in place to mitigate fires, gas explosions, aftershocks, and other secondary
earthquake effects.
During the earthquake those who are in buildings constructed to withstand
earthquakes should not attempt to move and should find cover under sturdy furniture
for protection from falling objects. They should avoid going outside during the quake
unless the building is in danger of collapse. Drivers of motor vehicles should make their
best attempt to come to a safe stop during the earthquake and remain in their cars with
seatbelts fastened. They should not attempt to drive until all ground vibrations have
subsided and should proceed cautiously, avoiding damaged road, ramp, and bridge
structures.

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 After the earthquake has abated, people should survey their surroundings for
signs of potential danger. People should leave buildings in danger of collapse. Gas or
other utilities should not be used since there may be damage to lines resulting in
increased risk of fire and explosion. Buildings that appear structurally unsound or are
partially collapsed should not be entered because subsequent aftershocks might cause
their collapse.
Basic preventive actions:
1. Prognosis by scientific methods – with seismic stations can follow the
activity of the earthquakes and using this information we can create
plans for action and prepare ourselves.
2. Creation of constantly active information systems – these systems
decrease the time for reaction.
3. Anti-seismic construction
4. Hospital planning for work in case of earthquakes.
5. Training of the population for correctly behavior, civics.
6. Creation of teams.
7. Material-technical insurance, crisis reserves.
VII. Emergency department treatment
As previously described, most injuries and fatalities occur within the first 24 hours
after the initial shock. The majority of injuries seen will be blunt trauma, crush injuries,
fractures, lacerations, abrasions, burns, and penetrating injuries in varying numbers.
Since the occurrence of earthquakes is unpredictable, it is important to have a
previously prepared and rehearsed disaster plan that can be rapidly activated. An
emergency department should be prepared to treat an anticipated post-event surge in
multi-trauma patients. In situations where local resources are overwhelmed, all efforts
should be made to stabilize critical patients and expeditiously transfer stabilized
individuals to other medical facilities outside the disaster zone. In situations where the
patient surge completely overwhelms the emergency department, it may be necessary
to implement a mass casualty triage approach to maximize the number of lives saved.
It is also important to ensure that the hospitals and emergency rooms are structurally
sound and in no potential danger from secondary earthquake effects.

GENERAL CHARACTERISTICS OF FLOODS. ORGANISATION OF MEDICAL

RESPONSE

I. Definition
Floods are natural occurrences of temporary water overflow onto a particular,
normally dry territory, caused by heavy rainfall, intensive snowmelt or river ways
blocked by ice jams or mud flow; by uprooted trees or building debris, etc. Floods can
also be caused by tidal waves (tsunami), submerging coastal regions, following
earthquakes, volcanic eruptions, cyclones or tornados.
II. Causes:
Objective – heavy rainfall; intensive snowmelt; onshore hurricanes; tidal
waves; demolished dams and protective embankments, as a result of earthquakes or
terroristic attacks;
Subjective – hydro-technical facilities design and construction flaws; lack of
proper maintenance and technical control over such facilities; use of geophysical
weapons /artificially triggered earthquakes/.

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 III. Classifications
With regard to territorial spread, floods fall in one of the following categories:
 Local (small-scale) floods – occur around particular rivers or river districts
 Medium-scale (mezzo-scale) floods – occur in regions with a number of
rivers
 Large-scale (comprehensive) floods – cover large territories with many
rivers
 Overall (widespread) floods – cover the larger part of a country or the
whole country
In Bulgaria, due to the uneven topography of the country, the mountainous
territories and the relatively small low river valleys, we only have floods belonging to
the first three categories.
Hydro-meteorologists have worked out the following classification of floods,
according to their intensity, repetitiveness and impact on the environment:
1. Minor river floods – occur once in 10-20 years. A river overflows its
banks in the lowest parts of the river way, not causing any damage. The event does
not stay long in the social memory.
2. Dangerous floods – recurrence rate of once in 20-40 years. River
waters inundate large parts of its floodplain and nearby territories, causing damage on
their way and threatens the life of people and animals. Such events stays long in the
social memory.
3. Very dangerous floods – recurrence rate of once in 40-80 years.
Dangerously deep river waters (above 1 metre) submerge a large area and the velocity
of the torrent is above 20 m/sec. Bridges, dams, buildings, etc. can be damaged. Such
floods are very dangerous and they are remembered as the worst floods in a lifetime.
4. Devastating floods – recurrence rate of once in 80-150 years. River
waters submerge the whole or the larger part of a river valley with a depth of 1.5 – 2
metres and the velocity of the torrent is 2.5 – 3 m/sec. The torrent travels down the
valley but not down the river bed, causing severe damage to bridges, buildings, hydro-
technical facilities, etc. Such floods cause huge human life and property loss. They
stay long in the social memory and personal experiences related to those are retold
from generation to generation.
5. Catastrophic floods – recurrence rate of once in 150-200 years. Huge
territories are inundated, the river valley is entirely submerged and the water torrent
travels down the whole river valley. Te depth and the velocity of the torrent are of
catastrophic dimensions. Devastating mud-slides and land-slides are triggered,
forming weirs and pools. Life and property loss is catastrophic. Such an event leaves
unforgettable traces in the social memory and memories of witnesses are transferred
from generation to generation.
IV. Characteristic features of the general and the medical situation:
 Huge property loss – devastated towns and villages; demolished and
severely damaged buildings, facilities, elevated and underground
communication lines, etc.;
 Mass cases of drowning, which are impossible to foresee;
 Dire hygiene and epidemiological conditions resulting from pollution and
contamination of inundated territories caused by silt, dead bodies of
people and animals and also by sewage coming out of damaged sewers
and water supply pipes, etc.;

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  Outburst of intestinal infections such as dysentery; salmonellosis;
cholera, etc. and transmissible infections like typhus; paratyphus;
malaria, etc.
V. Health care and medical response duties during flood relief operations
Important for reducing the scale of loss among the population is proper pre-
planning of medical response stages during catastrophic flood relief operations. All
regional, neighbouring regions’ or national medical services are supposed to
participate in dealing with the medical consequences of flood disasters.
In cases of flooding the medical services of the region have to cope with two
major tasks:
1. Organisation of medical care for injured and displaced people.
2. Organisation of hygiene and epidemic control in the region.
First aid should be provided by civilians themselves; teams of lifeguards;
Emergency Medical Assistance Centres; uninjured medical professionals in the region,
etc. For such first aid to be effective it is essential for the population of vulnerable
regions to be well trained in providing first aid to people who have experienced nonfatal
submersion event or drowning.
When given first aid, the rescued are transported to the nearest undamaged
hospitals in the region. Evacuation of all rescued to a hospital is necessary because of
the specific consequences of submersion and drowning, sometimes leading to
possible severe and irreversible damage.
Victims who need specialised medical care can be transferred to pulmonary
departments and clinics after their condition has been stabilised.
The first to evacuate should be pregnant women; mothers and small children;
bed-ridden diseased people; underprivileged people; people with chronic diseases,
who are in need to regularly go to hospital for procedures (such as hemodialysis for
example). Special attention is given to evacuate hospitalsed patients, children living in
social care institutions and old people living in residential homes;
Evacuation of patients of psychiatric clinics is executed after all actions have
been coordinated with respective specialists, under their supervision and guidance;
When evacuation is impossible the Directorate General for Fire Safety and Civil
Protection are responsible for providing the people who remain in the flooded region
with food; water; medication; clothes, etc., granted by the local authorities and the
Bulgarian Red Cross Organisation;
When the water retrieves Fire Safety and Civil Protection teams take an active
part in restoring normal living conditions: searching for missing or drowned persons
and animals; draining public buildings; hospitals; schools; homes, etc.
When the water retrieves, the flood terrain poses a potential risk of epidemic
outburst. Hygiene and epidemic control is exerted by the Regional Health Inspectorate,
with their specialised groups, teams and laboratories. That control includes the
following objectives:
 Biological investigation in the flooded residential areas and nearby territories;
 Organisation and execution of strict sanitary control on building and school
areas cleaning procedures;
 Anti-epidemic control and supervision on the burial of dead bodies of people
and animal, with regard to existing sanitary requirements;
 Execution and control on disinfection; disinsectisation and diratisation
procedures;

13
  Organisation and execution of epidemiologic monitoring of the population for
symptoms of infectious diseases and timely isolation of diseased people and their in-
contacts.
 Permanent sanitary control on drinking water; on food; warehouse storing
conditions, and on the soil is conducted. Water is distributed in alternative ways and
foods are destroyed if necessary or expert recommendations are made on how they
can be used after undergoing prescribed treatment.

GENERAL CHARACTERISTICS OF BREEDING AT CHEMICAL DISASTER.

FORECASTING AND TYPES OF MEDICAL LOSSES

Disasters involving exposures to hazardous materials are relatively rare events,

but they still represent one of the most common disasters in the community setting.
Experts agree there are over 100,000 hazardous materials in our society. Chemicals
are also effective terrorist weapons. These materials can be solids, liquids, or gases.
Exposures can result in significant morbidity. Acutely, these materials can produce
acute trauma such as burns, pulmonary edema, respiratory arrest, explosion injuries,
and neurological injuries.
Many accidents have occurred throughout the world that have led planners to
be particularly concerned about chemical accidents and our preparedness to deal with
them. The consequences of some chemical accidents for a community can be
devastating for many years to come.
A chemical accident is an unanticipated release, explosions, fires, or other
harmful incidents involving chemical substances that are toxic or hazardous materials.
While chemical accidents may occur whenever toxic materials are stored, transported
or used, the most severe accidents are industrial accidents, involving major chemical
manufacturing and storage facilities.
І. Definition. Causes of chemical disasters.
A chemical incident is the uncontrolled release of a toxic substance, resulting in
(potential) harm to public health and the environment. Chemical incidents usually
trigger a public health response, including, for example, assessment of exposure and
risk and/or provision of advice to authorities and/or the public.
Chemical incidents can have many manifestations, with different initiating
events (natural or anthropogenic), incident dynamics, injury types, and necessary
public health responses. Therefore, the term “chemical incident” might refer to
anthropogenic events such as the explosion of a factory which stores or uses
chemicals, contamination of the food or water supply with a chemical, an oil spill, a
leak in a storage unit during transportation or an outbreak of disease that is (likely to
be) associated with chemical exposure.
Chemical incidents can also arise from natural sources such as volcanoes,
earthquakes and forest fires. Natural disasters may disrupt chemical containment
systems and cause secondary anthropogenic chemical incidents (e.g. tank rupture
after flooding). Whatever the cause, the chemical incident might be discovered by
either knowledge of the contamination or knowledge of health conditions likely to have
a common chemical etiology, including disease outbreaks.
Chemical incidents can happen anywhere and at any time, even if there are no
chemical facilities in the area. Although most chemical incidents are small and involve
few people, the accumulated consequences may be just as serious as those of large

14
incidents in terms of illness, death, environmental and economic damage, and the
anxiety they generate for the public, emergency services personnel and employees.
Small incidents are often less visible and generate less publicity. However, the health
response should be as serious and professional as if it were a big event. In addition,
small incidents are occasions to verify the completeness and feasibility of the
preparedness plans and for responders to sharpen their skills.
A hazardous material is any substance that is potentially toxic to the
environment or to animals and humans. However, accurate and reliable data on the
public health consequences of hazardous materials releases are difficult to obtain. Few
agencies worldwide mandate reporting human exposure to hazardous materials to
governmental authorities. In the United States, the Agency for Toxic Substances and
Disease Registry (ATSDR) has maintained active state-based HazMat emergency
event system since 1990. ATSDR data reveal that 79% of these hazardous material
releases occur at fixed sites (i.e., industrial sites, schools, farms, and manufacturing
facilities) and 21% are transportation related. A single substance is released in 90% of
reported events. Volatile organic compounds, acids, chlorine, ammonia, pesticides,
and other organic substances are most commonly involved.
The most significant chemical accident in recorded history was the 1984 Bhopal
disaster in India, in which more than 3,000 people were killed after a highly toxic
vapour, (methyl isocyanate), was released at a Union Carbide Pesticides factory.
II. Examples of incident scenarios
Here are presented seven different manifestations of a chemical incident. The
incident types differ in initiating event, dynamics (time course), and the first risk
assessment and public health actions to be taken. Combinations of incident types are
possible.
Incidents can occur indoors and outdoors. The focus of the descriptions below
will be on outdoor releases, because these are often larger and have the potential to
affect more individuals than indoor releases. The consequences of outdoor releases
can extend to the indoor environment, and may result in exposures within buildings
and subsequent risks to health. The following types of incident scenario will be
described in terms of the typical course of the incident, and primary risk assessment
and public health actions.
1. Sudden evident outdoor release of gas or vapour
Typical course of the incident. A gas or vapour cloud with an acute time
course, possibly after evaporation from a pool of liquid. Inhalation exposure is possible
far downwind of the release site and there is a possibility of significant skin contact on-
site. The incident scene is accessible soon after the release has been terminated
because the vapour or gas cloud has moved downwind and been dispersed (unless a
pool is still present). Often rapid reports of odour or respiratory and eye irritation will
be received, but depending on the nature of the chemical, health effects can be
delayed for hours to days.
Risk assessment. In many cases only one or two chemicals are involved rather
than a completely unknown mixture of substances. Atmospheric conditions largely
determine the dispersion; gas pockets are possible, particularly after release of a heavy
gas. The population at risk can usually be determined quite rapidly from complaints
and dispersion modelling. The first environmental monitoring results will rarely come
in before 30–45 minutes following the chemical release. The possibility of delayed
health effects should be considered. The likelihood of secondary contamination outside
the incident scene is usually low.

15
 Public health key points. Usually advice to go indoors, shut all doors and
windows, disengage mechanical ventilation is appropriate for the population downwind
of the incident. Building characteristics determine the protectiveness and safe shelter
duration which is the length of time for which those at risk of chemical exposure should
remain in a safe shelter. The alert to shelter-in-place should include public alert
systems (sirens) supported by continuous and consistent communication through
multiple channels including radio, television, websites and telephone transmissions. If
the wind direction is expected to shift, preventive evacuation can be considered. After
the toxic cloud has passed, there are usually few or no restrictions on outdoor activities.
2. Sudden evident outdoor release of an aerosol
Typical course of the incident. A sudden emission of liquid or solid aerosol
occurs into the air outdoors and/or indoors; the material deposits on soil and
infrastructure, where it remains until it is removed either intentionally (e.g. in a cleanup)
or by natural mechanisms (e.g. wind or rain). The contaminated area outdoors can
range over kilometres, depending on the type of the event (e.g. explosion),
characteristics of the aerosol and environmental conditions. Inhalation exposure
usually occurs during and shortly after the emission. Primary exposure via the oral and
skin routes is possible on-scene and wherever deposited material persists.
Risk assessment. Usually information about the composition of the emitted
material and the particle size distribution is unavailable in the acute stage. Quantitative
assessment of exposure with modelling and monitoring is very difficult; usually
exposure is assessed by visual determination in the contaminated area.
Public health key points. Information about restrictions on access to the
outdoor area and clean-up is critical, particularly as long as the health risk has not been
determined. Compliance with health advice is generally high in areas where
contamination is visible, the occurrence of acute effects is recognized widely, and
concern about delayed effects (e.g. for carcinogenic substances) is communicated
clearly.
3. Sudden evident release to contact media other than air
Typical course of the incident. An immediately detected release of a
substance occurs in water, soil or directly into food (e.g. during food processing) or
other media (e.g. sediments or consumer products). It is often easier to avoid primary
human contact with the chemical for this scenario than it is to avoid contact with
airborne releases because it is often possible to discontinue exposure through these
media, at least for a short time. Secondary contamination of food, drinking-water and
consumer products can occur as well following release of a chemical to surface water
or soil. The time taken to respond to incidents of this type is usually a matter of hours,
rather than minutes as for types 1 and 2.
Risk assessment. The possible pathways for human exposure and the
resulting health risk depend on the physicochemical properties of the substance and
its eventual environmental fate. Volatile substances may evaporate quickly and be
detected by their odour or taste. Chemicals with low vapour pressure will partition
primarily between water and soil, or other substrates rich in organic matter, depending
upon their structure and solubility in water.
Public health key points. Warning the public to take immediate action is rarely
required, unless information needs to be provided about odour. The focus is on the
environmental incident.
4. Fire in a large building
Typical course of the incident. This type of incident includes fires in residential
and shopping areas, warehouses, fixed chemical storage and production sites, tunnels

16
and underground railways. Combustion products are determined by the burning
material and the type of fire. The heat of combustion influences the air dispersion of
the toxic smoke. Victims with serious injuries are mostly found inside or near such
burning structures. Secondary explosions may occur. Populations downwind of a
release point are at particular risk of exposure and subsequent immediate and delayed
health consequences. The size and constituency of this population at risk will
determine the scope of the response action.
Risk assessment. The characteristics of the affected building can provide a
rough indication of the materials on fire; identification of the material on fire has proven
very difficult for warehouses in which the inventory of stored products is varied and
may change over time. The initial risk assessment is based on smoke and combustion
products. Exposure modelling is complex; visual observation and environmental
monitoring often provide more useful estimates of exposure. It is often impossible to
make a quantitative risk assessment in the acute stage. Deposited material may cause
secondary contamination identical to that seen in type 2 incidents.
Public health key points. The safety of emergency responders is crucial,
particularly when explosions or contamination of fireextinguishing runoff are possible.
Since risk assessment is difficult, a precautionary approach is often used in providing
advice on sheltering and use restrictions. Evacuation of the building’s residents and of
neighbours with high exposure to smoke is advisable, and may need to be continued
for some days.
5. Explosion
Typical course of the incident. In many cases explosions have a forewarning
period. The affected area is roughly circular around the explosion site, although high
buildings may act as a shield. Explosions cause structural damage to buildings,
fragments, projectiles and glass splinters. In some cases a fireball or gas cloud
explosion occurs.
Risk assessment. The major types of injury are burns from thermal radiation
and traumatic (mechanical) injury due to the blast (gas filled organs and rupture of the
tympanic membrane), fragments and projectiles. These risks are relatively well
established. Toxicity is usually due to combustion products from secondary fires or
(resuspended) material on the soil or infrastructure.
Public health key points. In case of a forewarned explosion there may be time
to provide instructions on risk reduction to the at-risk population. In all cases the safety
of emergency responders is a primary concern: for a threat of explosion or after an
explosion (for example, owing to building instability and collapse). Experienced urban
search and rescue teams may be necessary. Access to the affected area may be
problematic if there is debris on access roads. Long-term shelter and provision of basic
essentials may be necessary for those who have lost their homes.
6. Disease outbreak
Typical course of the incident. In this case it is not the release of the chemical
that is detected, but an increase in the number of people with a more or less consistent
syndrome of signs and symptoms. Detection is usually through surveillance systems
and/or watchful clinicians, and usually takes days to weeks or months depending on
the specificity of the clinical syndrome and the geographical spread of the patients.
The common source may remain obscure for a long time, and all exposure routes and
contact media should be considered.
Risk assessment. The approach to risk assessment for this type of incident
involves strengthening disease surveillance, assessment and verification of clinical
presentation, and the search for the chemical hazard and a possible common source

17
of exposure (primary and/or secondary contamination), using toxicological and
epidemiological tools. Possible chemical hazards, sources and reported effects are
investigated simultaneously. After identification of the hazard and source, a detailed
exposure assessment should be made to verify the acute effects and predict possible
delayed or residual effects and the populations likely to be affected.
Public health key points. Key points are coordination of information,
investigations and communication. Most outbreaks will enter the public health system
as a suspected outbreak of an infectious disease. A well coordinated cooperation
between chemical and infectious disease experts may prevent loss of time in
identifying outbreaks with a chemical etiology.
7. Silent releases
Typical course of the incident. In the case of silent releases, the release of
the chemical into the contact medium is not detected until after the release, but before
it has been detected as a disease outbreak. This can happen when the occurrence of
an incident is brought out into the open after some time, or when a release is more
serious than anticipated at the time of the initial release.
Risk assessment. The first steps are verification of the chemical, an analysis
of all possible exposure pathways and populations, and a quantitative risk assessment
with focus on delayed or residual effects.
Public health key points. This type of incident may be a grey area between
response to a chemical incident and ”regular” environmental health provision. Health
investigations should establish a clear link between observed and anticipated delayed
health effects and exposure, including the development of case definitions. One of the
public health challenges in this scenario is that people who know about or have been
close to the event, but have NOT been exposed, may attribute signs and symptoms
related to another disease to the incident.
Incident types 1–5 are typically localized: there is an incident scene. In addition
to other common traits, public health management of events with an incident scene
may include concerns about health risks posed to emergency response personnel. The
detection and development of incidents of types 6 and 7 is typically much more diffuse
in time, place and person.
III. Injury mechanisms
Chemical incidents can cause injury through four basic injury mechanisms: fire,
explosion, toxicity and the experience of traumatic events. These injury mechanisms
may appear to be quite distinct, but in reality are strongly interrelated.
• Fire produces injuries through heat and exposure to toxic substances
(including combustion products). A secondary effect of a fire may be an explosion or
tank failure due to heating of tanks holding chemicals. Every major fire can be
considered a chemical incident.
• An explosion produces traumatic (mechanical) injuries through the resulting
shockwave (blast), fragments and projectiles. As a secondary effect an explosion may
result in a fire or loss of containment resulting in release of and exposure to toxic
chemicals (e.g. through penetration of an adjacent tank by fragments: so-called
domino effects).
• Toxicity may result when humans come into contact with a chemical released
from its containment, be it from storage or transport, or as reaction or combustion
products. Toxicity can cause harm by a wide array of toxic mechanisms ranging from
chemical burns to asphyxiation and neurotoxicity.
• Mental health effects, the final type of “injury” are not only determined by
exposure to the chemical, fire or explosion but also by “exposure to the event” itself.

18
Severe incidents have the potential to disrupt the lives of victims through injury, loss of
relatives, property or employment and societal disruption. A substantial proportion of
victims of major incidents have been shown to experience long-lasting mental health
problems.
IV. Injuries
Touching, breathing, eating or drinking harmful chemicals. Exposure to
chemicals can result in varying symptoms with different degrees of danger. Mild
reactions include burning and tearing of the eyes, throat, nose, chest and skin. Severe
reactions include coughing, wheezing, feeling faint, convulsions and even death.
V. Chemical incidents management
The first line of defence against adverse consequences of chemical incidents is
to prevent their occurrence and to limit their impact if they do occur. Prevention is
aimed at reducing the likelihood of an incident occurring and includes all technical and
organizational measures taken to reduce the severity of any incident that might occur
and to ensure that its impact is reduced to a minimum and that it does not become a
major event or disaster.
Despite the best efforts to eliminate risks and reduce the likelihood of their
occurrence, some residual risk will remain which can materialize in an incident. This
residual risk should form the basis for subsequent planning and preparedness. The
time taken during an incident to locate equipment and infrastructure, coordinate the
actions of the various stakeholders, establish links between agencies and emergency
services, establish a response plan and gather general information about the
pollutant(s) and the facility responsible for the incident will be time lost towards
minimizing the extent and consequences of a chemical incident. Hence, these tasks
should be accomplished prior to the incident, in order to ensure that immediate efforts
can readily be focused on the response to the incident. Therefore the incident response
system should be designed, the roles, responsibilities and competencies attributed,
personnel selected, trained and exercised, in the planning and preparedness stage.
Incident detection and alert is a continuous activity undertaken to pick up signals
that a chemical incident has occurred, and to ensure rapid alert for an appropriate and
timely response.
When an incident takes place, the operator, authorities and the public initiate the
incident response to terminate the incident and mitigate the consequences.
After the incident has been terminated the recovery may take years of clean-up,
health monitoring, evaluation and other activities that are aimed at restoring the
situation to how it was before the incident and contributing to prevention of recurrence.
VI. Responsibilities at a chemical incident
The police and fire services have a duty to ensure the safety and protection of
the public in general terms after incidents involving toxic or corrosive substances and
the health authorities have a responsibility to recover and care for any casualty—
however caused. Fire brigades have equipment to protect brigade personnel from the
effects of smoke and other toxic vapours. These will include full enveloping gas-tight
suits which, when worn with breathing apparatus, will give almost complete protection
from a hostile environment. The fire service, therefore, takes a leading role in incidents
involving toxic substances. The police will set up a cordon around the affected area.
They will be responsible for traffic diversions and evacuation of any area at risk. The
police would normally make contact with the owners or carriers of the substance
involved so that they can assist in removing or containing the hazard. The role of the
ambulance service is to provide aid to any casualties, to transport casualties from the
site to suitable medical facilities, either an established emergency department or, in an

19
incident of disaster proportions, to an improvised field hospital. From time to time
transport, direct to specialist hospitals, may be appropriate. Examples would be burns
units, plastic surgery units or hospitals equipped to deal with radiation contaminated
casualties.
Doctors or nurses may, from time to time, be called upon to assist at emergencies
where toxic or corrosive substances are involved. It is vital that such staff are given
adequate training and preparation for such incidents. They can then make a safe and
effective response to alleviate distress and treat injuries to casualties without putting
themselves at unnecessary risk.
VII. Decontamination
Decontamination would normally be effected by stripping and washing down
thoroughly. Water alone, or water and detergent, are the most suitable agents for
decontamination in almost all cases. On rare occasions, dry methods of decisions
about further management but may well take professional advice from an on-site
doctor.
VIII. Evacuation
In an incident where toxic chemicals are liberated into the atmosphere in the form
of smoke, powder, fumes or gases, it may become necessary to consider the possible
need to evacuate the area at risk. The extent of such an area is dependent on many
factors, such as wind velocity and direction, weather conditions and local topography.
Clearly the decision to evacuate is one of urgent priority, if necessary. Evacuation of
an area at risk would normally be undertaken by the police but, clearly, as they are not
trained and equipped with breathing apparatus and protective clothing, it is usual for
fire brigade members to deal with evacuation of the immediate area of contamination.
Cordons around the area and security of evacuated property is the responsibility of the
police. The local authorities are required to make contingency plans for mass
evacuation in such instances and may plan to open rest centres. These rest centres
are often in schools or halls and arrangements can be made for food, drinks, blankets
and other requirements. Often the voluntary aid societies and other bodies can be
mobilized to assist in them. The local authorities should also have plans for emergency
transport. For the walking wounded and the uninjured, this may include local bus
companies. Ambulance transport should only be used for those too ill, infirm or
handicapped to use other transport. Evacuation from toxic vapour clouds can generate
a great deal of panic and the whole operation needs firm and tactful policing.
A medical or first aid presence at each rest centre should be arranged to provide
care for the frightened or distraught and for those who, during the evacuation, forgot
important medication or left drugs behind. All those present at each centre should be
recorded and their disposal to other places documented.
Plans for major chemical incidents need to be prepared in advance, in just the
same way as most areas have plans for a train or air crash. Specified hospitals should
be equipped and staffed to deal with contaminated casualties and those suffering from
the acute effects of poisoning.
VII. Principles of first aid
Always use personal safety and protection equipment relevant to the known
hazard. Unconscious patients should be cared for in the normal way using the
recovery. Controlled or assisted ventilation and external chest compressions may be
necessary. Inhalation casualties should be removed to fresh air and given absolute
rest where possible. Oxygen should be administered in high concentrations and at an
appropriate flow rate for as long as is necessary. With smoke inhalation, there may
also be burns to the respiratory tract which may not be immediately apparent until the

20
secondary pulmonary oedema develops. Where there is contamination, all affected
clothes should be removed, together with wrist watches and shoes. The victim should
be washed copiously with water and soap. If the eyes are affected they should be
washed gently with a jet of water or normal saline. A simple arrangement is to use
normal saline and a standard giving set to irrigate the eyes continuously, with a tap to
control flow.
Skin Contact
 Remove all contaminated clothing, including shoes, watch and jewellery,
unless stuck to skin.
 Drench affected area with running water using soap as well, if appropriate.
 Check for burns and systemic signs of poisoning.
 Set up intravenous infusion.
 Refer to hospital, if required.
Eye Contact
 Wash eye thoroughly using normal saline for at least 10 minutes.
 Refer for specialist eye examination.
Ingestion
 Do not make casualty vomit.
 If unconscious, do not give anything by mouth.
 Check breathing and pulse. Give artificial ventilation, if necessary, using a
self-inflating bag (not mouth-to-mouth in cases of cyanide or hydrogen
sulphide ingestion) or automatic resuscitator. Give external chest
compressions, if necessary. Set up i.v. infusion.
 If unconscious, but with pulse and breathing normally, place in the
recovery position. Set up i.v. infusion.
 If conscious, give a pint of water to drink immediately. If the chemical is
corrosive, give 1 pint of milk unless the chemical contains phosphorus,
chlorinated hydrocarbons or degreasing solvents, in which case continue
giving water.
 Transfer to hospital.
Inhalation
 Remove from exposure, wearing appropriate protective clothing and
breathing apparatus.
 Check breathing and pulse, as above. Commence treatment with artificial
ventilation and external chest compressions, if required. Set up i.v.
infusion.
 If appropriate, use the recovery position for unconscious patients who are
breathing spontaneously.
 Give oxygen.
 Remove to hospital.
 Advanced resuscitative measures should be provided to supplement first
aid as soon as possible.

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 FIRE DISASTERS

As a type of manmade disasters, fires pose a main threat to human life and
health. On account of the possible causing factors and the type of damage they inflict
on people, fires can have different specific characteristics.
Fires have long been a current and constant concern since that kind of disaster
annually causes great damage and human losses in many parts of the world.
Large-scale fires also disrupt the ecological balance on large territories because
of the uncontrollably high temperatures and the large quantity of harmful gases and
evaporations they produce.
I. Causes
Depending on the cause of outbreak, fires can be classified as either manmade
(anthropogenic) or natural disasters. In the first case the cause of fire outbreak is
careless or irresponsible handling of fire; poor management and maintenance of
installations and facilities or disregard of safety at work standards and requirements.
In the second case, the cause of fire outbreak can be periods of extremely high
temperatures; lightning strikes or volcanic eruptions.
II. Definition
A fire is an incontrollable, complex, physicochemical process of burning. The
main phenomena related to the process of a burning fire are:
 The chemical reaction of burning;
 Heat release;
 Products of burning /toxic smoke/.
The regularities of fire phenomena and the interrelations between them
determine the fire situation, which depends on the following:
 The scope, the type and the speed of burning;
 The amount of heat released;
 The amount and the properties of other products of burning released in
the atmosphere.
The fire situation in each case determines the level of danger for people and
material objects.
III. Damaging factors
The effect of fire on living organisms can be fatal within a few seconds or it can
cause one of the most complex traumas to the human organism.
The main damaging factors causing harm to human health in cases of fire are
the following:
 Thermal factor
 Toxic factor
 Mechanical factor
 Stress factor
In most cases a combined type of trauma is observed because several
damaging factors affect victims of fire simultaneously.
Thermal factor
The thermal factor in cases of fire are the flames and the heat released as a
result of the process of burning. Their impact on people causes thermal burns of
different stages and severity:
First degree burns are associated with symptoms like skin redness, swelling and
mild pain in the affected area. Only the surface of the skin (the epidermis) is affected.

22
 Second degree burns cause skin blistering. If the blisters are popped, reddish
or white wounds can be seen beneath the raised skin. This type of burns are extremely
painful because not only the epidermis but also the dermis are damaged.
Third degree burns are black (charred), parchment-like or white in colour. This
type of wounds are not painful because they cause destruction of the sensory nerve
endings in the involved skin. Despite that, there are usually first and second degree
burns around a third degree wound, which are painful.

Toxic factor
The toxic factor in fires is presented by the toxic products of burning, released
in the smoke, which cause intoxications of different character and severity.
A great degree of vagueness exists in relation to the toxic factor, since it is
impossible to precisely predict the type of toxic substances released in different fires.
In most cases intoxications are caused by the effect of a few poisonous substances.
Most often the effect of the simultaneous action of the chemical substances released
in the process of burning is of additive, synergetic and, more rarely, of antagonistic
type.
The content of the poisonous substances released in the toxic smoke depends
on two groups of factors:

TYPE OF BURNING SUBSTANCE FACTORS FACTORS RELATED TO BURNING

CONDITIONS

Chemical characteristics of the substance burning Speed of burning

Quantity, shape and dimensions of the Rate of temperature increase while
object/substance burning burning
Contact of the substance burning with other materials Availability of oxygen

Traumatic /mechanical/ factor – fires are often accompanied by explosions,

buildings collapsing and sudden fall of different heavy objects, which often cause
damage and traumas of different nature.
Stress factor – the disastrous situations, which pose threat to human life and
health causes changes in the psychological state of people, typically associated with
panic, fear, and consequently, occurrence of depression, posttraumatic stress
syndrome, etc.
IV. Fire Prevention and Fire Response
The great number of specific characteristics of fires as a type of disaster and
the large number of damaging factors, which in their combined action take human life
and cause serious damage among the population affected call for the development of
a comprehensive prevention and fire response preparedness programme.
The development of such a programme is of vital importance because it can
either prevent or minimize the fire impact. It is a complex process which requires

23
precise analysis and consideration of the specific conditions, fire vulnerability and risks
in a specific place.
The development of a Fire Prevention Programme should take into
consideration four major guidelines:
 Fire prevention and fire response preparedness.
 Immediate response in the event of fire.
 Reconstruction of human and material losses during the period following
a fire incident.
 Further development after coping with the losses and eliminating the
effects of a fire.
An important step in the development of a fire prevention programme is carrying
out a comprehensive survey of a place or a situation in order to identify existing or
potential fire vulnerabilities and risks. Based on the information thus received an action
plan shall be developed in the form of a written document, which identifies and lays
down the objectives, priorities, management and control responsibilities, as well as the
time frame for task fulfillment. Each objective must be clearly defined, measurable,
achievable, appropriate and time-limited.
Measures should be identified in two main areas:
1. Fire prevention.
2. Response preparedness in the event of fire.
The actions related to these two areas are of different nature but of equal
importance for diminishing the risk of fires or restricting their impact on people and
property. The efficiency of fire response depends on the appropriateness and the
quality of preplanning, training and mock field exercises.
All structures in the sphere of production and services; public transport and
buildings; schools and hospitals need to have a specific fire prevention and response
system developed, which should reflect all specific details and peculiarities; the level
of risk available and the possible causes of a fire in each specific place or situation.
The development of such programmes depends on the quality of management
of each particular structure, their management policy and active participation in the
process of developing fire prevention and response preparedness measures.

BIOLOGICAL WEAPONS.
PARAMETERS OF THE BIOLOGICAL CONTAMINATION OUTBREAK

The biological weapons are on of the modern means for mass destruction.
Different pathogenic microorganisms can be used as biological weapon –
bacteria, viruses, fungi, rickettsiae and their toxins, designed for destruction of people,
pets and agricultural crops.
The purposeful application of biological agents for terroristic purposes is called
bioterrorism.
Biological weapons were used numerous times in the past. The achievements
of modern biology and immunology find even newer possibilities to apply them in such
scale that can lead to catastrophic consequences.
I. Biological weapons
In terms of bioterrorism the biological weapon has the following advantages:

24
 Cheap and accessible even for financially and technologically weak
countries and terrorist groups.
 Easily applicable and possible to use at a certain moment.
 Easy to hide and carry through border and other control structures.
 High levels of morbidity and mortality accompanied with manifestations
with mass hysteria among the people.
 Possibility to cover the attack and delay the discovery of the incident.
From biological perspective the bioagents are bacteria, viruses, rickettsiae,
deep mycoses, toxins, protozoa and helminths, which depending on the subject of
impact are divided into:
1. Homopathogenic agents – to this group belong infectious agents that have
pathogenic activity only on humans.
2. Zoopathogenic agents – infectious agents, specific only for the animals or
pathogenic for animals and humans.
3. Phytopatogenic agents – microorganisms and arthropods that affect
plants.
According to the type of the infectious agent:

DESEASES, WHOSE AGENTS /MICROORGANISMS OR TOXINS/ CAN BE

USED AS A BIOLOGICAL WEAPON

BACTERIAL RICKETTSIAL VIRAL MYCOSES INTOXICATIONS

ANTHRAX Q FEVER JAPANESE NORTH AMERICAN BOTULISM

ENCEPHALITIS BLASTOMYCOSIS
BRUCELLOSIS ROCKY
MOUNTAIN DENGUE SOUTH AMERICAN
CHOLERA SPOTTED FEVER FEVER BLASTOMYCOSIS STAPHYLOCOCCAL
INTOXICATION
DYSENTERY MARSEILLES SPRING- COCCIDIOIDOMYCOSIS
FEVER SUMMER
PLAGUE TICK-BORNE CRYPTOCOCCOSIS
EPIDEMIC ENCEPHALITIS
TULAREMIA TYPHUS HISTOPLASMOSIS
INFLUENZA
TYPHOID SCRYB TYPHUS
FEVER (TSUTSUGAMUSHI PSITTACOSIS
FEVER)
GAS SMALLPOX
GANGRENE
YELLOW
TETANUS FEVER

According to the level of threat to the national security the most probable
bioagents, ranked in descending gradation, are as follows:
 first group /category A/ - infectious agents posing the highest risk for the
national security; they can spread easily, be transmitted from person to person and
cause high mortality; they include anthrax, botulism, smallpox, tularemia, plague,
hemorrhagic fever;

25
  second group /category B/ - bioagents, which spread relatively easy,
cause moderate morbidity and low mortality, require increased monitoring of the
disease; they include Q fever, brucellosis, ricin toxin, cholera, etc.;
 third group /category C/ - dangerous pathogens with a potential for mass
dissemination in future; the group includes the virus causing encephalitis, viruses that
cause hemorrhagic fever, etc.;
Requirements, which the infectious agents should meet, when applied as a
biological weapon:
 Low infectious dose.
 High pathogenic effect.
 Resistance to the environment.
 Various and easy ways for dissemination and contamination.
 Lack of means for protection, prevention and treatment.
 Difficult and lengthy identification.
 Quick and cheap production.
In order to improve the biological weapon, in addition to choosing the
appropriate pathogenic triggers, their properties are modified as well. This modification
causes:
1. Enhanced virulence that increases the possibilities for mass morbidity
and leads to reduction of the incubation period.
2. Change in the immunobiological properties in order to overcome the
established immune barriers.
3. Enhanced resistance in the environment and searching possibilities for
contamination beyond the mechanisms typical for a certain infection.
4. Carrying by an untypical carrier.
The improvement of the bioagents is carried out through manipulation of the
genetic apparatus of the microorganisms. Different methods for irradiation with
ultraviolet and radioactive rays, chemical means, etc. are used.
Routes of administration:
1. Biological diversion, in which contaminated are water sources,
enterprises of food, pharmaceutical and cosmetic industries, mass contamination of
water, food, medicaments, and cosmetic products, which due to their mass use can
play a key role in the sharp deterioration of the epidemiological situation. This method
also includes the dissemination of infected arthropods, insects, rodents and birds,
which are a source for contamination. People are infected either directly through them
or by animals infected by them. In modern conditions the diversionary method has a
secondary significance.
2. The aerosol method is the most dangerous way for biological attacks. It
represents air contamination through the creation of aerosols made of pathogenic
microorganisms or toxins. There is a possibility to contaminate significant territories
with all the objects located in them – people, animals, plants, transport, food, water,
soil, air, etc. When a liquid culture of pathogenic microorganisms is disseminated then
the aerosol resembles fine mist, while in the dissemination of dried cultures and toxins
the aerosol is smoke-like. The formed aerosol cloud is spread following the direction
of the wind and contaminates the area. Under the aerosol method people can be
infected through their nose, mouth, conjunctivae and damaged skin. The aerosol
infection expands the doorways and the infectious process is harder and requires
longer treatment.

26
 The biological attack can be carried out through various technical means –
aviation bombs, rockets, artillery shells, mines, balloons, containers with infected
animals, generators with bacterial aerosols, etc.
The ammunitions are loaded with liquid or dried highly concentrated cultures of
pathogenic microorganisms or toxins.
Parameters of the biological weapons.
 The damaging capacity of the biological weapon depend on the biological
features of the disease agent used, the method of application, the routes for
dissemination of the infection.
 The biological weapon may include one infectious agent but it can also
include a combination of agents. It has a significant penetrating ability – it penetrates
all shelters, which are infiltrated by air and water.
 The use of biological weapons causes the contamination of large areas
entailing mass morbidity among the people. The biological weapon has high virulence
and prolonged activity.
 The biological weapon exercises its impact not only immediately at the
moment of the attack. People and animals can get infected at a later stage when the
healthy come into contact with infected people or contaminated objects.
 The duration of the contaminating activity of the biological weapon
depends on the used agent resistance to the environment.
 When using modern biological weapons it is possible to inhale not only
infections, for which this is the normal route for contamination, but also other infections,
which under natural conditions are not airborne.
 After the usage of biological weapons there is a period of precipitation of
microorganisms and/or toxic substances in water, air, soil, body surface and other
objects. The possible penetration routes for bioagents into the human organism are
the following:
o Airways: data shows that biological weapons are most efficient when
inhaled as an aerosol;
o Digestive tract: through the intake of contaminated food and drinking
water;
o Through the skin: the biological agents can penetrate both intact and
damaged skin.
The action of the biological weapon is visible after a certain incubation period
/the shortest one is for the toxins/ and is characterized by significant duration.
Depending on the agent various contagious diseases and epidemic outbreaks
develop.
II. Specifications of the epidemic situation at BCO
The application of biological weapons causes a biological contamination
outbreak /BCO/ – this is the territory, including the people, animals, plants that are
found in it and its adjacent atmosphere, in which you can find agents causing
contagious diseases or infected objects.
The epidemic process caused follows the general patterns, typical for natural
epidemic situations, however, the following specifications of the spreading of the
infectious agents, which are used as a weapon, can be observed:
1. Unexpectedly, without any causal link to the epidemic condition of the region
new massive epidemic outbreaks occur. It was calculated that their scope can reach
several hundreds square kilometers.

27
 2. The epidemic process that resulted from the usage of a biological weapon
will continue developing further naturally, however, we can suppose that at the very
beginning it will be highly intensive. This is facilitated by the following conditions:
a/ the aerosol method of using the biological weapon creates possibilities
for simultaneous airborne infection of a large number of people at one moment thus
creating a significant number of sources of infection that can further infect an even
bigger number of healthy people;
b/ the massive doses of microorganisms that are used for the contamination
are the reason for immunized people to be included in the epidemic process chain as
well;
c/ the intensive contamination of wide areas with all the objects of the
environment is the reason for the quick infection of more and more new people, who
pass through the contaminated territory, consume contaminated water or food, touch
contaminated objects;
3. It is possible to have many outbreaks in different territories at one and the
same time, which creates significant pressure in the organization of the anti-epidemic
provision for the population.
4. Several infectious agents and toxins can be used in one and the same
territory, which results both in diseases caused by various infections and intoxications
and many mixed infections. All of the above causes serious difficulties in the clinical,
microbiological and viral diagnostics.
5. While in the appearance and dissemination of a series of contagious
diseases in natural conditions there is certain seasonality, such cannot be considered
as regular when biological weapons are used.
6. A hidden action period is typical for the biological weapons. As it is known
there is an incubation period that varies in length for each contagious disease.
Therefore, the action of the biological weapon is not manifested immediately but after
a certain period of time.
When the biological attack was found in time, then the incubation period is a
favourable asset, since it allows quick preventive measures with significant effect to be
undertaken on time.
The situation is much different when the biological weapon was secretly
deployed. In this case, many people who were under the influence of the biological
weapon during the attack in a certain territory, will leave it before getting sick and after
the incubation period is over and the disease is manifested, they will end up being in a
different often quite remote region. Thus the infection can be carried away from the
biological contamination outbreak and it will lead to the occurrence of additional
epidemic outbreaks. The simultaneous manifestation of the sickness at both the
biological contamination outbreaks and at the additional epidemic outbreaks is the
reason for the place, where the biological weapon was used, to be hard for
identification.
III. Organization of the protection and medical provision for the citizens in
case of BCO. The protection activities can be grouped in the following sequence:
 measures prior to the BCO occurrence;
 measures at the occurrence of outbreak of biological impact;
 measures to eliminate the consequences.
Measures prior to the BCO occurrence. The measures for preliminary
preparation come down to:
• Planning the activities of the structures that react in case of threat or
occurrence of biological contamination outbreak.

28
 • Planning the type and number of staff and their training, maintaining
increased vigilance at all levels of state power and among the population;
• Developing specific protection measures and events, provided with the
necessary material, technical, financial and human resources.
Measures at the occurrence of BCO. The existing plans are immediately
drawn into action under the following sequence: notification, biological investigation
and isolation-restrictive measures /observation, quarantine/.
In terms of notification we have a developed system for constant interaction
between the different departments that are related to BCO by means of maintaining
24/7 duties and constant contact between the people on duty.
After establishing contamination by agents causing especially dangerous
infections /EDI/ the Director of Fire Safety and Civil Protection Chief Directorate
imposes a quarantine upon the region or the country following a report by the Minister
of Health. In the cases when it is found out that the infectious disease agents do not
belong to the group of EDI, observation is imposed – i.e. a system of measures,
envisaging increased medical monitoring at the outbreak, undertaking medical-
prophylactic and isolation-restricting measures that prevent the spreading of the
infection. The main difference is that the observation does not envisage isolating the
outbreak by armed guards, even though in case of observation the entry and exit are
limited and controlled.
Measures to eliminated the BCO and treatment of the contagious patients.
The organization of the medical provision of the affected is following the
“treatment on the spot” system. Evacuation from the BCO is absolutely forbidden.
For the medical provision /MP/ of the affected are included all healthcare
personnel, formations and treatment facilities that are within the outbreak of the
contamination. The main measures undertaken at the outbreak are early detection,
isolation, hospitalization and treatment of the contagious patients, urgent and specific
prophylactics, disinfection of the territory, facilities, transport means and sanitary
treatment of the population, health control over the food and the drinking water.
IV. Methods and means for protection against biological weapons
Collective means for protection. The air-raid hermetically sealed shelters are
used. They are built deep under the ground in order to be used for protection against
nuclear weapons and are equipped with special absorbing filters to purify the air
coming from outside.
Personal means for protection.
The gas mask is the most secure means for protection of the respiratory organs
and the eyes from biological weapons.
The respirator also provides protection of the respiratory organs. It is lighter than
the gas mask and does not impede breathing so much.
Cotton-gauze mask. It is made of 4 up to 8 layers of gauze and one layer of
cotton and is tied to the face with four ties.
Protective goggles. They are used for eye protection. They should fit tightly and
are secured additionally with cotton around the nose.
Protective clothing. It protects the body from contamination in case of aerosol
attack or if using infected arthropods. It consists of hooded overall, rubber boots and
rubber gloves.
Preventive immunizations. Immunity against contiguous diseases can be
achieved through the usage of vaccines, toxoids, serums, gamma-globulins and
bacteriophages.

29
 Urgent prevention. Application of antibiotics and sulfonamides to prevent the
people, who were exposed to danger of getting infected by pathogenic microorganisms
or toxins, to get sick.
Protection of the drinking water. When central water sources are
contaminated with biological weapon, then the supply from them is interrupted until the
complete water disinfection. For drinking and household needs is used water from local
sources /pumps, wells/. They should be kept in good hygienic condition and be
protected from contamination. In the event of immediate danger the wells are covered
with polythene, canvas or other impenetrable cover. The population should provide for
themselves water supply that is protected from contamination. Water is stored in well
cleaned and disinfected barrels, casks, cans and other vessels that can be closed,
which are placed in well closed premises and are covered with a impenetrable cover.
Before usage the drinking water should be boiled for a period of 30-40 minutes.
Protection of food. Securely protected from biological contamination is all food
that is in sealed /metal, glass, plastic/ packaging. To protect them from contamination
the packages with food are placed in tightly closed boxes and cupboards or are
covered by polythene. Food from animal origin is protected by being placed in fridges
or tightly closed cupboards. Bread, bakery products and bulk food are placed in
polythene packaging and are stored in tightly closed cupboards. Liquid food is placed
in tightly closed glass vessels. Food, which is not stored in sealed packaging, should
be consumed only after thermal treatment. Food that cannot be thermally treated is
destroyed.
Personal hygiene. Maintaining personal hygiene is of great importance for the
protection against getting infected: washing hands with water and soap before eating,
often having a bath and changing of the underwear, sterilizing the cutlery, etc.
Disinfection. Methods:
 Mechanical – washing with warm water and soap using a brush and
rinsing thoroughly.
 Physical – boiling/sterilization of food, cutlery, kitchenware and different
objects.
 Chemical – using chemical disinfectants /chloramine, chlorinated lime
(calcium hypochlorite), etc./.
Disinsection. Methods :
 Physical – boiling/sterilization, ironing with a hot iron, treatment with hot,
dry or humid air, etc.
 Chemical – applying contact insecticides /heksachloran, neguvon, etc./.
Deratization. It is done through:
 Preventive measures – protecting the premises from rodents who can
penetrate them and breed in them.
 Extermination measures – mechanic/traps/ and chemical/zinc phosphide
and coumarin products/means.

IONIZING RADIATION. RADIATION DANGER

Radiation
In physics, radiation describes any process in which energy emitted by one
body travels through a medium or through space, ultimately to be absorbed by another
body. Non-physicists often associate the word with ionizing radiation (e.g., as occurring
in nuclear weapons, nuclear reactors, and radioactive substances), but it can also refer

30
to electromagnetic radiation (i.e., radio waves, infrared light, visible light, ultraviolet
light, and X-rays) which can also be ionizing radiation, to acoustic radiation, or to other
more obscure processes. What makes it radiation is that the energy radiates (i.e., it
travels outward in straight lines in all directions) from the source. This geometry
naturally leads to a system of measurements and physical units that are equally
applicable to all types of radiation. Some radiations can be hazardous.
Ionizing radiation
Ionizing radiation consists of subatomic particles or electromagnetic waves
that are energetic enough to detach electrons from atoms or molecules, ionizing them.
The occurrence of ionization depends on the energy of the impinging individual
particles or waves, and not on their number. An intense flood of particles or waves will
not cause ionization if these particles or waves do not carry enough energy to be
ionizing. Roughly speaking, particles or photons with energies above a few electron
volts (eV) are ionizing.
Examples of ionizing particles are energetic alpha particles, beta particles, and
neutrons. The ability of an electromagnetic wave (photons) to ionize an atom or
molecule depends on its frequency. Radiation on the short-wavelength end of the
electromagnetic spectrum — high frequency ultraviolet, x-rays, and gamma rays — is
ionizing.
Ionizing radiation comes from radioactive materials, x-ray tubes, particle
accelerators, and is present in the environment. It is invisible and not directly detectable
by human senses, so instruments such as geiger counters are usually required to
detect its presence. In some cases it may lead to secondary emission of visible light
upon interaction with matter, as in Cherenkov radiation and radioluminescence. It has
many practical uses in medicine, research, construction, and other areas, but presents
a health hazard if used improperly. Exposure to radiation causes damage to living
tissue, resulting in skin burns, radiation sickness and death at high doses and cancer,
tumors and genetic damage at low doses.
Types of radiation
 Alpha (α) radiation consists of a fast moving Helium-4 (4He) nuclei and is
stopped by a sheet of paper.
 Beta (β) radiation, consisting of electrons, is halted by an aluminium plate.
 Gamma (γ) radiation, consisting of energetic photons, is eventually absorbed
as it penetrates a dense material.
 Neutron (n) radiation consists of free neutrons which are blocked using light
elements, like hydrogen, which slow and/or capture them.
Various types of ionizing radiation may be produced by radioactive decay,
nuclear fission and nuclear fusion, and by particle accelerators.
In order for a particle to be ionizing, it must both have a high enough energy and
interact with the atoms of a target. Photons interact electromagnetically with charged
particles, so photons of sufficiently high energy also are ionizing. The energy at which
this begins to happen with photons (light) is in the high frequency end of the ultraviolet
region of the electromagnetic spectrum. Charged particles such as electrons,
positrons, and alpha particles also interact electromagnetically with electrons of an
atom or molecule. Neutrons, on the other hand, having zero electrical charge, do not
interact electromagnetically with electrons, and so they cannot directly cause ionization
by this mechanism. However, fast neutrons will interact with the protons in hydrogen
(in the manner of a billiard ball hitting another, sending it away with all of the first ball's
energy of motion), and this mechanism produces proton radiation (fast protons). These
protons are ionizing because they are charged, and interact with the electrons in

31
matter. A neutron can also interact with an atomic nucleus, depending on the nucleus
and the neutron's velocity; these reactions happen with fast neutrons and slow
neutrons, depending on the situation. Neutron interactions in this manner often
produce radioactive nuclei, which produce ionizing radiation when they decay, then
they can produce chain reactions in the mass that is decaying, sometimes causing a
larger effect of ionization.
Unlike alpha or beta particles, gamma rays do not ionize all along their path, but
rather interact with matter in one of three ways: the photoelectric effect, the Compton
effect, and pair production. By way of example, the figure shows Compton effect: two
Compton scatterings that happen sequentially. In every scattering event, the gamma
ray transfers energy to an electron, and it continues on its path in a different direction
and with reduced energy.
In the same figure, the neutron collides with a proton of the target material, and
then becomes a fast recoil proton that ionizes in turn. At the end of its path, the neutron
is captured by a nucleus in an (n,γ)-reaction that leads to a neutron capture photon.
The negatively-charged electrons and positively charged ions created by
ionizing radiation may cause damage in living tissue. If the dose is sufficient, the effect
may be seen almost immediately, in the form of radiation poisoning. Lower doses may
cause cancer or other long-term problems. The effect of the very low doses
encountered in normal circumstances (from both natural and artificial sources, like
cosmic rays, medical X-rays and nuclear power plants) is a subject of current debate.
A 2005 report released by the National Research Council (the BEIR VII report)
indicated that the overall cancer risk associated with background sources of radiation
was relatively low.
Radioactive materials usually release alpha particles, which are the nuclei of
helium, beta particles, which are quickly moving electrons or positrons, or gamma rays.
Alpha and beta particles can often be stopped by a piece of paper or a sheet of
aluminium, respectively. They cause most damage when they are emitted inside the
human body. Gamma rays are less ionizing than either alpha or beta particles, and
protection against gammas requires thicker shielding. The damage they produce is
similar to that caused by X-rays, and include burns and also cancer, through mutations.
Human biology resists germline mutation by either correcting the changes in the DNA
or inducing apoptosis in the mutated cell.
Non-ionizing radiation is thought to be essentially harmless below the levels that
cause heating. Ionizing radiation is dangerous in direct exposure, although the degree
of danger is a subject of debate. Animals (including humans) can also be exposed to
ionizing radiation internally: if radioactive isotopes are present in the environment, they
may be taken into the body. For example, radioactive iodine is treated as normal iodine
by the body and used by the thyroid; its accumulation there often leads to thyroid
cancer. Some radioactive elements also bioaccumulate.
Ionizing radiation
Some types of radiation have enough energy to ionize particles. Generally, this
involves an electron being 'knocked out' of an atom's electron shells, which will give it
a (positive) charge. This is often disruptive in biological systems, and can cause
mutations and cancer.
These types of radiation generally occur in radioactive decay.
Alpha radiation
Alpha (α) decay is a method of decay in large nuclei. An alpha particle (helium
nucleus, He2+), consisting of 2 neutrons and 2 protons, is emitted. Because of the
particle's relatively high charge, it is heavily ionizing and will cause severe damage if

32
ingested. However, due to the high mass of the particle, it has little energy and a low
range; typically alpha particles can be stopped with a sheet of paper (or skin).

Beta (+/-) radiation

Beta-minus (β-) radiation consists of an energetic electron. It is less ionizing
than alpha radiation, but more than gamma. The electrons can often be stopped with
a few centimeters of metal. It occurs when a neutron decays into a proton in a nucleus,
releasing the beta particle and an antineutrino.
Beta-plus (β+) radiation is the emission of positrons. Because these are
antimatter particles, they annihilate any matter nearby, releasing gamma photons.
Gamma radiation
Gamma (γ) radiation consists of photons with a frequency of greater than 1019
Hz. Gamma radiation occurs to rid the decaying nucleus of excess energy after it has
emitted either alpha or beta radiation.
Non-ionizing radiation
Non-ionizing (or non-ionising) radiation, by contrast, refers to any type of
radiation that does not carry enough energy per photon to ionize atoms or molecules.
Most especially, it refers to the lower energy forms of electromagnetic radiation (i.e.,
radio waves, microwaves, terahertz radiation, infrared light, and visible light). The
effects of these forms of radiation on living tissue have only recently been studied.
Instead of producing charged ions when passing through matter, the electromagnetic
radiation has sufficient energy only for excitation, the movement of an electron to a
higher energy state. Nevertheless, different biological effects are observed for different
types of non-ionizing radiation.
Neutron radiation
Neutron radiation is a kind of non-ionizing radiation that consists of free
neutrons. These neutrons may be emitted during either spontaneous or induced
nuclear fission, nuclear fusion processes, or from other nuclear reactions. It does not
ionize atoms in the same way that charged particles such as protons and electrons do
(exciting an electron), because neutrons have no charge. However, neutron
interactions are largely ionizing, for example when neutron absorption results in
gamma emission and the gamma subsequently removes an electron from an atom, or
a nucleus recoiling from a neutron interaction is ionized and causes more traditional
subsequent ionization in other atoms.

33
Units
The units used to measure ionizing radiation are rather complex. The ionizing
effects of radiation are measured by units of exposure:
 The coulomb per kilogram (C/kg) is the SI unit of ionizing radiation exposure,
and measures the amount of radiation required to create 1 coulomb of charge
of each polarity in 1 kilogram of matter.

34
  The roentgen (R) is an older traditional unit that is almost out of use, which
represented the amount of radiation required to liberate 1 esu of charge of
each polarity in 1 cubic centimeter of dry air. 1 Roentgen = 2.58×10 −4 C/kg
However, the amount of damage done to matter (especially living tissue) by
ionizing radiation is more closely related to the amount of energy deposited rather than
the charge. This is called the absorbed dose.
 The gray (Gy), with units J/kg, is the SI unit of absorbed dose, which
represents the amount of radiation required to deposit 1 joule of energy in 1
kilogram of any kind of matter.
 The rad (Roentgen absorbed dose), is the corresponding traditional unit
which is 0.01 J deposited per kg. 100 rad = 1 Gy.
Equal doses of different types or energies of radiation cause different amounts
of damage to living tissue. For example, 1 Gy of alpha radiation causes about 20 times
as much damage as 1 Gy of x-rays. Therefore the equivalent dose was defined to give
an approximate measure of the biological effect of radiation. It is calculated by
multiplying the absorbed dose by a weighting factor W R which is different for each type
of radiation (see above table).
 The sievert (Sv) is the SI unit of equivalent dose. Although it has the same
units as grays, J/kg, it measures something different. It is the dose of a given
type of radiation in Gy that has the same biological effect on a human as 1
Gy of x-rays or gamma radiation.
 The rem (Roentgen equivalent man) is the traditional unit of equivalent
dose. 1 sievert = 100 rem. Because the rem is a relatively large unit, typical
equivalent dose is measured in millirem (mrem), 10−3 rem, or in microsievert
(μSv), 10−6 Sv. 1 mrem = 10 μSv.
For comparison, the average 'background' dose of natural radiation received by
a person is around 2.4 millisieverts (240 mrem) per year. The lethal full-body dose of
radiation for a human is around 4 - 5 sieverts (400 - 500 rem).

Weighting factors WR for equivalent dose

Radiation Energy wR

x-rays, gamma rays, electrons, positrons, muons 1

neutrons < 10 keV 5

10 keV - 100 keV 10

100 keV - 2 MeV 20

2 MeV - 20 MeV 10

> 20 MeV 5

protons > 2 MeV 2

alpha particles, fission fragments, heavy nuclei 20

35
Maximum acceptable doses and dose limits in case of irradiation from
technological sources of ionizing radiation.
Natural and artificial radiation sources are similar in their effects on matter.
Above the background level of radiation exposure, the U.S. Nuclear Regulatory
Commission (NRC) requires that its licensees limit human-made radiation exposure
for individual members of the public to 100 mrem (1 mSv) per year, and limit
occupational radiation exposure to adults working with radioactive material to 5,000
mrem (50 mSv) per year.
The average exposure for Americans is about 360 mrem (3.6 mSv) per year, 81
percent of which comes from natural sources of radiation. The remaining 19 percent
results from exposure to human-made radiation sources such as medical X-rays, most
of which is deposited in people who have CAT scans. This compares with the average
dose received by people in the UK of about 2.2 mSv. As already mentioned, an
important source of natural radiation is radon gas, which seeps continuously from
bedrock but can, because of its high density, accumulate in poorly ventilated houses.
The background rate for radiation varies considerably with location, being as
low as 1.5 mSv/a (1.5 mSv per year) in some areas and over 100 mSv/a in others.
People in some parts of Ramsar, a city in northern Iran, receive an annual absorbed
dose from background radiation that is up to 260 mSv/a. Despite having lived for many
generations in these high background areas, inhabitants of Ramsar show no significant
cytogenetic differences compared to people in normal background areas. This has led
to the suggestion that high but steady levels of radiation are easier for humans to
sustain than sudden radiation bursts.
Some human-made radiation sources affect the body through direct radiation,
while others take the form of radioactive contamination and irradiate the body from
within.
Medical procedures, such as diagnostic X-rays, nuclear medicine, and radiation
therapy are by far the most significant source of human-made radiation exposure to
the general public. Some of the major radionuclides used are I-131, Tc-99, Co-60, Ir-
192, and Cs-137. These are rarely released into the environment. The public also is
exposed to radiation from consumer products, such as tobacco (polonium-210),
building materials, combustible fuels (gas, coal, etc.), ophthalmic glass, televisions,
luminous watches and dials (tritium), airport X-ray systems, smoke detectors
(americium), road construction materials, electron tubes, fluorescent lamp starters, and
lantern mantles (thorium). A typical dose for radiation therapy might be 7 Gy spread
daily over two months.
Of lesser magnitude, members of the public are exposed to radiation from the
nuclear fuel cycle, which includes the entire sequence from mining and milling of
uranium to the disposal of the spent fuel. The effects of such exposure have not been
reliably measured due to the extremely low doses involved. Estimates of exposure are
low enough that proponents of nuclear power liken them to the mutagenic power of
wearing trousers for two extra minutes per year (because heat causes mutation).
Opponents use a cancer per dose model to assert that such activities cause several
hundred cases of cancer per year, an application of the controversial Linear no-
threshold model (LNT).
In a nuclear war, gamma rays from fallout of nuclear weapons would probably
cause the largest number of casualties. Immediately downwind of targets, doses would
exceed 300 Gy per hour. As a reference, 4.5 Gy (around 15,000 times the average
annual background rate) is fatal to half of a normal population, without medical
treatment.

36
 Occupationally exposed individuals are exposed according to the sources with
which they work. The radiation exposure of these individuals is carefully monitored with
the use of pocket-pen-sized instruments called dosimeters.
Some of the radionuclides of concern include cobalt-60, caesium-137,
americium-241, and iodine-131. Examples of industries where occupational exposure
is a concern include:
• Airline crew (the most exposed population)
• Industrial radiography
• Medical radiology and nuclear medicine
• Uranium mining
• Nuclear power plant and nuclear fuel reprocessing plant workers
• Research laboratories (government, university and private).

RADIOECOLOGY. NATURAL BACKGROUND RADIATION

Radioecology is a branch of radiobiology that examines the relationship

between living organisms and ionizing radiation emissions. It studies the rules
governing the migration of technogenic radionuclides in the biosphere and their
accumulation in organisms, plants and other objects in the environment.
Sources of ionizing radiation:
 Natural background radiation.
 Technogenic sources:
 Sources used in medicine
 Ionizing radiation in manufacturing
 Nuclear explosions
 Nuclear accidents
I. Natural background radiation
The natural background radiation is based on the natural sources of ionizing
radiation and consists of the emissions of naturally occurring radionuclides that are
dispersed over the Earth’s surface, the ground-level atmosphere, food products, water
and the human body. One of its typical characteristics is its relative constancy. These
emissions have been affecting all living organisms since life first appeared on this
planet.
It has been estimated that, depending on location, the exposure to natural
background radiation of the planet’s human population varies from 1 to 10 mSv, with
the average value of the effective dose being 2.4 mSv per person worldwide and 2,3
mSv for Bulgaria.
The natural background radiation has two components:
 Cosmic rays.
 Emissions of naturally occurring radionuclides within the lytho-, hydro-,
atmo- and biosphere.
1. Cosmic rays
The background radiation produced by cosmic rays accounts for almost half of
the external radiation exposure of the human population originating from natural
sources of radiation – around 0.3 mSv per year. Cosmic rays consist of:
 Primary cosmic rays. This radiation consists of high-energy ionizing
emissions that enter the Earth’s atmosphere from outer space. Primary cosmic rays

37
consist of 92% protons, 7% α-particles, 0.78% nuclei of carbon, oxygen, nitrogen,
lithium, beryllium and 0.22% nuclei of other elements. The origin of this radiation has
not been conclusively determined. According to one of the theories it includes:
 galactic cosmic rays – formed outside the Solar System; ionizing
radiation emanating from the nebulae in the galaxy originating from the explosion of
supernovae;
 solar radiation – consists of protons and α-particles primarily released
in solar eruptions.
As they pass through the atmosphere, primary cosmic rays interact with gas
molecules and gradually lose their energy. Only 0.05% of them reach sea level, which
means that they are predominately found in the upper layers of the atmosphere.
 Secondary cosmic rays. Secondary cosmic rays are the result of the
interaction between the radioactive particles of primary cosmic rays entering the
atmosphere and the atoms in the air. This interaction causes the atoms of the
atmosphere to split producing neutrons, protons, photons, electrons and mesons. They
in turn also collide with other atoms in the air forming new secondary particles. The
exposure to secondary cosmic rays is not uniform. The doses at the poles of the Earth
are higher than those at the equator, because the Earth’s magnetic field deflects some
of the radiation. Secondary cosmic rays have 2 components :
 directly ionizing radiation;
 neutron component;
The level of exposure to secondary cosmic rays increases with altitude, because
of the thinner layer of air serving as a screen. It is highest at an altitude of 20-30 km. It
is most intense in the highest parts of mountains and sharply decreases at sea level,
where the effects of directly ionizing radiation predominate. The neutron component
increases with altitude and becomes the most important one at altitudes higher than 6
km. The interaction of cosmic rays with the upper layers of the atmosphere results in
the formation of the so-called cosmogenic radionuclides: 3Н, 14С, 7Ве, 22Na.
2. Emissions of naturally occurring radionuclides in the lytho-, hydro-,
atmo- and biosphere.
The naturally occurring radionuclides in the lytho-, hydro-, atmo- and biosphere
are present in small quantities and can be divided into 3 groups:
 elements belonging to the radioactive families with progenitors 238U,
235U /Actin Uranium/ и 232U /thorium/ - they have been present in the Earth’s crust since

the planet was formed→ primary radionuclides;

 elements that do not belong to radioactive families – 40К, 48Са, 87Rb,
etc.;
 cosmogenic radionuclides – they are formed when cosmic rays interact
with the air – 14С, 3Н /tritium/, etc.
Natural radionuclide content in the soil. Most commonly, soils contain the
radioactive isotopes of uranium, thorium and their daughter products – radium, radon
and thoron. 40К and 87Rb also have a significant presence. The content of radioactive
elements in the soil depends on their concentration in the rocks that served as the
foundation for that soil. Volcanic rocks exhibit higher natural radioactivity than
sedimentary ones. Clay soils are characterized by higher radioactivity than sandy ones
because of their superior absorption properties. Naturally occurring radionuclides are
unevenly distributed in the soil. In different part of the Earth’s surface, the levels of
radiation vary from 0.3 до 0.5 mSv per year. Certain geographic areas are
characterized by higher content of radioactive elements in the soil /some states in
India, areas in Brazil, etc./

38
 Concentration of naturally occurring radioactive elements in the air. The natural
radioactivity of the air is determined by:
 its cosmogenic radionuclide content / 14С, 3Н/;
 the amount of radioactive gases coming from the Earth’s surface;
The most important cosmogenic radionuclide is 14С. It is formed as a result of
the interaction between secondary cosmic ray neutrons and the nitrogen in the
atmosphere. It is produced at an altitude of 9 km. Every year approximately 10 kg of
14С are produced in the Earth’s atmosphere and its overall quantity is approximately

80 tons. It is a pure β-emitting isotope with a half-life of 568 years.

The most important radioactive gases originating from the Earth’s surface are the
radioactive elements of the uranium and thorium series – radon, thoron, actinon and
their daughter products. Radioactive gases enter the atmospheric air from the Earth’s
surface via diffusion. As the half-life of Rn is significantly longer than that of thoron and
actinon, most of the air’s radioactivity is associated with Rn.
The ground-level layers of the atmosphere also contain 40К – it is attached to dust and
dust particles.
Concentration of naturally occurring radioactive elements in the water. It varies
over a wide range and is determined by the type of water – sea, river, lake,
atmospheric, ground.
 atmospheric water – it has a very low content of radioactive elements; these
are primarily cosmogenic radionuclides and insignificant quantities of 40К and 238U,
lifted by winds from the Earth’s surface;
 ground water – its radiochemical composition depends on the quantities of
soluble radionuclides in the different layers it passes through; the most important
radionuclides are 40К, 222Rn, 226Ra;
 open bodies of water – their radioactivity depends on the type of inflow –
surface or ground;
 surface water /rain, snow/ - it contains insignificant quantities of radioactive
elements, mainly 40К, 238U, 226Ra.
Concentration of naturally occurring radionuclides in living organisms. All
radionuclides in the natural environment participate in the metabolism of living
organisms. There are 2 groups of radioactive elements:
 radioactive elements mixed with their stable isotopes that play an active role
in metabolism; some of these are 40К, 14С, 3Н; their concentration in the organism
depends on the quantity of their stable isotopes;
 radioactive elements, whose quantities in tissues of plant and animal origin
depend on their concentration in the environment /mostly soil and water/ - 238U, 226Ra,
232Th; their quantity is higher in plants.

Because of the ubiquity of the stable isotope К in the natural world, a significant
portion of the radioactivity of plants and animals is due to 40К. Its quantity in plants is
higher than that in animals. The radioactivity of the human body is primarily determined
by the concentration of 40К, 14С и 3Н in the tissues.
Concentration of naturally occurring radionuclides in the human body. The
background radiation, formed by cosmic rays and the emissions of naturally occurring
radionuclides in the environment, creates a certain absorbed dose in the organs and
tissues of every human being. This is the so-called background radiation exposure.
The human body is exposed to radiation in two ways:
 external exposure to emissions originating from the radionuclides in the
surrounding environment;

39
  internal exposure to radionuclides that have entered the human body as
part of the food, water and air it takes in /incorporation of radioactive substances/.
The total annual dose of the exposure to natural background radiation is 2.4
mSv/a /average value of 2.8 mSv/a for Bulgaria/.

Values of the average annual effective doses received from

different sources of radiation

External exposure to cosmic rays 0.4 mSv/a

External gamma exposure 0.4 mSv/a
Internal exposure 1.6 mSv/a

The biological significance of the natural background radiation has not been
completely clarified. Different hypotheses exist:
 hypothesis І – background radiation is harmful and it induces some of the
spontaneous mutations.
 hypothesis ІІ – background radiation has a stimulating effect, resulting in the
production of biologically active substances that affect biomembranes and the
synthesis of certain enzymes and amino acids.
 hypothesis ІІІ – ionizing radiation is a necessary factor for the existence of
life on the planet, as attempts to reduce exposure to background radiation result in
radiation deficiency.
II. Technogenic sources of radiological contamination
Radioactive materials are used in different fields of human activity: medicine,
industry, energy development, science, etc., and this leads to the real possibility of
releasing radionuclides in the environment. Significant radiological contamination is
produced by the testing and use of nuclear weapons of mass destruction /nuclear
explosions/. Radionuclides are also released when accidents occur in nuclear power
plants / nuclear accidents/.
1. Sources used in medicine. One of the main sources of additional radiation
exposure for the population is the use of ionizing radiation for diagnostic and
therapeutic purposes in medicine. X-ray diagnostic procedures are the most common
source of exposure in medicine.
Average values of the effective doses in X-ray examinations

Type of examination Еср /mSv/

Computed tomography scan of the abdomen 20

Computed tomography scan of the thorax 10
Barium enema of the large intestine 7
Angiography 7
Upper gastrointestinal tract 4
Urography 3
Lumbosacral region 1,7
Cholecystography 1,5

40
 Pelvic region 1,2
Abdomen 1,1
Mammography 1
Thoracic cavity /thoracoscopy/ 1
Femoral 0,9
Thoracic cavity /thoracography/ 0,14

The diagnostic nuclear medical examinations performed in Bulgaria are

relatively fewer in number and their contribution to the total radiation exposure of the
population is smaller.
Average values of the effective doses in diagnostic nuclear medical examinations
Type of examination Еср /mSv/

Brain 6
Bones 4,5
Cardiovascular 8
Lung perfusion scan 1,5
Lung ventilation scan 1
Thyroid scan 2
Thyroid uptake 15
Kidneys 1,5
Liver / spleen 1,7

The use of radioisotopes for diagnostic purposes also contributes to the

radiation exposure of the population. Different isotopes are used, most commonly
iodine-135, which causes higher radiation exposure. Recently, it has been replaced by
iodine-125, which produces lower radiation exposure.
Medical radiation exposure also includes exposure with a therapeutic purpose.
Radiotherapy is primarily used to treat malignant diseases. Different sources of
ionizing radiation are used for this purpose – X-ray apparatus for superficial and deep
therapy, gamma therapy installations, electron accelerators, etc. Local irradiation is
normally performed and the doses needed for therapeutic effect are around 50-70 Sv.
Despite the relatively high individual doses, the contribution of radiotherapy to the
additional radiation exposure of the population as a whole is relatively small as a
comparatively low number of people undergo such procedures.
2. Sources used in manufacturing
A segment of the population, who come into contact with artificial sources of
radiation as part of their profession, could receive a higher dose than the natural
background radiation under certain circumstances.
They only account for a relatively small percentage of the population – 0,1-0,2 %.
These are the people who work with defectoscopes in metallurgy, health workers in
radiobiological laboratories, workers in nuclear power plants, etc.
3. Nuclear explosion
Nuclear weapons (NW) tests were a main source of contamination of the
environment with radioactive elements (RE) until the ban on experimental nuclear

41
explosions in 1963 with a treaty signed by the USA, England and the former USSR.
France and China continued to perform smaller-scale tests until 1974 and 1980
respectively. Between 1945 and 1980 423 nuclear weapons tests were conducted.
Types of nuclear weapons. Three generations of nuclear weapons have
been designed. Their action is based on the release of internal nuclear energy at the
moment of the explosion:
 atomic bomb – the internal nuclear energy is released as a result of
a fission chain reaction involving the radioactive uranium-235;
 hydrogen bomb– the internal nuclear energy is released through a
thermonuclear reaction of light nuclei fusion;
 neutron bomb– the internal nuclear energy is released as a result of
a fission reaction;
An enormous amount of energy is released in these reactions within a millionth
part of a second and in a comparatively small volume, which is why they occur as an
explosion.
Types of nuclear explosions. Nuclear weapons cause different types of damage
depending on the location where the explosion takes place:
 Atmospheric nuclear explosion – the
nuclear bomb is detonated above the surface of the earth
or above water and the fireball does not come into contact
with them;

 Surface nuclear explosion (ground or

water) – the nuclear bomb is detonated on the surface of
the earth or on the water surface and the fireball comes
into contact with them;

 Underground /underwater/ nuclear

explosion – the nuclear bomb is detonated underground
or in water and no fireball is formed;

The most dangerous nuclear explosions from a radiation fallout standpoint are
those that take place on the earth’s surface. They result in the formation of local
radioactive deposition. A fireball is formed immediately after a nuclear explosion.
Because of the gradual cooling of the fireball, the gases it contains condense and form
a mushroom-shaped cloud composed of the bomb’s solid particles, radioactive
substances, water vapors and a large quantity of soil and rock debris from the ground
surface.
The radioactive cloud continues to rise for some time and then it begins to move
horizontally in the direction of the wind. The radioactive substances it contains begin
to fall to the earth’s surface in the order determined by their size, forming the so-called
radioactive cloud trace.
The trace of the radioactive cloud refers to the area over which radioactive
products fall under the impact of horizontal air currents. Around 90 % of these products
are large in size – over 40 microns. This area is shaped like a giant cigar extending
along the direction of the wind, with a length of up to 400-500 km and a width of 30-40
km. Depending on the level of contamination, this area is divided into 4 zones.

42
 Trace of the radioactive cloyd
А – Zone of moderate contamination
B – Zone of strong contamination
C – Zone of dangerous contamination
D – Zone of extremely dangerous
contamination

Atmospheric nuclear explosions take place several hundred meters above the
ground. They result in the formation of tropospheric and stratospheric fallout.
The fireball is composed primarily of the materials of the nuclear device and
generally contains no land debris. The cooling of the fireball creates the conditions for
the formation of oxides of the elements the bomb casing is composed of and the
products of nuclear fission. Tropospheric fallout contains radioactive particles with a
size under 5 microns. They can be carried over very long distances, can pass over
several continents and their deposition can continue for 2-3 months. Meanwhile, the
short-lived radionuclides decay and radioactive contamination is much weaker.
Stratospheric fallout consists of the longest–lived radionuclides. Their particles are
under 1 micron in size, they can circle the planet floating and continue to deposit for
years.
4. Nuclear accidents
Nuclear accidents are events that occur in a facility or installation and disrupt
the normal working process, resulting in a threat of irradiation for the staff and the
population that resides close or further away from the site.
Accidents in nuclear power plants expose large groups of people to the effects of
radiation. The scale of the accident and the environmental impact can vary over a very
wide range.
All three types of fallout are present when there is a nuclear accident, with local
ones being the most prevalent. A radioactive cloud is formed in the reactor as a result
of the steam explosion. It spreads in the direction of the wind and an area with a certain
shape and size is contaminated with radioactive substances – the trace of the
radioactive cloud.
The shape and contours of the radioactively contaminated area are determined
primarily by the amount of energy released in the explosion, the meteorological
conditions at the time of the accident, the terrain, the size of the particles, the duration
of the ejection of materials, the physicochemical state of the decay products. When the
winds are weak, the radioactive cloud spreads only in the vicinity of the reactor. When
the winds are strong, the radioactive trace begins to resemble a winding river.
The sanitary protection zone around a nuclear power plant /3 km./ is the most
contaminated area, which is the reason why no civilian sites are allowed there.
III. Radioactive fallout
Radioactive elements in the form of aerosols fall to the surface of the earth,
becoming local, tropospheric and stratospheric depositions. As a result of this, they
accumulate in soils, plants, animals and open water bodies. Radioactive elements can
enter the human body directly via the air we breathe or following the food chain.

43
 In the air
/Aerosol/

Soil Plants Animals Water

Man

Every link in this chain consists in turn of multiple intermediate sections divided
by barriers. Different barriers are characterized by different permeability and their
function can change the concentration of the isotope as it moves from section to
section. If the concentration of an isotope decreases as it passes through a certain
barrier, we talk about protection coefficient, while the increase is referred to as
accumulation. Normally, every consecutive section in the chain causes a reduction in
the activity of the radioisotope, but it is also possible to observe an increase in
concentration /e.g. fish are a typical accumulator of 90Sr/.
Studies of the regularities in the migration of the radioecologically significant
strontium-90 and cesium-137 in different objects in the biosphere have shown that the
former isotope is distributed similarly to calcium, while the latter – to potassium.
Maximum accumulation of strontium-90 in objects in the biosphere is observed
among those that are rich in calcium /bones, eggshells, etc./, while the maximum
concentration of cesium-137 is found in objects rich in potassium /muscles/.
If we have introduced more calcium and potassium in the organs in a situation
of increased radiation, the accumulation of strontium and cesium will be lower. This
phenomenon is called discrimination.
Radioactive fallout. Types.
Local /early/ radioactive fallout – these depositions are formed in nuclear
accidents and underground and surface nuclear explosions. They fall in the vicinity of
the accident, most commonly over a zone that is tens of kilometers in size. The shape
and contours of the radioactively contaminated area are determined primarily by the
amount of energy released in the explosion, the meteorological conditions at the time
of the accident, the terrain, the size of the particles, the duration of the ejection of
materials, the physicochemical state of the decay products. Local radioactive
depositions fall to the surface of the earth over a period of 24 hours. In chemical terms,
they are a mixture of nuclear decay products dominated by short-lived isotopes. Iodine-
131 is the main radioisotope. Depending on the degree of radioactive contamination,
a gamma field of different strength is formed on the terrain.
Tropospheric fallout – powerful explosions /nuclear accidents and athmospheric
nuclear explosions/ cause decay products to enter the troposphere.
They fall from this altitude very slowly, over a period of approximately 30 days. This
results in the formation of a wide radioactive trace that is also several thousand
kilometers long. The density of the contamination of the earth’s surface with these
materials is similar to that of local fallout, but slightly lower. Rains are the most
important factor contributing to the cleansing of the troposphere from radioactive
elements.
Stratospheric fallout – it is typical of atmospheric nuclear explosions.
Radioactive elements remains in the atmosphere for a long time – between 6 months

44
and 5-7 years on average. During this period, short-lived isotopes decay and for that
reason the stratosphere contains primarily the long-lived strontium-90 and cesium-137.
Under the impact of various types of processes /physicochemical, meteorological/
radioactive elements spread in all directions while they remain in the stratosphere. It is
typical of stratospheric fallout that it consists of minute particles with a very low
concentration because the radioactive cloud spreads over long distances in all
directions.
IV. Migration of technogenic radionuclides in the natural environment
1. Radioactive fallout in the soil
The fate of radioactive substances (RS) entering the soil depends on a multitude
of factors: the physicochemical properties of the isotopes, the types of chemical
compounds, certain parameters of the external environment, etc. One of the main
properties of radioactive elements that determines their behavior in the soil is their
solubility in water. Around 1% of the decay products formed in a radiation accident are
soluble. These include the compounds of strontium, cesium and iodine. The remainder
of the radionuclides that have fallen to the surface of the earth are not soluble.
The large, insoluble particles of the decay products remain in the upper layers
of the soil. Their ability to penetrate further down is limited. The smaller particles stick
to the soil components.
The speed of migration and the depth of the penetration depend on the type of
soil and the groundwater level. Heavy clay soils hold radioactive elements /RE/ better
than sandy soils. Up to 80% of the radioisotopes deposited on the surface of the earth
stay in the upper layers /0-25 cm./ of clay soils.
2. Accumulation of radioactive fallout in the water
The contamination of open water bodies /rivers, lakes, dams/ with radioactive
elements can occur in the following ways:
 inflow of liquid radioactive elements;
 emergency release of radioactive elements from a nuclear power plant,
which are then deposited on the water surface
 rainfall-induced runoff from radioactively contaminated areas in the vicinity
of the water body;
The behavior of radioactive elements entering the body of water depends on the
following factors: the type of compound, the content of the water, the temperature, etc.
The isotopes attached to the solid particles floating in the water are slowly deposited
to the bottom. A small part of the radioactive elements are deposited over aquatic
plants and plankton and penetrate them directly through their surface. Radioactive
elements can also enter fish and other aquatic animals through the gills or through the
digestive tract. The distance travelled by the radionuclide in the body of water depends
on its solubility and half-life. Soluble, long-lived radioisotopes can cover huge
distances. Radioactive elements can also migrate beyond the borders of the water
bodies. This occurs when rivers or lakes overflow; they can also be carried by insects;
by amphibians, aquatic and swamp birds; by livestock drinking from the body of water;
or through irrigation using radioactively contaminated water.
3. Accumulation of radioactive fallout in plants
The concentration of radioactive elements in plants depends on the quantity of
the radioactive depositions in the area, the terrain /in mountainous areas plants contain
more radioactive elements compared to low-lying areas/, the physicochemical
properties of radioactive elements /water solubility/, the presence of wind / there is
higher radioactivity in plants exposed to winds, compared to those that are found in

45
areas protected from the wind/, the rainfall, the type of plant, the way it is cultivated,
etc.
There are two main paths of radioactive contamination in plants – through the
root and through the surface of the shoot. The leaves are the primary path of
penetration, while the root are secondary.
Different types of plants absorb radioactive elements to a different degree. This
depends on the structure of their leaves and roots, their age, etc. For example, leaves
that are more rugged hold more radio-aerosols and perennial plants are characterized
by higher activity than annual ones.
Radioactive elements are distributed unevenly among the different part of the
plant. Grains, seeds and fruits contain fewer radioactive elements than leaves and
stems. Their concentration is higher in the dermal tissue than in the pith.
4. Accumulation of radioactive fallout in animals
Radioactive elements can enter the animal organism in two ways – digestion
and respiration. The path via the digestive tract is of primary significance. In this way
iodine-131, barium-140, cesium-137 and other elements enter the animal organism.
Through the bloodstream they spread to different organs and tissues. Osteotropic
radioactive elements /strontium/ are deposited in the bones. Cesium is deposited in
muscles and iodine – in the thyroid gland. The amount of radioactive elements that
enter the animal organism depends on the degree of contamination of the grazing
ground.
Game meat contains more radioisotopes than the meat of livestock /
mountainous area are more polluted and the feed given to livestock is cleaner/.
Radioactive iodine enters the body of the animals with the food and it is secreted in
their milk. Every liter of cow’s milk releases 1.5 % of the daily dose the animal has
received, while with goat’s milk the percentage is higher -25%.
V. Radionuclide contamination of food products of plant and animal
origin. Means and methods of decontamination.
1. Means and methods connected with sowing, soil treatment and the
manner of storing grains:
 selection of soils fit for sowing – heavy (chernozem) and clay soils have
a more pronounced ability to fix radioactive elements; heavily contaminated soils are
appropriate for sowing industrial crops; for medium level of contamination – earth-up
and fodder crops; low contamination – cereals and vegetables.
 ameliorative activities and fertilization – plants develop faster and absorb
smaller amounts of radioactive elements;
 ensilaging and drying of plants lead to a reduction in the amount of
radioactive elements they contain, because of the natural decay of their radionuclides;
 when collecting grass, the second and third windrows are used primarily,
while the first one is destroyed;
2. Means and methods of fruit and vegetable decontamination:
 mechanical cleansing is used in the case of superficial contamination
- washing and peeling, which results in the elimination of up to 50% of
radioactive elements;
- fruits and vegetables can be kept in a solution of water, 1% hydrochloric
acid and 0.1 % detergent for 60 min. and then washed extensively with water;
 methods used in radioactive contamination of the flesh of fruits and
vegetables:
- boiling, which transfers some of the radioactive elements into the broth;
the addition of table salt extracts the radiostrontium and radiocesium from the broth;

46
 - the quantity of radioactive elements can also be minimized by means
of drying and canning;
3. Means and methods of meat decontamination
The quantity of radionuclides in this product depends on the degree of
contamination of the vegetation used for grazing, the type of animal, etc. Mutton is
several times more contaminated than beef. Primarily cesium-137 accumulates in
meat. Sometimes smaller amounts of zinc-65 can also accumulate. The strontium-90
content is much lower. It mainly accumulates in bones. Iodine-131 accumulates in the
thyroid gland.
The concentration of radionuclides in meat is reduced by means of:
 salting and boiling with added salt; boiling causes certain quantities of
cesium-137 to pass to the broth; the most effective way is to salt the meat first by
soaking it for a long time in a 25% salt solution and then to boil it /radiocesium is
reduced by up to 90%/; dry salting is not considered particularly effective;
 soaking in a solution of water and 10% vinegar for 24 hours, followed by
thermal processing /mutton/; radiocesium is reduced by up to 95%;
 blanching the meat in a solution of water and 10% vinegar /poultry/; then
the meat is canned without the broth; radiocesium is reduced by up to 50%;
 meat processing into longer-lasting products; the concentration of
radioactive elements is reduced by 46 to 85%;
4. Means and methods of milk decontamination
Strontium-90 and cesium-137 are always found in milk, while strontium-89,
barium-140 and iodine-131 periodically appear after every series of nuclear tests /prior
to the nuclear test ban treaty/ or a small-scale accident in a nuclear power plant. The
concentration of cesium-137 is 5 to 7 times higher than that of strontium-90. Iodine-
131 was found in milk only during the nuclear weapons test period or following
significant nuclear accidents. It can be dangerous to the human being only when milk
is consumed immediately after the milking process. In durable dairy products it
disappears after two months. The following methods are used to cleanse milk:
 preliminary processing of the milk with clinoptilolite; degree of cleansing
– 90% for cesium and 50% for strontium-90;
 milk processing into durable dairy products; radionuclides can pass
through almost all durable dairy products, but their quantities vary over a wide range;
processing milk into cheese, yellow cheese and butter is a form of cleansing in itself;
 acidification of milk with lactic acid /40-70%/ contributes to better
cleansing of strontium-90;
5. Means and methods of egg decontamination
Feeding hens with radioactively contaminated food leads to migration of some
radionuclides into the eggs. The content of radiostrontium is highest in the eggshell;
cesium-137 – in the egg white; iodine 131 – in the yolk. Radioiodine poses the biggest
danger and it can be avoided if eggs are consumed after a certain period, so that the
isotope can decay sufficiently until it reaches safe doses.
6. Means and methods of fish decontamination
Different radioactive elements accumulate in different tissues and organs in
the fish. Strontium-90 accumulates in the skeleton, the fins and the scales, while
cesium-137 accumulates in the soft tissue. The effective biological half-life of
radiocesium in the soft tissue of the fish is 5-7 days. This leads to the conclusion that
the fish releases this radioisotope relatively quickly and becomes edible. The lengthy
period of release of strontium-90 from the skeleton of the fish means that contaminated
fish meal cannot be used for different commercial purposes.

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 BIOLOGICAL EFFECTS OF IONIZING RADITION

The exposure to ionizing radiation in living organisms causes a specific

biological effect that can be different depending on the conditions of emission
exposure.
Characteristics of the biological effects of ionizing emissions
1. During the first few minutes following an incident of external irradiation,
even when it is high-dose, many animals as well as humans do not feel the effects of
the ionizing emissions. This is due to the fact that they lack specific receptors and
analyzers for ionizing radiation.
2. All reactions of the organism exposed to ionizing radiation can be
divided into 3 categories:
 radiosensitivity – the lowest dose to which a certain tissue
responds with non-prolonged physiological reactions that do not have lasting
effects;
 radio damage – the lowest dose that causes disruption in the
function or morphological damage to organs, system and the entire organism;
 compensatory processes – emergence of different recuperative
mechanisms in an organism exposed to radiation;
3. The effects of radiation are a combination of:
а/ direct action arising from the impact of ionizing emissions on the
tissues of the organism;
b/ indirect action – secondary damage to the biosubstrate and
receptor mechanisms;
This is the reason why the primary physicochemical and biochemical changes
at the molecular level are examined first, then the changes in the cell, followed by the
changes at the tissue and organ levels and finally, the changes in the organism as a
whole.
I. Theories explaining the biological effects of ionizing radiation
1. Theory of the direct action of ionizing radiation
Ionizing radiation affects directly vital parts of cells and damages them in the
process. It is theorized that every biological object contains two types of living matter
that differ significantly in terms of their size, composition and sensitivity to ionizing
emissions. The radiosensitive segment, which is spatially differentiated, is
characterized by high susceptibility to radiation damage. This segment is much smaller
in mass compared to the entire cell and for that reason it is called a target or critical
mass. If this target is directly hit by the ionizing particle, this results in irreversible
damage and the death of the entire cell.
The accumulation of experimental evidence shows that it is difficult to explain
the biological effect only with the direct impact of ionizing radiation on certain biological
structures within the organism. Without denying the possibility of the direct action of
radiation on these organic structures, great importance is attached to the indirect action
of the radical products of water, which emerge under the impact of irradiation, on the
different cell components.
2. Theory of indirect action
The exposure of biosubstrates to ionizing radiation causes chain reactions,
which increase and aggravate the harmful effect of radiation. These reactions appear
when every radical or chemically active molecule immediately causes the formation of

48
new active molecules and radicals. The latter serve as catalysts and in turn induce the
appearance of new active molecules and particles.
This theory posits that the biological effect results from the formation of
strongly active chemical substances that increase the primary damage to the cell. As
water is a main component of the cell, it is believed that these substances are products
of water radiolysis; i.e. the primary effect of ionizing radiation on living tissue is its
interaction with water molecules. Direct evidence has already been obtained of the
existence of radicals and peroxidates in water exposed to radiation.
This theory posits the existence of several fast-transition phases that merge
into one another.
• First phase /physical/ - absorption of the radiation energy by the cells
in the organism. The water molecules become ionized. When an electron separates
from the water molecules, this results in the creation of a positive water ion, while the
addition of an electron to another, electrically neutral molecule results in the
emergence of a negative water ion:
H2O H2O+ + e-

H2O + e- H2O-

This phase occurs instantaneously – within 10-16 to 10-13 s.

• Second phase /physicochemical/ - formation of chemically active
atoms and molecules with an unstable position of the electrons in their orbit. Ionized
water molecules are unstable and they dissociate into free radicals.
H2O+ H+ + OH0

H2O- H0 + OH-

This phase takes 10-13 to 10-5 s.

If the electron rejoins the water molecule it has separated from, the latter
becomes electroneutral again, but it enters into an excited state. The energy given out
in the dissociation of the excited molecules can also cause the production of free
radicals:
H2O H2O+ + e- H2O H0 + OH0

Free radicals are very chemically active. The hydroxyl radical is a powerful
oxidizer, while the hydrogen atom is a reducer. A number of reactions occur between
these radicals, as well as between them and the free oxygen in biological tissue –
recombination, radical transfer, etc.
 Third phase /biological/ - the products of water radiolysis and
peroxides react with different molecules of the cell substrate. This disrupts the normal
cycle of biochemical reactions in the organism and results in atypical products of
metabolism that damage the cell. The third phase develops gradually throughout the
process of receiving radiation damage. Because radiation damage develops gradually,
it is characterized by the presence of a latent period. Even when experimental animals
have been exposed to lethal doses, no visible changes can be found immediately after
the irradiation.
The next stage of radiation damage is the disruption of the normal
physiological processes in the organism. Changes appear in the humoral environment
and the neurohumoral regulation, which contribute significantly to the development of
the pathological process.

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 II. Biological effect of ionizing radiation at the subcellular level
There is significant and irrefutable evidence in vitro and in tissue cultures
describing the effects of ionizing radiation on the molecules of the cell substrate. In a
living organism, the radiobiological effect is not merely the accumulation of the primary
radiation damage that has occurred in the cells. It is determined by a number of
neuroregulatory, humoral and defense mechanisms present in the organism. For that
reason, it is not separate molecules or cells that respond to the impact of irradiation,
but the entire organism.
Nucleic acids are especially susceptible to the impact of ionizing radiation.
DNA is the first target of the action of ionizing radiation in a cell. In chromosomes, DNA
can be found in the form of Deoxyribonucleoprotein (DNP). In radiosensitive tissues
DNP dissociates during the first few minutes following the irradiation. The reasons for
the weakening of the bond between the protein and DNA are not clear. The weakening
of the nucleoprotein complex and the presence of free DNA makes them more
susceptible to the effects of ionizing radiation. It causes rupture of the hydrogen bonds
in the double helix structure of DNA, release of phosphoric acid, separation of amine
groups, etc. The following types of lesions are most commonly observed – single-
strand breaks, double-strand breaks and damage to the bases. It has been
experimentally proven that pyrimidine bases are more radiosensitive than purine
bases.
Under the impact of low doses of radiation, DNA synthesis is disrupted
relatively quickly. The DNA degrading ferments /deoxyribonuclease/ are activated as
early as the first few minutes following the irradiation. RNA sustains similar damage.
The intense dissociation of nucleic acids in the organism can be detected based on
the increased release of their degradation products in the urine in the first few days
after irradiation has occurred.

Single-strand break Double-strand break

The effect of ionizing radiation on proteins has been studied thoroughly. Small
doses of radiation can lead to their degradation. Irradiation with small doses causes
biochemical changes in proteins. Reactions of deamination, decarboxylation,
oxidation, rupture of hydrogen bonds, etc. occur as a result. This damages the amino
acids and produces biologically active substances that change the cellular metabolism.
For instance, the irradiation of cyclic amino acids /phenylalanine, tyrosine, tryptophan,
histidine/ results in the production of biologically active substances – tyramine,
dioxyphenylethylamine, tryptamine, histamine. These are protein-based radiation
toxins that affect the primary metabolic processes.
It is also important that biochemical processes lead to the production of atypical
proteins that are foreign to the organism and cause allergic reactions. Changes occur
in plasma proteins under the impact of ionizing radiation. Protein fractions are altered.
The reasons for that are the disturbances in the synthesis, the permeability, the

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immunological and hormonal reactions. The quantitative changes in plasma proteins
depend on the severity of the radiation-induced damage, the type of living organism
and the condition of its metabolism. A reduction is observed in the fractions of albumin
and gamma globulin, and an increase in alpha and beta globulins.
Carbohydrate metabolism is closely linked to the provision of energy for the
living cell. The high-molecular-weight carbohydrate glycogen is an important energy
reserve for the organism. As far back as the beginning of the 1950s, intensive synthesis
and increased glycogen content in the liver were observed in different animals
subjected to radiation. This effect is one of the most prominent metabolic changes
registered after a period of irradiation. Most authors believe that because glycogenesis
is mostly stimulated by the corticosteroids of the adrenal gland and the pituitary-adrenal
system affects the increase in glycogen content, it follows that when irradiation occurs,
intensive synthesis of glycogen takes place in the liver, possibly with the participation
of this hormonal system. It is important to note that when the organism is irradiated,
the blood glucose levels increase.
Lipid metabolism also deviates from the norm as a result of the exposure to
ionizing radiation. The study of the changes in lipid metabolism is a matter of present
interest in connection with the early radiochemical reactions that occur in lipids. This
refers to the emergence of self-accelerating chain reactions, whose end products are
toxic substances. Among them, unsaturated fatty acids hold a special place as they
are unstable and prone to oxidation with molecular oxygen. For that reason, they easily
degrade to lipid peroxides – epoxides, aldehydes and ketones, quinones, ortho-
quinones and semiquinones. These are lipid radiotoxins, which are chemically very
active and play an important role in the intensification of the initial radiation effect.
In normal conditions the use of fats by the organism is connected with their prior
oxidation /into ketone bodies/, which takes place in the liver. The latter substances are
then transported to the tissues and cells, where they are used directly. In the event of
radiation damage, there is mobilization of fats in the adipose depots and the fats are
transitioned into the liver. This is the cause of the fatty infiltration of the liver, where
fats, which normally comprise no more than 5% of the organ, can reach up to 50%.
The accumulation of fats in the liver and the formation of acetone bodies during the
later stages of radiation damage leads to acetonemia and acetonuria, as the organism
cannot cope with the oxidation of an inordinately high amount of acetone bodies.
Acetonemia can also lead to acidosis, which exhausts the alkaline reserve in the
tissues.
Changes in enzyme activity are observed with exposure to relatively low doses
/0,5 – 5 Gy/. Many biochemical changes occur within a short amount of time /24-48
hours/.
In the early stages following the incident of irradiation, the enzymes that are
activated are the ones responsible for nucleic acid degradation, the proteolytic enzyme
/deoxyribonuclease, catepsin/, as well as those connected with the metabolism of
phosphorous compounds, primarily phosphatases and others. These enzymes are
characterized by protease activity and therein lies their significance for the autolysis of
tissues. On the other hand, other enzymes become inactive.
The fluctuations in enzyme activity are not the result of radiation-induced
chemical changes in their molecules as these are observed only in case of exposure
to higher doses. After irradiation has taken place, it is possible that abnormal
distribution of low-molecular-weight substrates and metabolic inhibitors will be
observed, which will affect their activity.

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 Ionizing radiation also has an effect on mineral metabolism. Exposure to high
doses leads to significant changes in the water balance and the electrolyte levels.
Radiation causes a disruption in the regeneration of the intestinal epithelium, which
changes the physiological barrier between the intestinal wall and the organism’s
internal environment. This is accompanied by massive loss of fluids and some
electrolytes – sodium, chlorine and potassium, which leads to lower levels of these
electrolytes in the blood. For that reason, the administration of large quantities of saline
solution has a beneficial medicinal effect on the organism. In cases of irradiation with
sublethal doses, a reduction in the amount of sodium and potassium ions in cell nuclei
is observed. The effects of ionizing radiation on bone tissue metabolism are also noted
- lower levels of potassium and phosphorous are present in the bones.
III. Biological action of ionizing radiation at the cellular level. Effects.
The changes in the cell are non-specific. The physical, physicochemical and
biochemical processes that take place can cause different types of damage to the cell,
including its death. The following are possible effects of ionizing radiation on the cell:
 The cell may be left undamaged by the dose of ionizing radiation.
 The cell may be damaged, recover successfully and continue to function
normally.
 The cell may be damaged, recover with defects and continue to function
abnormally.
 The cell may die as a result of the damage caused by ionizing radiation.
The degree of damage to the cells is determined by the following characteristics:
а/ the radiosensitivity of the cell – it varies over a wide range; it is
proportional to the reproductive ability of cells and inversely proportional to their degree
of differentiation;
b/ the primary damage to the cell – it is characterized by the changes that
occur within the cell under the impact of ionizing radiation until mitosis takes place;
Based on the radiosensitivity, cells can be divided into the following three
categories:
 Young, undifferentiated cells /those of the hematopoietic and the
reproductive tissue/, characterized by high radiosensitivity;
 Cells in the process of maturation – medium radiosensitivity;
 Mature cells – characterized by low radiosensitivity, often able to maintain
their function.
Radiosensitivity in regard to the phases of the cell cycle can be classified into
two categories:
• Concerning reproductive death, the cell is most sensitive in mitosis;
• Concerning chromosome damage, the cell is most sensitive if it is
exposed to radiation after mitosis has occurred.
The changes that determine the primary damage to the cell appear within a
short time after irradiation has occurred. Those can be as follows: granularity and
changes in cell nuclei, different degenerative changes in the cytoplasm, disrupted
permeability of cell membranes, changes in coloration, etc.
As far as the radiosensitivity of the different structural elements of a cell is
concerned, it has been determined that the nucleus is far more susceptible than the
cytoplasm and the changes that occur in it are irreversible.
Mitochondria are characterized by a high degree of radiosensitivity. Their
oxidative phosphorylation is inhibited and various morphological changes take place
in them. Damage to the membrane of the lysosomes and the release of their acid

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hydrolases leads to interphase cytolytic death. It should be noted that cells in a state
of mitotic inactivity are more resistant to radiation.
Ionizing radiation is a powerful mutagenic factor. It has been categorically
proven that there is an increase in mutation frequency in cases of supplementary
exposure /higher than background radiation/. Based on their significance for the
individual and the human population as a whole, ionizing radiation-induced mutations
fall into two large categories:
 Mutations in somatic cells.
 Mutations in reproductive cells.
Mutations in somatic cells are important for the individuals directly exposed to
radiation, while mutations in reproductive cells determine the role of ionizing radiation
for the future generations.
There is significant evidence showing increased frequency of chromosome
aberrations in persons exposed to radiation. There is also a proportional relationship
with the absorbed radiation dose. The most common type of aberrations observed are
the stable ones – translocations, inversions and deletions. There are also unstable
chromosome aberrations – dicentric chromosomes.
IV. Biological effects of ionizing radiation at the tissue level
Based on their radiosensitivity, tissues can be divided intro three main groups –
tissues with high, medium and low radiosensitivity.

Low Medium High

Lymphatic tissue Skin CNS

Bone marrow Endothelium Muscles
Gastrointestinal epithelium Lungs Bone and cartilage
Gonads Kidneys Connective tissue
Embryonic tissue Liver
Eye /lens/

1. Central nervous system /CNS/

Under the effects of ionizing radiation, CNS manifests early functional changes.
At the beginning, there are functional phase changes. The first few minutes after the
period of exposure are characterized by increased activity of the cerebral cortex,
followed by reduced and finally completely suppressed activity. This state of
suppressed activity spreads not only to the surface of the cerebral cortex, but also to
the subcortex. Evidence of this can be found in the lowered blood pressure, disrupted
breathing and weakened unconditioned reflexes. The disturbances in the
functional state of the vegetative centers can be seen in the different aberrations that
occur in the organism following a period of exposure to radiation. Changes are noted
in thermoregulation, blood pressure, phase changes in the secretion of gastric acid
and in intestinal motorics.
2. Hematopoietic tissue
It manifests high radiosensitivity. The red bone marrow, the lymph nodes and
other lymphoid organs are affected. Exposure to high doses of radiation causes
destructive changes in hematopoietic organs. If we compare the two components of
hematopoiesis, namely red bone marrow and lymphoid tissue, the latter manifests
higher radiosensitivity.

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 Following exposure to high doses of radiation, devastation of lymph nodes and
destruction of the follicles in the spleen are observed. The lymphoid tissue associated
with the digestive system is also severely damaged.
Termination of mitosis and destructive changes in the cells of the bone marrow
are observed within a short time.
Irradiation results in inhibited proliferation, cell death and exhaustion of the
proliferative pool – stem cells and progenitors. Exhaustion results from the inability to
renew the differentiation pool – precursors and aplasia.
Lymphocytes are the most radiosensitive subgroup of the formed elements of
blood. Degenerative changes showing direct damage to them already appear within
hours after exposure to radiation. As time goes on, the amount of degenerative
changes increases. Lymphocytopenie occurs as early as the first day following the
irradiation of the living organism. In addition to the quantitative and morphological
changes in lymphocytes, irradiation also results in an increase in the frequency of
chromosome aberrations.
The changes in the count of leukocytes /the granulocyte series/ in the peripheral
blood are different in character. Changes in the granulocytes in the peripheral blood
usually occur in phases and depend on the dose. The most commonly observed
phases with doses of 2-5 Gy are the following:
 Lag phase that includes the phase of initial neutrophilia.
 First degenerative phase.
 Abortive surge.
 Second degenerative phase.
 Recovery phase.
Thrombocytes in the peripheral blood decrease slowly. They reach their lowest
count at the end of the latent phase of the acute radiation syndrome. The erythrocyte
count decreases even more slowly. There is evidence showing that the lifespan of the
erythrocytes in the peripheral blood is reduced by half. Therefore, pancytopenia occurs
only in cases of severe radiation damage.
Under the impact of ionizing radiation biochemical changes take place in
proteins, fats, carbohydrates, enzymes and electrolytes in the blood. At later stages
coagulation is disrupted /the period of bleeding and clotting increases/ and toxic
products emerge.
A summary of the research evidence presented in scientific literature on the
changes in the count of the formed elements of blood upon incorporation of
radionuclides leads to the conclusion that higher doses result in anemia, leukopenia,
and thrombopenia. Anemia and thrombopenia are not as pronounced with lower
doses. Leukopenia predominates in that case.
3. Reproductive tissue
Depending on the absorbed dose, ionizing radiation can cause the death of
some of the reproductive cells. This determines the cellular radiosensitivity of
reproductive cells. The radiosensitivity of the surviving reproductive cells, which
become defective, determine the genetic radiosensitivity of reproductive cells.
The male gonads are characterized by high radiosensitivity. Stem cells and
proliferating spermatogonia are highly radiosensitive to cell death and radioresistant to
genetic damage. Spermatids and spermatozoa are resistant to cell death and
susceptible to genetic damage. The interstitial cells in the testicle, which control the
production of hormones, are resistant. Permanent sterility develops with exposure to
doses between 3.5 and 6 Gy. Temporary sterility occurs at a dose of 0.15 Gy.

54
 Female gonads are also highly radiosensitive. Under the effects of ionizing
radiation, the ova and the follicles in the process of maturation usually die. This leads
to reduced hormone production. Radiogenic sterility is accompanied by menopause
and has a significant effect on the secondary sex characteristics. Doses of 2 Gy cause
permanent sterility in women over the age of 40, but only temporary sterility in women
under 35 years of age.
4. Digestive system
The small intestines are the most susceptible to radiation damage when
exposed to high doses. The intestinal epithelium is destroyed and its physiological
functions are disrupted. The intestinal epithelium is highly susceptible to radiation
damage because of its high proliferation rate. The exposure to radiation terminates the
mitosis in the crypts, which severely disrupts the regenerative ability of the epithelium.
The intestinal motorics are also disrupted. Initially they are produced via
neurological mechanism and manifests themselves as increased intestinal peristalsis.
Later on, peristalsis is suppressed resulting in intestinal stasis. The damage to the
intestines causes disrupted digestion, malabsorption and malnutrition, disrupted
permeability of the intestinal barrier and severe disturbances in the water and sodium
balance in the organism. Autoinfection and sepsis can develop as a result of the
suppressed natural immunity of the irradiated organism and the free access of
intestinal flora into the bloodstream. These often cause the death of the organism.
There are changes in the blood and lymph circulation of the intestinal wall.
Hemorrhages appear in the intestinal mucosa, which can turn into necrosis and ulcers.
5. Cardiovascular system
Tachycardia and hypotonia are observed. Capillary permeability is reduced and
capillaries become brittle leading to hemorrhaging.
6. Endocrine system
At the beginning endocrine glands are simulated, while later on their functions
are suppressed. The pituitary and adrenal glands are the most radiosensitive ones.
7. Immunobiological reactivity of the organism
The immune system is the most radiosensitive one and for that reason immune
suppression is observed during the earliest stages following a radiation exposure
incident. Both the non-specific defense responses and the factors of specific
defense are affected. The suppressed immunobiological reactivity of the
macroorganism results in endogenic and exogenic infections, which often cause the
death of the irradiated organism.
In the most general terms, as far as non-specific defense is concerned, it can be
concluded that the bactericide properties of liquids are affected. The activity of the
complement system is hampered with exposure to doses that are almost lethal. The
phagocytic activity of neutrophil cells is disrupted in its first phase – the migration to
the object that will be phagocytized. Discoordination and dysfunction of the different
enzymes are observed and the strict order of their activity in the digestion of the
phagocytized object is disturbed. Lymphocytes are exceedingly radiosensitive. Doses
around 0.2 Gy cause morphological changes and changes in their count. B
lymphocytes are significantly more radiosensitive than T lymphocytes. Ionizing
radiation has a significant effect on antibody production. The degree of disruption it
undergoes is directly proportional to the dose of radiation.
V. Biological effects of ionizing radiation on the organism as a whole
The biological action of ionizing radiation on the human organism depends on a
number of factors. The most important ones are: the type of radiation, the absorbed

55
dose and its power, the size and the localization of the irradiated area, the organism’s
reactivity.
As a result of a number of processes that take place at the molecular, cellular,
tissue and organ levels under the impact of ionizing radiation, the following types of
radiation damage occur in the organism:
А. Somatic effects:
 Early somatic effects – they appear within several weeks after
irradiation /deterministic/.
 Late somatic effects – they appear years or decades after
irradiation /stochastic effects/.
B. Genetic effects – they affect the generations that come after the
irradiated individual /stochastic/.
1. Early somatic effects.
They are also called deterministic as the severity of the damage in those cases
is proportional to the absorbed dose, if a certain clinical manifestation threshold is
surpassed. The existence of a threshold dose for the manifestation of a certain effect
is explained with the fact that damage by ionizing radiation received in small doses
below the threshold results in recovery processes in the organism that can compensate
for the damage. With doses higher than the threshold, the severity of the damage
increases proportionally to the dose received, because of the higher rate of cell
destruction compared to the rate of cell reproduction. The graph illustrating the
dependence dose-effect in this type of radiation damage is a sigmoid curve.
For one-time, whole-body exposure of short duration, the threshold dose is 0.2-
0.3 Sv. This dose of radiation does not make the individual feel ill, but there are
disturbances in the functions of a number of radiosensitive organs /red bone marrow,
lymph nodes, spleen, reproductive glands, the mucous membrane of the
gastrointestinal tract and the respiratory system, etc./
The organism’s recovery systems are capable of compensating for the damage
caused by exposure to small doses of radiation /0.3 Sv/. These compensatory abilities,
however, are not sufficient for higher doses. In human beings this occurs when doses
of around 1 Sv are received – symptoms of acute radiation sickness appear. Doses of
around 4 Sv /called LD50/ result in the death of approximately 50 % of the irradiated
persons. Doses higher than 6-7 Sv /LD100/ are almost always lethal.
The manifestation of deterministic effects is different for different individuals. It
depends not only on the characteristics of the exposure incident and the dose, but also
on the physiological state of the organism.

Values of threshold doses for different deterministic effects

Organ Dose /Gy/ Effect

Whole body 8 Early death

Whole body 1 Acute radiation syndrome
Whole body 0,5 Bone marrow suppression
Liver 30 Failure, ascites
3-10 Erythema
Skin 8-12 Dry desquamation
15-20 Wet desquamation
25 Necrosis
Lung 15 Early death
5 Pneumonitis

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 Thyroid gland 5-10 Hypotheroidism
Testicles 0,15 Temporary steriliry
3,5-6 Permanent sterility
Ovaries 0,65 Temporary sterility
2-6 Permanent sterility
Lens 2-10 Cataract

2. Stochastic effects
These include the late somatic effects and the genetic effects. In this case, the
normal cell is modified under the impact of low doses of ionizing radiation, but it still
retains its reproductive ability. These effects are not determined by the dose and there
is no threshold that needs to be surpassed in order for them to appear.
Concerning the dose-effect dependence, we can observe a stochastic /
probabilistic/ distribution of cases, i.e. the increase in the dose of radiation means a
higher probability of illness occurring, but it bears no relationship to its severity as is
the case with deterministic effects. Therefore, when we discuss these effects, we talk
about radiation risk. Stochastic effects are random by nature and their manifestation
depends on the physiological characteristics of the organism. Because the modified
cells retain their reproductive ability, they produce their own population. This population
could be destroyed by the organism’s defense mechanisms. However, if that does not
happen for a number of reasons, after a certain latency period, the stochastic effect
will manifest itself. The probability of its appearing depends on the number of modified
cells that emerge after the exposure incident. The higher their number, the more likely
they are to survive.
 Late somatic effects. They include new malignant formations /different
forms of carcinoma and leucosis/. These stochastic effects typically appear after a
prolonged latency period – between several years and whole decades. The
mechanisms of malignization are not clear. The emergence of inherited changes in the
genetic apparatus of the cell is of crucial importance.
 Genetic effects. They are caused by the exposure of reproductive cells
to radiation prior to or during the reproductive age, which results in additional mutations
that are transmitted to the next generation. Ionizing radiation is a powerful mutagen
and the most common types of genetic damage it causes are genetic mutations and
chromosome aberrations.
3. Carcinogenic risk
The carcinogenic risk is primarily connected with the appearance of late somatic
effects. The radiation-induced malignant diseases are forms of leucosis and solid
tumors.
The main characteristics of radiation-induced leucosis are:
 The incidence is proportional to the dose.
 The risk is higher, the lower the age when the exposure took place.
 The peak of its manifestations is observed 7-8 years after irradiation.
 Leukemic risk is observed in individuals exposed to doses higher or equal
to 1 Gy.
The characteristics of radiation-induced solid tumors are:
 The risk of developing cancer increases with the dose.
 Carcinogenic risk is higher the lower the age when the exposure took
place.
 Unlike leucosis, in the case of solid tumors the latent period increases if
irradiation has occurred at a younger age. Furthermore, the effect

57
 becomes noticeable at an age when spontaneous cancer morbidity rates
are already higher.
Types of dose-risk dependence for assessment of carcinogenic risk:
1. With higher doses the dose-risk dependence is linear no-threshold, i.e.
the additional risk /R/ is directly proportional to the dose /D/. R=k.D, where k stands for
risk coefficient. It is estimated for the more common malignant lethal diseases and
used to calculate the risk resulting from one-time irradiation with a certain dose for the
remainder of the irradiated persons’ lives /coefficient of lifelong risk/.
2. With very high doses and power of the dose, the dose-risk dependence
is linear-quadratic, i.e. the additional risk decreases faster as the dose is reduced.

Carcinogen risk assessment is very difficult to make because of the high rate of
spontaneous occurrence of tumor diseases and its annual fluctuations. It is possible to
detect carcinogenic diseases caused by the effect of ionizing radiation if their number
is higher than the average value of the fluctuations.
Risk assessment is conducted through observation of groups of people exposed
to higher doses, because only those groups manifest higher rates of new malignant
formations documented by multi-year research. The results of these observations
make it possible to create models of the dependence dose-additional risk and these
models can be extrapolated for smaller doses.
The additional risk of leucosis and tumors over time (after exposure to radiation) is
illustrated in the graph below, which is based on observations of Japanese citizens
following the atomic bombings of Hiroshima and Nagazaki and the linear no-threshold
model of the stochastic effect. Additional cases of leucosis are not observed two
years after irradiation. Then their number increases, peaking six-eight years after
irradiation. The number gradually goes down to 0 after 27 years. The risk period for
leucosis is 25 years.
Additional cases of other malignant diseases are not observed over the first 10
years after irradiation. During this latency period there is no carcinogenic risk. Then
the risk increases, peaking 30 years after irradiation. After the maximum has been
reached, there are 3 possibilities: the risk decrease, it remains constant or continues
to grow.

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 4. Genetic risk
The assessment of the genetic risk caused by the effects of ionizing radiation is
very difficult to perform because of the high spontaneous rate of genetic disorders. The
relationship dose-genetic risk is also characterized by linear no-threshold dependence.
Genetic risk assessment can be performed in two ways:
 The first method is to express genetic risk using the rate of genetic
disorders per unit of radiation dose.
 The second method is to express genetic risk through the dose that
doubles the natural mutation rate.
Recently it has been observed that there is an increase in the doses needed to
double genetic mutations, which means that genetic risk has decreased compared to
the situation in the past.
The International Commission on Radiological Protection states that in cases of
low doses and power of the dose, the nominal probability coefficient for severe genetic
effects in regard to all generations and in connection with the gonad doses received,
distributed for the entire population, is 1.3 х 10-2 Sv-1.

SPECIFIC CHARACTERISTICS OF THE BIOLOGICAL EFFECTS OF IONIZING

RADIATION IN CASE OF EXTERNAL EXPOSURE AND INCORPORATION OF
RADIONUCLIDES IN THE ORGANISM

Nuclear accidents can result in the contamination of the biosphere and increase
the likelihood of radionuclides /RN/ entering the human body.
The term incorporation refers to the entry of radionuclides into the human body through
the skin, through inhalation or perorally.
Once they have been incorporated, radionuclides remain in the human body for
a certain period of time and become a source of internal radiation exposure. Their rays
are absorbed fully or partially by the tissues and this results in a certain degree of
radiation load.
I. Specific characteristics of the damage incurred by the organism when
radionuclides are incorporated
The biological action of the incorporated radionuclides is similar to that observed
in external exposure, but it is characterized by a number of specific features connected
with the rules governing the behavior of radioactive substances in the organism. They
are important for the calculation of the absorbed dose.
Measuring the magnitude of the absorbed tissue dose when there is
incorporation of RN into the organism is significantly more complicated than

59
determining the doses in case of external exposure. Certain mathematical models are
used in this process. The established quantitative regularities of the behavior of RN
along the complex path they follow in the organism serve as a necessary basis for
calculating the absorbed dose.
When radioactive substances are incorporated into the organism, the absorbed
dose is the sum of the following 3 constituents:
 The quantity of radionuclides in the tissues.
 The type and energy of the emission.
 The duration of the contact between radiation and tissues.
The section devoted to the study of the regularities in the behavior of
incorporated radioactive substances and the effects of internal radiation exposure on
the organism is called radiotoxicology. The term radiotoxicity has been introduced to
describe the degree of biological action of a given radionuclide resulting from its
radioactivity.
The active quantities of radioisotopes have insignificant weight and for that
reason they are not measured in units of weight, but in units of activity.
If a radioactive substance is incorporated with high activity, is easily resorbed,
accumulates in significant amounts in critical organs, is eliminated slowly from them
and is characterized by a long physical half-life, this means that it is highly
radiotoxic.
The biological action of the radionuclides incorporated into the organism is
primarily determined by the following 2 factors:
 The magnitude of the absorbed dose.
 The response of the corresponding organs and tissues.
The magnitude of the absorbed dose depends on:
 the type and energy of the emission – when radionuclides are
incorporated into the organism, the severity of the damage depends on the ionization
density of the radiation and not on its penetrating ability as is the case with external
exposure; therefore it is the alpha particles that cause the worst damage in case of
internal exposure, followed by beta particles and gamma quants;
 the quantity of radionuclides in the tissues;
 the duration of the exposure, i.e. the distribution of the absorbed dose
over time – it is characterized by the change in the concentration of radionuclides in
tissues; this change depends on the rate of the physical decay and biological
elimination of the radionuclide, as well as on the duration of its entry into the organism;
 distribution of the absorbed dose in space /within the volume of the
organ/ - the uneven distribution of RN in organs and tissues leads to uneven
distribution of the absorbed tissue dose;
 physicochemical properties of RN – they determine the metabolism of
RN in the organism: the path of entry, the features of the distribution and dynamics of
the metabolism, the shape of the complex compounds it forms with the biosubstrate;
the degree of solubility of RN at the entry determines the pathway and characteristics
of its movement within the organism; the metabolism of radioisotopes in the organism
is determined to a significant extent by the groups, subgroups and periods they fall into
according to Mendeleev’s periodic table; the metabolism of radioactive isotopes within
the same group of the periodic table has many common characteristics; radioisotopes
participate in the same metabolic processes as their stable counterparts; radionuclides
that fall into different groups have significantly different chemical properties and thus a
different behavior in the organism;

60
  the importance of the carrier – when assessing the biological effect, it
is important whether the isotope has been introduced in its pure form or with a carrier;
“carrier” refers to the amount of a certain substance that has entered into a chemical
reaction with the same amount of another substance; there are isotopic and non-
isotopic carriers; an isotopic carrier is the stable isotope of the given element; its
chemical properties are identical to those of its radioactive isotope; e.g. the stable
phosphorus-31 /carrier/ with respect to the unstable phosphorus-32; non-isotopic
carrier refers to the stable isotope of the chemical analog of the radioisotope; the latter
is analogous to the carrier only in regard to their group-determined chemical properties,
e.g. stable calcium /carrier/ with respect to strontium-90;
 absorption magnitude – the absorption magnitude of radionuclides,
expressed through the coefficients of resorption at the different entry points, has a
significant impact on its toxicity; this is primarily expressed in quantitative and not
qualitative differences, but it influences the biological effect; the absorption coefficient
is directly proportional to the amount of radioactive isotopes entering the organism.
Response of the respective organs and tissues
The biological effects of the incorporated RN depend on the radiosensitivity of
the respective organs and tissues in which they accumulate. The most radiosensitive
organs /hematopoietic system, reproductive tissue/ incur the most severe damage.

The biological action of the RN incorporated into the organism is of two

types:
1. Direct action – determines the damage at the point of entry or in the organs
resulting from selective accumulation of RN.
2. Indirect action – manifests itself as a reaction of the entire organism.
Specific characteristics of the biological action of the incorporated RN:
1. Single entry of evenly distributed RN into the organism. General injury to
the organism affecting all its organs and systems is observed. Diverse injuries emerge
early on. Changes in the radiosensitive organs are the first to appear. RN characterized
by this type of distribution are Cs137, Na22, Co60, etc.
2. In case of incorporation of difficult to dissolve RN, the entire absorbed dose
is absorbed in the gastrointestinal tract leading to the development of severe radiation
responses of this system /Cerium-144/.

61
 3. In case of single entry of RN with selective tropism, the critical organs are
damaged the most and the general responses of the organism are not particularly
pronounced.
An important indicator for the assessment of the radiotoxic action of nuclides is
the formation time of the absorbed dose:
1. In case of single entry of easily dissolved isotopes distributed evenly in
the organism and an absorbed dose of 1-1.5 Gy accumulated over the course of 2
months since the start of the exposure, acute radiation sickness /ARS/ develops.
2. In case of single entry of compounds of RN that are difficult to dissolve
through the gastrointestinal tract, damage to the digestive system is observed with
doses of 1.5-3 Gy for a day. The accumulation of this dose over the course of 1 year
with daily introduction of RN causes Chronic Radiation Sickness (CRS).
3. The prolonged impact of small doses of RN leads to the development of
CRS of varying severity and the emergence of tumors. Most commonly, the localization
of the tumors is in the critical organ.
II. Pathways for radionuclide entry into the organism
 Undamaged skin
 Damaged skin surface
 Respiratory system
 Digestive system
1. Undamaged skin. The behavior of radionuclides that come into contact with
the skin is determined by the following factors:
 State of aggregation and physicochemical properties of RN.
 State of the skin surface.
 Conditions in which the radioactive contamination appears.
RN become attached to the surface of the skin as a result of adhesive forces.
The degree of fixation depends on the size of the particles and the state of the skin.
The partial resorption depends on the character and intensity of the secretion and
excretion processes occurring in the skin and on the depth of penetration into the
pores. Radionuclides on the skin are distributed in three layers:
 Superficial – it consists of mechanically deposited particles.
 Middle – it consists of radioactive particles that are deposited
based on physicochemical interaction between RN and the skin’s structures.
 Lower – it consists of particles that have reached a certain depth
as a result of ion exchange between radioactive substances and the skin’s surface.
A significant portion of RN that have come into contact with the skin penetrate
it deeply through the epidermis or through the sudoriferous and sebaceous glands, as
well as through the hair follicles. The biological barriers of the skin that are difficult for
RN to penetrate are the hydro-lipid layer covering the skin and the stratum corneum. If
a radionuclide has passed through the stratum corneum, the lower layers of the skin
can offer no resistance to its further movement.
RN that have penetrated the dermis are absorbed into the blood and lymph
capillaries and reach the liquid environment of the organism. Resorption in blood
capillaries is higher than that in lymph capillaries.
A typical characteristic of the distribution of RN in the skin is that they interact with
proteins on all levels. For that reason, the character and rate of their metabolism
depend on the character and rate of the metabolism of these complex compounds.
2. Damaged skin. The behavior of RN is determined by 2 main factors:
 The physicochemical properties of RN.
 The type of wound.
62
 The most important of the physicochemical properties of RN is the solubility of
the chemical compound containing the RN that interact with the damaged skin. If
oxides and carbonates of heavy metals that are difficult to dissolve come into contact
with the wound, they remained fixed at the point of entry and undergo almost no
resorption by the blood. Soluble nitrates and chlorine compounds of plutonium quickly
enter the bloodstream in large quantities. Alkaline, alkaline-earth and halogenic RN
demonstrate the highest level of absorption through the wound surface.
The type of wound is very important for the degree of resorption of RN. Incised
and puncture wounds results in the highest level of absorption. Skin- and muscle-
penetrating wounds are characterized by lower resorption. The lowest level of
resorption is observed in tears and contused wounds.
The explanation for the reduced resorption in skin- and muscle-penetrating wounds,
tears and contused wounds is the large-scale tissue injury accompanied by damage to
blood and lymphatic vessels and slower movement of blood and lymph inside them.
For first and second degree thermal burns, the resorption is not different than
that in the case of undamaged skin. In third degree thermal burns, the necrotic tissue
serves as a barrier, which greatly reduces the degree of resorption of RN.
It has been determined that the swelling and inflammation, which accompany all
wounds and spread into the connective tissue and along the nearby vessels, contribute
to the distribution of RN into the tissues surrounding the wound.
3. Respiratory system. The respiratory system serves as an entry point of
different RN both in regular working and emergency conditions. The behavior of RN
upon their entry depends on the following factors:
 The properties of the inhaled radioactive aerosol:
а/ the size and shape of the radioactive particles;
b/ the propensity for chemical bonding with liquids;
c/ the density of the particles;
d/ the chemical properties of the particles;
 Anatomic and physiological characteristics of the respiratory tract:
а/ the respiratory minute volume;
b/ the respiratory rate;
c/ the surface area of the lungs and the bronchi;
The size of the particles is of primary importance:
а/ particles over 5 μm remain in the upper respiratory tract;
b/ particles between 0.5 and 5 μm penetrate the lungs;
c/ particles under 0.5 μm can penetrate and exit the lungs
undeterred;
When particles enter the nasopharynx, some of them pass through the trachea
and the bronchi, while others go through the oral cavity and into the digestive system.
A certain portion of RN moving through the ciliated epithelium of the trachea and the
bronchi go back into the oral cavity and end up in the stomach via this route.
Via the respiratory tract, the RN that have not been pushed back out continue
on their way to the surface of the lung. The soluble radioactive substances are
absorbed into the blood and the lymph. They are carried by these fluids throughout
the entire organism.
The third part are the insoluble radioisotopes, which are deposited into the
nearby lymph nodes.
The general pattern presented above does not completely reflect the multitude
of diverse processes that take place when radionuclides are absorbed through this
entry point, but it can help understand the basic principles. It needs to be pointed out

63
that the magnitude and speed of the absorption of RN from the lungs into the
bloodstream are primarily determined by their solubility in the liquid environment of the
respiratory system.
4. Digestive system. This system is of prime importance as an entry point of
RN into the organism.
Radionuclides entering the organism with ingested food and water are mixed
with the contents of the gastrointestinal tract and move along the tract, irradiating the
stomach and intestinal walls in the process. The soluble RN are resobred through the
intestines. Resorption is the strongest in the upper sections of the small intestine.
Resorption in the stomach and the large intestine is insignificant, except for that
of radioiodine. Insoluble RN are not resorbed and they are eliminated from the
organism with the fecal matter.
The resorption of RN through the gastrointestinal tract depends on the following
factors:
 The chemical properties of RN.
 The physiological state of the digestive system.
 The contents of the food ration.
Cesium, iodine, sodium, potassium, rubidium and bromine are almost fully
resorbed. 10-40 % of alkaline earth metals are absorbed.
The most important chemical property is the solubility of the chemical compound
containing the RN that enters the digestive tract.
The physiological state of the digestive system affects the rate of passage,
which in turn determines the amount of time RN contaminated foods remains in the
organism.
III. Principles of the distribution of RN in the organism
The radionuclide mixture entering the organism consists of different isotopes
that have their own path of distribution and do not affect one another. At all levels of
metabolism, the physicochemical properties and the form of the compounds resulting
from their interaction with the liquid environment of the organism are a determining
factor.
The solubility of RN at the entry point determines the pathway, character and
form of their chemical compounds for their ensuing distribution in the organism.
Two main groups of radioisotopes have been recognized, each with its own
distribution mechanisms:
 Radioisotopes, whose compounds can be dissolved in the liquid
environment of the organism.
 Radioisotopes, whose compounds are not dissolved easily in the liquid
environment in the organism.
The radioisotopes that form soluble compounds at the entry point into the
organism are absorbed into the bloodstream and enter the intercellular fluid, which
serves as a boundary between blood and organs. Some of these RN are distributed
evenly in the organism’s cells. Others accumulate selectively in certain organs and
tissues.
The rate of passage of RN between the three sections, namely blood plasma –
intercellular fluid – cells, is not uniform. Their transition from the blood to the
intercellular fluid and back is faster. The process of return of RN from the cells of the
tissues and organs where they have accumulated is slower. The reason for this is the
fact that RN form stable bonds with cellular contents in the tissues. RN that form
unstable bonds in the tissues, as well as those found in the blood plasma and the
intercellular space, are eliminated from the organism the quickest. The speed of

64
elimination of RN that have accumulated in a certain organ depends on the metabolic
processes occurring in said organ and the half-life of the specific RN.
The organs affected by the selective tropism and accumulation of RN are
subjected to the highest degree of radiation exposure. They are called critical organs.
If RN accumulate selectively in several organs, the critical organ will be the one in
which the radioisotope accumulates the most intensively and from which it is eliminated
at the slowest rate. Critical organs are characterized by high radiosensitivity.
Based on their accumulation in critical organs, RN are divided into 5 groups:
а/ evenly distributed in the organism (22Na, 40K, etc.);
b/ accumulating in the bones (strontium-89, phosphorus-32 , etc.);
c/ accumulating in the kidneys and the spleen (polonium-210, lead-210, etc.);
d/ insoluble RN with weak resorption through the intestines, for which the
critical organ is the digestive tract (60Со, etc.);.
e/ radioisotopes selectively accumulating in separate organs and tissues –
iodine-131 in the thyroid gland, iron-59 in the erythrocytes, zinc-65 in the
pancreas, etc.;
The bones and the digestive tract are the critical organs for the most common
types of RN.
The radioisotopes that form insoluble compounds at the first link in the metabolic
pathway become attached to and accumulate in the cells of the mononuclear
phagocytic system.
RN in the blood plasma are caught by the reticuloendothelial cells of the liver,
the spleen and the bone marrow, which are located along the length of the capillaries.
The cells extract RN directly from the blood and deposit them in the liver, the spleen
and the bone marrow.
RN from the lungs are caught by the reticuloendothelial cells located in the
lymph nodes. These RN are deposited in Ly nodes.
In the cells of the reticuloendothelial system, RN undergo changes that can lead
to their becoming soluble. In this way they are eliminated from the organism or
accumulate for the second time in certain organs.
IV. Dynamics of the metabolism of RN in the organism
The deposition of the incorporated RN in different organs and tissues is not
stable. Their quantities, and thus their radioactivity, change over time. The changes in
the concentration of radioactivity in a given organ or tissue determine the degree of
internal exposure.
The dynamics of the metabolism of RN in the organism is primarily determined
by the following 2 processes:
 Physical radioactive decay of RN.
 Biological half-life of RN.
The physical radioactive decay is a continuous process which is characterized
by release of ionizing emissions and a reduction in the quantity of RN until it becomes
a stable isotope.
To quantify the physical radioactive decay, we use the term half-life – it refers
to the time it takes for the initial activity of RN to be reduced by half. The value of this
quantity is determined by the biological effectiveness of the radioactive substance.
The damaging effect of the short-lived isotopes takes place over a shorter period
of time compared to long-lived ones because of their faster decay rate.
Under the conditions of irradiation with a mixture of RN, the overall rate of
reduction of its radioactivity is equal to the sum of the rates of decay of the different

65
isotopes it contains. The radioactive mixture is characterized by variability as the
daughter products emerging in the process are also radioactive.
The biological half-life of RN is a combination of complex biological processes
of accumulation, distribution and elimination of radioactive substances from the
organism. These processes lead to a reduction in the quantity of RN in the organism
achieved via biological means. In order to determine the dynamics of RN, we need to
take into account the rate of these biological processes at the following stages of their
metabolism:
1. Resorption of RN into the bloodstream from the entry point.
2. Transition of RN from the blood into the organs and tissues.
3. Elimination of RN from the organism.
In the case of mixed decay products, the sum total of the interaction of the rates
of these processes for the different RN determines the dynamics of the biological
reduction of radioactivity in the organism.
For the purposes of interpreting the dynamics of the metabolism of RN in the
organism, the following models have been developed and the following mathematical
expressions have been formulated. Based on such a mathematical model, the
reduction in the concentration of RN in a given organ as a result of its elimination is
described using the following exponential function:

Nt = No . e -λcp.t

Where:
Nt – number of radioactive atoms at time t;
No – number of atoms at t = 0;
λcp – decay constant.

This expression can serve as a simple foundation for the mathematical

interpretation of the metabolism of RN and it is commonly accepted as a way to
describe their elimination from the organs.
The quantity characterizing the physical decay of RN, which is used to
determine the dynamics of their metabolism, is called the decay constant. It is
calculated as “day-1“.
The biological elimination leads to a reduction in the number of isotopes as a
result of metabolic processes and it is characterized using the so-called biological
decay constant (λb) - /day -1/.
The decrease in the radioactivity in the organism caused by the physical and
biological decay is called the effective decay constant (λеf).

λеf = λср + λb

The dependence between the physical and the biological decay can be
demonstrated using the effective half-life. It shows the time /in days/ that it takes for
the RN content in the organism to be reduced by half:

Тph . Тb Тef – effective half-life

Теf = ------------ Тph – physical half-life
Тph +Тb Тb – biological half-life

66
 The mutual dependence between λеf and Теf can be expressed in the following
way:
0,693 0,693
Т = ---------- λ = ---------
λ Т
The dynamics of the metabolism of RN in the organism can also be described
using the so-called chamber model that demonstrates the rate of movement of RN in
the organism. The following principle of grouping RN into different chambers is used:
1. Concentration principles – the organs and tissues that have the
property of concentrating RN to the same extent under stationary conditions are
grouped together in the same chamber.
2. The structural elements of the system in which RN is found in an
identical chemical state can be put together in the same chamber.
3. The organs and tissues that are equally functionally important in one
and the same phase of the metabolism of RN can be grouped together in the same
chamber.
The concentration of the radioisotope in a certain organ is primarily determined
by the relationship between the radioactivity (A) and the mass of the organ (m).

А
С = ---
M

V. Elimination of radionuclides from the organism

The pathways for elimination of radioisotopes from the organism are as follows:
the gastrointestinal tract, the kidneys, the bile ducts, the salivary, mammary and
sudoriferous glands, and the lungs. The largest quantity of radioisotopes in the
organism is eliminated with the feces and the urine.
Elimination is most active during the first couple of day following the
incorporation. The highly soluble radionuclides that are evenly distributed in the
organism are eliminated primarily with the urine. Those radioisotopes that stay in the
liver are eliminated mainly through the bile ducts in the intestines.
It is a common rule that the pathways for elimination of radionuclides from the
organism are determined to a significant extent by the pathways through which they
have entered the body. The radionuclides that have entered the organism through the
oral cavity are eliminated mainly as part of the fecal matter during the first couple of
days. This is especially typical of radioisotopes that are not dissolved easily. As time
goes on, the elimination pathway changes. Elimination through the urine becomes
more prevalent.
Those radioactive aerosols that have not been deposited in the lungs can be
eliminated from the organism via the exhaled air. Most commonly these are
compounds of tritium, radon, carbon, oxygen. All radioisotopes found in the
intercellular fluid can be eliminated through the sweat.

67
 SPECIFIC CHARACTERISTICS OF THE DAMAGE CAUSED TO THE
ORGANISM BY PROLRNGED EXPOSURE. BLAIR’S THEORY

In the case of prolonged exposure, the ionizing radiation does not impact the
organism only one single time and momentarily, but continues to affect it over a certain
period of time as the intensity of the exposure gradually decreases. An example of
prolonged exposure can be the exposure caused by the gamma field that has emerged
in the zone of the local radioactive fallout following an accident in a nuclear power
plant.
Prolonged exposure has a number of specific characteristics that have been
thoroughly investigated using experimental research on animals. The tests have
helped to determine that the longer the exposure period, the higher the total dose that
causes damage of a specific severity, because of the action of the recovery processes
in the organism.
According to this theory, prolonged exposure to ionizing radiation causes two
processes to take place:
 Process of incurring damage, which depends on the exposure dose.
 Process of recovery, which depends on the time of the exposure episode
and the rate of the recovery mechanisms in the organism.
The difference between the absorbed dose and the dose compensated by the
recovery processes determines the magnitude of the true damage to the organism. It
is also referred to as pure damage to the organism or biologically effective dose.
The true damage is not compensated by recovery processes. As more time
passes from the start of the exposure, the magnitude of the true damage decreases,
because most of the injuries are influenced by the recovery processes.
Based on his studies of the processes of incurring and recovering damage to
the organism exposed to radiation for a prolonged period of time, Blair constructed a
theoretical curve that describes the dependence between these two processes. He
posited that the daily recovery rate is 10%.
The analysis of the curve demonstrates that the recovery rate at the beginning
is in a constant percentage interrelation with the pure damage. At the later stages, a
certain unrecoverable part of the damage manifests itself. The late-stage effects are
its clinical manifestation. The magnitude of the irreversible damage is directly
proportional to the total applied dose.

All these regularities have been discovered through experiments with animals.
In order to determine the responses of the human organism to prolonged exposure,
Blair studied the following indicators connected with the human being:
Magnitude of the daily recovery of the human organism or half recovery period.
It has been estimated through analysis of the half recovery periods of different animals
/mice, guinea pigs, dogs/ and extrapolation of that data to humans. The data are
68
examined using a number of indicators that animals and humans share. The main
indicator is the number of leukocytes as these are the cells in the organism that are
most susceptible to radiation damage. Thus, it has been estimated that the half
recovery period for humans is 30 days.
Irreversible portion of the damage – it is determined on the basis of the familiar
parameters of the ionizing radiation that appears in the zone of radioactive fallout in
nuclear accident. Its value is approximately 10-12 % of the total dose.
Based on these 2 indicators relating to the human being, Blair’s theory can be
used to estimate the radiation injury to the human organism caused by prolonged
exposure. A mathematical formula is used that accounts for the sum total of the actions
of all the processes occurring in the organism exposed to radiation for a prolonged
period of time:

Dt = D [f + (1-f)e-βt]

Dt – pure damage
f – irreversible portion of the damage
1-f – irreversible radiation injury
D – single exposure dose
β – daily rate of recovery in %
t – number of days
е – base of natural logarithms

Conclusions drawn from Blair’s theory:

 The effective dose is used only to determine the short-term effects of
exposure to radiation.
 The late-stage effects of exposure on the organism increase in parallel
to the total dose. This conclusion is based on the fact that the slower the
effective dose reaches its maximum value, the higher the ratio between
the total dose and the maximum effective dose.
 Two different types of exposure that share the same maximum
magnitudes of the effective doses can result in similar short-term effects,
but different late-stage ones.

TREATMENT AND PREVENTION MEASURES IN THE EVENT OF RADIATION

IMPACT

Principles.
Treatment and prevention measures are needed when radioactive elements
have been incorporated into the organism. The first principle is that the application of
treatment and prevention measures is reserved for cases in which the incorporated
radioactive elements /RE/ surpass the maximum permissible dose limits. The factors
that determine the treatment and prevention measures are: the type of RE, the
incorporated quantity, the pathway of entrance, the beginning and end of the entrance,
the magnitude of the dose of external exposure, etc.
The presence of a nuclear accident accompanied by release and ejection of
radioisotopes into the outside environment, or even merely suspicions that an accident
has occurred and radionuclides might enter the organism, can serve as grounds for
the application of treatment and prevention measures.

69
 The effectiveness of the prevention measures depends on their timely
execution. It is reduced significantly if they are delayed for a few hours.
The treatment and prevention measures that are conducted in the event of a
nuclear accident can be classified into two groups:
 General measures
 Specific measures
1. General treatment and prevention measures
These are used for all radioisotopes for the purpose of removing them
mechanically:
а/ radioactively contaminated skin surfaces are washed thoroughly with
running water and detergent for 15-20 min.; this procedure should not take place later
than 1-1.5 hours after the skin surface has been contaminated;
b/ the oral cavity is washed with a 1-2% solution of sodium bicarbonate or
simply with clean water if this solution is available; the mucous membranes of the eyes
and the nose are washed with the same solution using a pipette; when bathing the
eyes, the stream of water needs to be directed from the inner to the outer corner of the
eye in order not to contaminate the tear ducts; the ears are cleaned with separate
plastic syringes; the teeth are brushed with toothpaste if available;
c/ when RE enter the digestive tract, the treatment measures are aimed at
reducing the absorption of radionuclides, their elimination from the upper sections of
the digestive tract and their accelerated elimination from the intestines; the main
measure is to perform gastric lavage using a tube and 2-3 liters of clean water; inducing
vomit has also been applied successfully – either mechanically or by administering
medicaments /5-10 mg. of apomorphine percutaneously/; absorbents are applied after
the stomach has been emptied of its contents /activated charcoal, antidotum
metallorum/; then laxatives are administered /magnesium sulfate/; the use of castor oil
is not recommended as it accelerates the resorption of some radionuclides; after the
intestines have been cleansed, a regular or siphon enema is performed;
d/ when radionuclides enter the respiratory system – the nasopharynx and
the oral cavity are washed in the manner described above; all the aforementioned
actions to cleanse the digestive tract are also carried out; additionally, expectoration is
induced by applying Broncholytin (1 tablespoon/2 hrs.), Bromhexine (3X2 tablets), etc.;
e/ in the case of radioactively contaminated wounds, the first measures to
prevent the entry of radionuclides into the blood need to be taken immediately;
Esmarch bandage is temporarily applied; then the wound is washed thoroughly with
an appropriate solution and the wound is dressed; after that there are two possible
approaches – conservative and surgical:
Conservative treatment is applied in case of small, superficial wounds that
have been contaminated with short-to-medium lived radionuclides with low toxicity – it
includes:
 Irrigating the wound with saline and dressing it with a sterile pad;
 Dosimetric control of the cleansing fluids and the primary wound
dressing;
 Anti-tetanus anatoxin – if necessary.
Surgical treatment is applied in case of wounds with a large area and
severe contamination with long-lived radionuclides with high toxicity:
 Irrigating the wound with saline or 3% hydrogen peroxide solution;
 Application of Esmarch bandage /tourniquet/ over the wound and
removal of the contaminated tissue under anesthesia;
 Measuring the radioactivity of the wound surface;

70
  Second surgical intervention – if necessary;
 Second irrigation of the wound;
 Application of wound dressing;
 Anti-tetanus anatoxin – if necessary;
 Analysis of blood radioactivity;
 Removal of the Esmarch bandage.
2. Specific treatment and prevention measures
а/ application of compound formers – the mechanism of their action is
based on the principle of formation of incorporated radionuclides of soluble compounds
that are easily eliminated from the kidneys; it is important to establish quick bonds with
the radionuclides before the later have entered into a durable chemical bond with tissue
components; radioisotopes found in the blood and the intercellular fluid are the most
prone to forming compounds; the compound formers used in the medical practice are
classified into three groups:
 Derivatives of polyamino-polycarbonate acids – Trilon B, Tetacium
calcium, pentacene, DESTA; the most commonly and successfully used medicament
in the clinical practice is pentacene /ampoule 0.25 gr);
 Derivatives of diethyl compounds – 2,3 Dimercaprol /Unithiol/, etc.;
 Compound formers that are found naturally in the organism –
bicarbonates, sodium citrate, etc.
b/ application of the method of saturation of the organ with a
corresponding stable isotope or its analog – it is based on the principle of saturating
tissues with non-radioactive isotopes, which results in lower levels of radioactive
isotopes being incorporated into them / e.g. iodine prophylaxis/;
c/ direct elimination of RE from the blood through hemodialysis – it is
used in case of incorporation of large quantities of RE; it is most effective during the
first 4 hours; this method is not applicable in case of massive injury;
d/ stimulated elimination through the urine – diuretics are used in this
process, which reduces the degree of resorption of radioisotopes in the kidneys and
contributes to their faster elimination through the urine.

RADIATION DAMAGE

Radiation damage (injuries) are diseases of the body caused by exposure to

ionizing radiation. Radiation injuries are 3 types:

 Acute radiation syndrome or sickness (ARS)

 Chronic radiation syndrome or sickness (CRS)
 Cutaneous radiation injury (CRI)

A radiation doesn’t have to be toxic, the administration of a very low dose of

radionucleid could even have some benefit. We call this phenomenon hormesis.
The occurrence of the radiation injuries after exposure depends on many
factors:
1. The type of radiation. Nuclear reaction produce radionucleid divided in two
major type:
 Molecule radiation : electron, positron and helium. Helium is the most
dangerous one.
 Electromagnetic radiation : x-ray and gamma radiation.

71
 The four types of radiation that can cause injury include alpha, beta, gamma,
and neutron. Alpha particles cause no significant threat by external exposure but if
taken internally can cause local injury. Beta particles are known to cause skin and eye
injury with external contamination and similar damage as alpha particles when
internalized. The radiation from gamma and neutron particles penetrates significantly
and can cause severe whole-body exposure.
2. The doses. Higher the dose is more important are the lesion.
3. The fractionation of the dose. If the all amont of radiation is receive in one
in one times the consequences are higher, when the dose is highly fractionate the
consequences are minimal.
4. The type of tissue. Some tissue are highly resistant to radiation, other are
sensible like skin or bone marrow for exemple.
5. The type of exposure. It exists two type of exposure - external and internal.
 External exposure happens when the radiation source is outside of our
body. At turn it is divided in two subtype:
 Distant external exposure (irradiation). The patient is exposed to
penetrating radiation from an external source that is not deposited
on the body's surface. Exposure stops when the patient leaves the
area of radioactive contamination. The patient is not contaminated
and poses no risk to others.
 Direct contact exposure (external contamination). The patient is
exposed to radiation when radioactive material is deposited on the
body's surface. The patient poses a risk to others and must be
decontaminated.
Those external radiation comes from :
 Nuclear weapons or accidents (Tchernobyl nuclear plan explosion).
 Cosmic ray for space travellers.
 Natural radiation comming from water or soil.
 Most of the time medical radiation : radiotherapy for cancer or
scintigraphy.
 Internal exposure (internal contamination). The patient is exposed to
radiation when radioactive material is incorporated into the body through
ingestion, inhalation, or absorption through intact or wounded skin. The
patient exposure continues until the material is expelled from the body.
The patient poses a risk to others and must be externally
decontaminated. Definitive treatment is specific to each radioactive
material.

ACUTE RADIATION SYNDROME

Definition
Acute Radiation Syndrome (ARS) (sometimes known as radiation toxicity or
radiation sickness), it is a constellation of health effects which occur within several
months of exposure to high amounts of ionizing radiation in a very short period of time
(usually a matter of minutes). The major cause of this syndrome is depletion of
immature parenchymal stem cells in specific tissues.
Atomic bombs and nuclear accidents are the main causes for ARS. Till 2000
more than 417 nuclear accidents have been reported with 127 casualties, while others
state that the nuclear accidents were 580 and fatal casualties 180. These figures may

72
be even higher. Nuclear accidents may terrorize communities, far away from the site
of the actual accident.
Examples of people who suffered from ARS are the survivors of the Hiroshima
and Nagasaki atomic bombs, the firefighters that first responded after the Chernobyl
Nuclear Power Plant event in 1986, and some unintentional exposures to sterilization
irradiators.
The required conditions for Acute Radiation Syndrome (ARS) are:
• The radiation dose must be large (i.e., greater than 0.7 Gray (Gy) or 70
rads).
• Mild symptoms may be observed with doses as low as 0.3 Gy or 30 rads.
• The dose usually must be external (i.e., the source of radiation is outside
of the patient’s body).
• Radioactive materials deposited inside the body have produced some
ARS effects only in extremely rare cases.
• The radiation must be penetrating (i.e. able to reach the internal organs).
• High energy X-rays, gamma rays, and neutrons are penetrating
radiations.
• The entire body (or a significant portion of it) must have received the
dose.
• Most radiation injuries are local, frequently involving the hands, and these
local injuries seldom cause classical signs of ARS.
• The dose must have been delivered in a short time (usually a matter of
minutes).
• Fractionated doses are often used in radiation therapy. These are large
total doses delivered in small daily amounts over a period of time. Fractionated doses
are less effective at inducing ARS than a single dose of the same magnitude.
Clinical picture
The exposure to radiation leads to physical manifestation. Those symptômes
appears chronologocaly in four phases:
 Prodromal phase. It is characterise by primary symptômes developement :
 Vomiting and nausea : 10 to 50 % of people present this sign two
hours or more after the exposure.
 Slight headache
 Diarrhea and abdominal pain.
 Eye burning.
 Fever.
The symptoms occur from minutes to days following exposure. The symptoms
may last for minutes up to several days.
 Latent phase. In this phase, the patient looks and feels generally healthy
for a few hours or even up to a few weeks. During this time the mature cells are
progrssively replaced by impaired cells.
 Manifest illness phase. In this phase the symptoms depend on the
specific syndromes and last from hours up to several months. The third phase is called
critical phase. It begins about 30 days after the prodrome and it’s duration depends on
dose and underlying host factors. The three classic ARS Syndromes are:
1. Hematopoietic (0.25 to 10 Gy). This syndrome is marked by a drop in the
number of blood cells, called aplastic anemia. This may result in infections due to low
white blood cells, bleeding due to low platelets, and anemia due to low red blood cells.
These changes can be detected by blood tests after receiving a whole-body acute dose
as low as 0.25 Gy, though they might never be felt by the patient if the dose is below

73
1 Gy. Conventional trauma and burns resulting from a bomb blast are complicated by
the poor wound healing caused by hematopoietic syndrome, increasing mortality.
2. Gastrointestinal. This syndrome often follows absorbed doses of 6–30
Gy (600–3000 rad). Nausea, vomiting,loss of appetite, and abdominal pain are usually
seen within two hours. Vomiting in this time-frame is a marker for whole body
exposures that are in the fatal range above 4 Gy. Without exotic treatment such as
bone marrow transplant, death with this dose is common. The death is generally more
due to infection than gastrointestinal dysfunction.
3. Neurovascular. This syndrome typically occurs at absorbed doses
greater than 30 Gy (3000 rad), though it may occur at 10 Gy (1000 rad). It presents
with neurological symptoms such as dizziness, headache, or decreased level of
consciousness, occurring within minutes to a few hours, and with an absence of
vomiting. It is invariably fatal.
4. Cutaneous radiation syndrome. Within a few hours after irradiation, a
transien redness (associated with itching) can occur. After the prodromal phase
blistering and ulceration of the irradiate site are visible. This phenomenon could be
reversible (scar formation) or leads to necrosis. Hyperpigmentation, dry
desquamtation, burns are commonly observed.
 Recovery or death. The fourth and last phase is called recovery or death
phase according to the current events. Sometimes Stem cells could recovers their
function leeding to a proliferative response. Even after recovering a life treatement is
necessary.

Relatively to the doses the manifestation are differents. Those scale show the
response and the manifestation function to the dose.

1-2 GRAY

2-4 GRAY

4-6 GRAY

74
 Exposure (Gy)
Phase Symptom
1–2Gy 2–6Gy 6–8Gy 8–30Gy >30Gy
Nausea and 5–50% 50–100% 75–100% 90–100% 100%
vomiting
Time of onset 2–6h 1–2h 10–60 min < 10 min Minutes
Duration < 24h 24–48h < 48h < 48h patients die in <
48h
Diarrhea None None to Heavy Heavy Heavy
mild (<10%) (>10%) (>95%) (100%)
Time of onset — 3–8h 1–3h < 1h < 1h
Headache Slight Mild to Moderate Severe Severe
Prodromal moderate (80%) (80–90%) (100%)
(50%)
Time of onset — 4–24h 3–4h 1–2h < 1h
Fever None Moderate Moderate to Severe Severe
increase severe (100%) (100%)
(10-100%) (100%)
Time of onset — 1–3h < 1h < 1h < 1h
CNS function No Cognitive Cognitive Rapid Seizures, Tremo
impairmen impairment impairment > incapacitat r,Ataxia,Letharg
t 6–20 h 24h ion y

28–31 7–28 days < 7 days none None

Latent
days
Mild to Moderate to Severe Nausea patients die in <
moderate severe Vomiting 48h
Leukopenia Severe
Leukopeni Leukopenia High fever diarrhea
a Purpura Diarrhea High fever
Fatigue Hemorrhag Vomiting Electrolyte
Illness
Weakness e Dizziness disturbanc
Infections Disorientatio e
Epilation n Shock
Hypotension
Electrolyte
disturbance
Without care 0–5% 5–100% 95–100% 100% 100%
With care 0–5% 5–50% 50–100% 100% 100%
Mortality
Death 6–8 wks 4–6 wks 2–4 wks 2 days– 1–2 days
2 wks

75
Diagnosis
The diagnosis of ARS can be difficult to make because ARS causes no unique
disease. Also, depending on the dose, the prodromal stage may not occur for hours or
days after exposure, or the patient may already be in the latent stage by the time they
receive treatment, in which case the patient may appear and feel well when first
assessed.
If a patient received more than 0.05 Gy (5 rads) and three or four CBCs
(complete blood count) are taken within 8 to 12 hours of the exposure, a quick estimate
of the dose can be made. If these initial blood counts are not taken, the dose can still
be estimated by using CBC results over the first few days. It would be best to have
radiation dosimetrists conduct the dose assessment, if possible.
If a patient is known to have been or suspected of having been exposed to a
large radiation dose, draw blood for CBC analysis with special attention to the
lymphocyte count, every 2 to 3 hours during the first 8 hours after exposure (and every
4 to 6 hours for the next 2 days). Observe the patient during this time for symptoms
and consult with radiation experts before ruling out ARS.
If no radiation exposure is initially suspected, you may consider ARS in the
differential diagnosis if a history exists of nausea and vomiting that is unexplained by
other causes. Other indications are bleeding, epilation, or white blood count (WBC)
and platelet counts abnormally low a few days or weeks after unexplained nausea and
vomiting. Again, consider CBC and chromosome analysis and consultation with
radiation experts to confirm diagnosis.
Treatment and Diagnostic Evaluation
Treat vomiting, and repeat CBC analysis, with special attention to the
lymphocyte count, every 2 to 3 hours for the first 8 to 12 hours following exposure (and
every 4 to 6 hours for the following 2 or 3 days). Precisely record all clinical symptoms,
particularly nausea, vomiting, diarrhea, and itching, reddening or blistering of the skin.
Be sure to include time of onset.
Note and record areas of erythema. If possible, take color photographs of
suspected radiation skin damage. Consider tissue, blood typing, and initiating viral
prophylaxis. Promptly consult with radiation, hematology, and radiotherapy experts
about dosimetry, prognosis, and treatment options. Call the Radiation Emergency
Assistance Center/Training Site (REAC/TS) at (865) 576-3131 (M-F, 8 am to 4:30 am
EST) or (865) 576-1005 (after hours) to record the incident in the Radiation Accident
Registry System.
After consultation, begin the following:
1. In giving medical care and treatment to patients with the ARS, we first,
must wash and clean the skin of the contaminated person, from radiation dust and ask
him/her to wear clean clothes. We, then, must clean any injuries using warm water and
soap and then disinfectant, in order to clean and also lower the radiation emitted from
these injuries till twice above background. Note that injuries that have already been
healed are sensitive to reoccur even after years.
2. Prevention and treatment of infections. Antibiotics should be given against
both aerobic and anaerobic bacteria.
3. Stimulation of hematopoiesis by use of growth factors or factors for
regenerating granulocytes.
4. Stem cell transfusions, red blood cells or platelet transfusions.
5. Psychological support.
6. Careful observation for erythema, hair loss, skin injury, weight loss, or
fever.

76
 7. Confirmation of initial dose estimate using chromosome aberration
cytogenetic bioassay when possible. Although resource intensive, this is the best
method of dose assessment following acute exposures.
8. Consultation with experts in radiation accident management.
9. For all the above mentioned forms of ARS, we also use symptomatic
treatment with anti-emetics, painkillers and antidiarrheal drugs.
It is considered that the overall condition of patients who received either smaller
doses (1-2Gy) or very high doses (8-12Gy) of radiation shall not change much, after
medical care and treatment. This is because the small doses group of patients has a
0%-5% chance of fatal results within the next 2 months, while in the higher doses group
all patients are expected to die within the next 14 days. For patients who received the
intermediate level of doses (between 2-8Gy), medical treatment may increase survival
by 50%. Not to forget that in this intermediate group of patients death may also appear
in 5% of the cases, unrelated to medical treatment. It has also been reported that
without medical care 50% of patients who received more than 4Gy shall die within the
next 30 days.
Epidemiology
The most important causes of acute radiation symdrome in the history was
probably due to human disasters. Hiroshama and Nagasaki, Tchernobyl and currently
Fukushima are probably the most well known.
In the case of Tchernobyl the casualties were particullary hight indeed on the
500 000 liquidator who worked in Tchernobyl to stop the catastroph 20 000 are already
dead and 200 000 are incapacited. However in Tchernobyl the worst enemy was not
the radiation but the lack information. Indeed officially during 20 years only 56 death
are attribut to Tchernobyl.

CHRONIC RADIATION SYNDROME

Definition
Chronic radiation syndrome or chronic radiation sckness follows after small
radiation doses that may be repeated. Furthermore, doses from a flux of radiation
greater or about 0.1Gy/h or from an accident during radiotherapy or during a sun
explosure emitting radiation, received by astronauts during an interplanetary voyage
or absorbed doses from radioactive waste or from accidental misuse of
radiopharmaceuticals in medicine may cause CRS.
The severity and time of occurrence of pathological changes in the affected
organs and their systems, which is caused mostly by the nature of radiation, which can
be both general and local, total radiation dose, its type and intensity, as well as the
physiological characteristics of the structure and function of an organ. Chronic radiation
sickness is characterized by the duration and undulating current, due to a combination
of progressive deterioration effects distinct restorative and adaptive responses.
Clinical picture
In the course of chronic radiation sickness distinguished three periods: the
formation of the disease, the recovery period and the consequences and outcomes of
chronic radiation sickness.
With increasing doses, and, depending on individual characteristics of the
organism the development of clinical manifestations can be mild (I) moderate (II)
severe (III) and very severe (IV), which are essentially phases in the development of a

77
single pathologic process, and with continued irradiation at sufficiently high doses,
sequentially replace each other.
Fabric and patterns, having a large pool of relatively immature cells, intensively
exchanging your cellular structure under physiological conditions (the epithelium of the
skin, intestine, hematopoietic tissue, the seminiferous epithelium), long-lasting
capabilities of the morphological reconstruction.
Developing changes in the circulatory system can be described as a syndrome
of vegetative-vascular dysfunction or neurocirculatory dystonia. He expressed total
and regional (in the retina and the cerebral vessels) arterial hypotension, mild
bradycardia, rapid high reflex response to clino-orthostatic load. Typical for the
expanded clinic chronic radiation sickness are not common, and regional violations of
peripheral blood circulation in the skin, extremities, and less frequently the brain,
manifested in the form of headaches, pains in the limbs, increased chill, General
weakness, sometimes transient neurological symptoms. Changes in cardiac activity
are characterized by mild pronounced symptoms of cardiomyopathy.
Upon irradiation in the range of total doses of 0.7-1.5 Gy with minor changes
from the digestive tract for a long time not accompanied by any subjective or objective
indigestion. When the total radiation doses exceeding 1.5-4 Gy, reduced secretory
activity of the glands of the mouth, occur slightly marked focal atrophic processes in
the mucous membrane of the mouth and gastrointestinal tract.
Functional changes of the nervous system in preclinical stage of the disease,
corresponding to the total dose level in the range of 0.15 to 0.7 Gy, are of a reflex
nature and often accompanied by involvement in the response of the endocrine and
cardiovascular systems.
With increasing total doses and irradiation intensity can distinguish three
consistently developing neurological syndrome of chronic radiation sickness.
Primarily refers to a syndrome of disorders it viscerally regulation observed with
an increase in total dose to 0,7-1,5 Gy. It is characterized by an asymmetric increase
of the tendon and decrease cutaneous reflexes, transient vestibular disorders. Patients
complain of fatigue, headaches, pain in the extremities, dizziness, sweating.
For asthenic syndrome (when the total dose of 1.5-4 Gy) characterized by
general hypotonia, impaired physiological distribution of tone, light, impaired
coordination, decreased cutaneous reflexes, sensitivity disorders (generalized
reactions to spontaneous pain and pain stimulation).
The third syndrome of organic lesions of the nervous system is developing at
high doses (more than 4 Gy in total, 10-15 Gy local irradiation). In these cases, there
are symptoms common to varying the location and nature of the pathological process
(ischemia, hemorrhage, cyst, necrotic area).
Minor changes in the morphological composition of peripheral blood detected in
patients who received the maximum allowable dose and exceeding them periodically
2-3 times. They are expressed in terms of transient leukopenia, thrombocytopenia,
retikulocitoza.
The sequence of changes in the blood system when the doses of 0.001-0.1 Gy
per day is characterized by typical dynamics. During the formation of chronic radiation
sickness reveals a growing cytopenia due to the reduction in the number of neutrophils,
lymphocytes, and later, and platelets. The appearance of anemia is always a bad
prognostic sign and is observed only at high cumulative doses of intense exposure.
Information about the state of the endocrine areas with chronic exposure to
small. The development of persistent irreversible male sterility occurs only in patients
who underwent radiation therapy with a local dose to the testes in 30-40 Gy. Women

78
subjected to overall irradiation in total doses up to 4 Gy, revealed no discernible shift
in time of the onset of menopause, as well as in the quantity and for pregnancies,
childbirth.
When I degree of severity observed expressed mild neuro-regulatory
disturbances of various organs and systems, especially cardiovascular, unstable and,
moreover, reasonable leykosytopeniya, rarely thrombocytopenia.
When the severity of the II degree show signs of functional insufficiency,
especially of the digestive glands, cardiovascular and nervous systems, as well as
depression of hematopoiesis with the presence of persistent leukocyte and
thrombocytopenia, metabolic disorders.
When the severity of the III degree revealed signs of a more profound bone
marrow suppression with anemia, found atrophic processes in the mucosa of the
gastrointestinal tract, as well as myocardial dystrophy, multiple entsefalomielit.
Weakening of immunity entails infectious and septic complications. Observed
hemorrhagic syndrome, circulatory disorders.
In chronic radiation sickness IV degree of observed diarrhea, pronounced
depletion. Due to the fact that such manifestations of the disease currently meet the
selection in classification IV (very severe) degree is conditional.
Treatment
Treatment of chronic radiation sickness based on the termination of contact with
sources of radiation.
When I and II degrees of severity of the disease is systemic and symptomatic
drug therapy (tonics, vitamin therapy, tranquilizers, drugs bromine, hypnotics),
physiotherapy, medical gymnastics, rational psychotherapy.
With the development of infectious and septic complications are broad-spectrum
antibiotics.
Special attention deserves the so-called radiation sickness from internal
exposure, which develops by ingestion of radioisotopes inside the body and has its
own distinctive features. On the basis of the causal principle of its formation are
distinguished polonium, radium, plutonium disease. Radioactive substances can enter
the body by inhalation through the respiratory tract, through the gastro-intestinal tract
(food and water), and through the skin, especially damaged.
Mainly radiation sickness from internal exposure is a chronic disease, although
when hit in a short period of time large quantities of radioisotopes, particularly able to
be distributed more evenly, may occur and acute radiation syndrome.
Clinical manifestations of radiation sickness from internal irradiation are formed
of the common symptoms and organ damage predominant intake of radioactive
substances, their deposition and excretion. So, in inhalation poisoning is dominated by
the defeat of the bronchi and lungs, in the gastro-intestinal - disorders of the digestive
tract. Hematopoietic tissue is usually involved in the process, as the majority of
radioactive substances or relatively evenly distributed in the body, causing its total
exposure, or is deposited in the bones, lymphoid, histiocytic tissue. Other substances
are deposited mainly in the liver, kidney, spleen.
To accelerate the elimination of natural and artificial radioactive isotopes from
the body have been offered drugs Ca2, hormones, vitamins, agents that stimulate
metabolic processes, chelating agents. However, in General, the problem of removal
from the body of radioisotopes cannot be considered to be finally resolved, as many of
the recommended tools are serious complications, the most significant of which are
associated with kidney damage.

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 CUTANEOUS RADIATION INJURY

Definition
Injury to the skin and underlying tissues from acute exposure to a large external
dose of radiation is referred to as cutaneous radiation injury (CRI). Acute radiation
syndrome (ARS) will usually be accompanied by some skin damage; however, CRI
can occur without symptoms of ARS. This is especially true with acute exposures to
beta radiation or low-energy x-rays, because beta radiation and low-energy x-rays are
less penetrating and less likely to damage internal organs than gamma radiation is.
CRI can occur with radiation doses as low as 2 Gy or 200 rads and the severity of CRI
symptoms will increase with increasing doses.
Early signs and symptoms of CRI are itching, tingling, or a transient erythema
or edema without a history of exposure to heat or caustic chemicals. Exposure to
radiation can damage the basal cell layer of the skin and result in inflammation,
erythema, and dry or moist desquamation. In addition, radiation damage to hair follicles
can cause epilation. Transient and inconsistent erythema (associated with itching) can
occur within a few hours of exposure and be followed by a latent, symptom-free phase
lasting from a few days to several weeks. After the latent phase, intense reddening,
blistering, and ulceration of the irradiated site are visible. Depending on the radiation
dose, a third and even fourth wave of erythema are possible over the ensuing months
or possibly years.
In most cases, healing occurs by regenerative means; however, large radiation
doses to the skin can cause permanent hair loss, damaged sebaceous and sweat
glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or
necrosis of the exposed tissue.
With CRI, it is important to keep the following things in mind:
• The visible skin effects depend on the magnitude of the dose as well as
the depth of penetration of the radiation.
• Unlike the skin lesions caused by chemical or thermal damage, the
lesions caused by radiation exposures do not appear for hours to days
following exposure, and burns and other skin effects tend to appear in
cycles.
• The key treatment issues with CRI are infection and pain management.
Clinical picture
CRI will progress over time in stages and can be categorized by grade, with
characteristics of the stages varying by grade of injury.
Prodromal stage (within hours of exposure). This stage is characterized by early
erythema (first wave of erythema), heat sensations, and itching that define the
exposure area. The duration of this stage is from 1 to 2 days.
Latent stage (1–2 days postexposure). No injury is evident. Depending on the body
part, the larger the dose, the shorter this period will last. The skin of the face, chest,
and neck will have a shorter latent stage than will the skin of the palms of the hands or
the soles of the feet.
Manifest illness stage (days to weeks postexposure). The basal layer is repopulated
through proliferation of surviving clonogenic cells. This stage begins with main
erythema (second wave), a sense of heat, and slight edema, which are often
accompanied by increased pigmentation. The symptoms that follow vary from dry
desquamation or ulceration to necrosis, depending on the severity of the CRI.
Third wave of erythema (10–16 weeks postexposure, especially after beta exposure).
The exposed person experiences late erythema, injury to blood vessels, edema, and

80
increasing pain. A distinct bluish color of the skin can be observed. Epilation may
subside, but new ulcers, dermal necrosis, and dermal atrophy (and thinning of the
dermis layer) are possible.
Late effects (months to years postexposure; threshold dose ~10 Gy or 1000 rads).
Symptoms can vary from slight dermal atrophy (or thinning of dermis layer) to constant
ulcer recurrence, dermal necrosis, and deformity. Possible effects include occlusion of
small blood vessels with subsequent disturbances in the blood supply; destruction of
the lymphatic network; regional lymphostasis; and increasing invasive fibrosis,
keratosis, vasculitis, and subcutaneous sclerosis of the connective tissue. Pigmentary
changes and pain are often present. Skin cancer is possible in subsequent years.
Recovery (months to years).
Diagnosis
The signs and symptoms of CRI are as follows:
• Intensely painful burn-like skin injuries (including itching, tingling,
erythema, or edema) without a history of exposure to heat or caustic chemicals. Note:
Erythema will not be seen for hours to days following exposure, and its appearance is
cyclic.
• Epilation
• A tendency to bleed
• Possible signs and symptoms of ARS
As mentioned previously, local injuries to the skin from acute radiation exposure
evolve slowly over time, and symptoms may not manifest for days to weeks after
exposure. Consider CRI in the differential diagnosis if the patient presents with a skin
lesion without a history of chemical or thermal burn, insect bite, or skin disease or
allergy. If the patient gives a history of possible radiation exposure (such as from a
radiography source, x-ray device, or accelerator) or a history of finding and handling
an unknown metallic object, note the presence of any of the following: erythema,
blistering, dry or wet desquamation, epilation, ulceration.
Treatment
Prodromal Stage. Use antihistamines and topical antipruriginous preparations,
which act against itch and also might prevent or attenuate initiation of the cycle that
leads to the manifestation stage. Anti-inflammatory medications such as
corticosteroids and topical creams, as well as slight sedatives, may prove useful.
Latent Stage. Continue anti-inflammatory medications and sedatives. At
midstage, use proteolysis inhibitors.
Manifestation Stage. Use repeated swabs, antibiotic prophylaxis, and anti-
inflammatory medications, to reduce bacterial, fungal, and viral infections
• Apply topical ointments containing corticosteroids along with locally
acting antibiotics and vitamins.
• Stimulate regeneration of DNA and later, when regeneration has started,
biogenic drugs.
• Stimulate blood supply in third or fourth week.
• Puncture blisters if they are sterile, but do not remove them as long as
they are intact.
• Treat pain according to the individual patient's condition. Pain relief is
very difficult and is the most demanding part of the therapeutic process.
• Debride areas of necrosis thoroughly but cautiously.

81
 EXOGENIC INTOXICATION. BASIC TERMS IN TOXICOLOGY. FACTORS
DETERMINING THE COURSE OF ACUTE INTOXICATION. CLASSIFICATION OF
POISONS AND TYPES OF POISONING

Toxicology is the study of the harmful effects of chemical substances on living

organisms. The subject field of toxicology are the laws of interaction between living
organisms and poisons. It studies the changes which the toxic factors cause on tissue,
cell and molecule level.
The main objectives of toxicology are the following:
 To reveal and define the toxic properties of chemical substances which
can cause pathological changes in living organisms.
 To study the necessary conditions for the appearance, manifestation and
disappearance of the toxic properties of chemical substances.
 To study the clinical and pathomorphological symptoms of poisoning in
different ways of poison intake into an organism. The toxic effect is measured my
means of functional and structural changes in bodily organs and systems.
Presently we can identify three main areas of development in toxicology:
theoretical (experimental); preventive (hygienic) and clinical.
Toxicodynamics studies the mechanisms through which a certain poison affects
the organism. The subject field of toxicokinetetics are the biotransformations of a
particular poison in the organism, the access ways, distribution mechanisms and
mechanisms of taking the poison out of the body.

I. Basic Terms in Toxicology

1. Poison (toxic / poisonous substance). It is any chemical substance,
introduced into the organism in quantities which can cause disruption to life supporting
bodily functions and thus threaten life. As early as in XVI century Paracelsus noted that
all substances are poisonous and there are no such substances which are not
poisonous. It is the dose that differentiates medicine from poison (the dose makes the
poison).

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 2. Toxicity. It is the property substances have to cause pathological changes in
the living organisms, when introduces in certain quantities. It is measured by means of
the values of toxic dose (concentration) and lethal dose (concentration).
Toxic dose (concentration) is the smallest quantity of a substance per kilogram
of bodyweight (milligram per cubic meter of air, respectively) which causes pathological
changes in living organisms.
Lethal dose (concentration) is the smallest quantity of substance per kilogram
of bodyweight (milligram per cubic meter of air, respectively) which causes death to
animals in laboratory experiments. In experimental toxicology the widely-used toxicity
measurements are LD50 (CD50) – the average lethal dose or concentration and
LD100 (СD100) – the absolute lethal dose, or concentration respectively.
The smaller the quantity (the dose) causing disruption of physiological functions,
the higher the toxicity of a particular substance.
3. Poisoning (Intoxication). It is a pathological condition, developed as a result
of the interaction between the poison and the organism.
The biological effects of different toxic chemical compounds vary widely. Acute
poisoning occurs at single exposure to high dose levels. Prolonged absorption of small
quantities of a poisonous substance causes chronic poisoning.
In a large number of acute intoxication cases different degrees and severity
values are observed: minor; moderate and severe intoxication. Exposure to very high
doses (concentration) causes instant poisoning, which can, in many cases, be fatal:
fudroyant (instant, severe acute) type of poisoning.
It is known that some poisonous chemical compounds cause impairment of
different nature, depending on the manner of administration – single or multiple intake.
For example the acute benzene intoxication primarily relate to central nervous system
depression, while chronic benzene exposure is associated with impairment of the
haemopoietic system.
Delayed effects occur in cases of small quantity intake of poisonous substances.
Gonad-toxic; embryo-toxic; mutagenic and carcinogenic effects are observed. A lot of
chemical agents can act as antigens and thus cause allergic reactions.
Continuous intake of some chemical substances, such as morphine; arsenic;
organic solvents, etc. do not cause noticeable or clinically compatible changes in the
organism. This phenomenon is known as acquired poison tolerance and today is
viewed as a stage of chronic intoxication.
4. Cumulation
Cumulation is the property of chemical substances to increase their toxic effects
on living organisms in consecutive exposure. It can be material: accumulation of the
chemical substance in tissues, or functional: accumulation of the toxic effects of the
substance. The quantity of cumulation is measured by means of the value of
cumulation quotient:
 below 1 – excessive cumulation;
 from 1 to 3 – noticeable cumulation;
 from 3 to 5 – moderate cumulation;
 over 5 – slightly notice cumulation.
II. Characteristics of the Factors Determining the Course of Acute
Poisoning:
1. Type and dose of the poison: the type of the poison is determined by its
physical and chemical properties and by its origin.
This criterion has also been used as the basis of one of the toxic substances
classifications, according to which they fall into the categories of inorganic or organic

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substances; toxic gases; medicines with dose-dependent toxic properties; plant and
animal poisons (venoms), etc.
Of great importance to toxicology are the values of toxic and lethal doses, which
are different for the different chemical substances and depend on the type of poisonous
substance, the conditions of the case of poisoning and peculiarities of the organism.
2. Exposure Conditions – the ambient environment where the exposure
occurred. Based on that factor we distinguish the following types of intoxication:
Workplace intoxications – they occur in industrial factories; in agriculture; test
laboratories. The toxic agent which causes the intoxication is a chemical substance
which is used in the process of production or is a sub-product or an end-product of that
substance.
Domestic intoxications – they occur in household environment; restaurants and
cafes; during relaxation outdoors activities or when travelling. The most common type
of intoxication, occurring in such conditions are food and alcohol poisoning; poisoning
caused by plant and animal toxins or by organic solvents.
Medication intoxications – they occur when the intake of medicinal substances
reaches toxic or lethal doses, in the course of therapy or with suicidal intentions.
Environmental intoxications – these are intoxications caused by poisons of
various physical and chemical properties, which are present in the environment we live
in.
3. Peculiarities of different organisms – they are responsible for the
manifestation of intoxication symptoms in a particular organism.
The factors which are of great importance are: sex; age; general health
condition of the organism /fatigue; cold; quantity of food intake; exhaustion, etc./; the
metabolic rate; past and current illnesses.
The interaction of the above mentioned factors determines the clinical
characteristics of each particular case of intoxication, forming two main tendencies:
1. Increased damaging effects of toxic agents - observed in exposure to
highly toxic agents; when the people exposed are in a vulnerable health condition
/especially in children and elderly people/; in the presence of concomitant illnesses or
in cases of decreased common and immune resistance. In such cases the value of the
toxic and lethal doses of a particular poison can be considerably lower than the officially
determined ones and substances of weaker toxic properties may reveal much stronger
toxic aggression.
2. Uncommon, atypical course of intoxication – observed in contact of a
person with a toxic agent in specific conditions regarding the intoxication determining
factors, such as: type of poison; time of exposure; preceding and accompanying
changes in the organism. Such is the case, for example, with allergic patients.
III. Toxic Hazard of Chemical Substances in Emergency Situations
The toxic hazard of chemical substances is determined by the Marshall method.
The assessment is made using the following criteria:
 Dispersal capacity – it determines the speed of poisoning. Gases like
chorine and ammonia have strong dispersal capacity;
 Stability of the toxic substance;
 Frequency of usage /application/ - toxic chemicals of frequent and wide
application in industrial production and other fields of business activity have a higher
degree of toxic hazard than chemicals of limited application;
 Toxicity;
 Penetration capacity;
 Presence of delayed effects;

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  Ratio of the number of affected to the number of dead persons.
The above mentioned criteria are assessed in the following way: up to 8 points
are given for degree of toxicity; up to 4 points – for degree of application and up to 2
points for the remaining criteria.
The Marshall method is used to make a quantitative analysis of the toxic hazard
of chemicals.
IV. Classification of toxic substances which are of importance to disaster
medicine
Numerous classifications have been created, based on different principles:
 by chemical structure of toxic substances;
 by characteristics of the biological effect of a toxic substance and clinical
manifestation of poisoning;
 by degree of toxicity.
Of greatest importance to disaster medicine is the toxicological classification,
according to which the toxic substances, which can have a disastrous effect in
emergency situations fall into the following main groups:

TOXICOKINETICS OF POISONOUS SUBSTANCES IN EXOGENOUS POISONING

Toxicokinetics in exogenous poisoning reflects the interaction between the toxic

substance and the organism. It consists of two types of phenomena:
 Movement and metabolism of the toxic agent /route of administration and
distribution, biotransformation and elimination/;
 Changes in the organism caused by the poison and its metabolites;

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 Toxicokinetics consists of three stages:
 initial /absorption/;
 haematogenous;
 organ and cell absorption stage.
During these stages of movement of the poison in the body, the interaction of
the toxic substance and the organism is determined by the physical and chemical
properties of the substance and the permeability of the cell membranes. The main
mechanisms of interaction between the toxic substance and the organism are
absorption, transportation, distribution, metabolism, biotransformation and elimination
mechanisms.
I. Initial absorption stage
Тhis is the stage of poison intake into the organism via a particular site of toxic
application. Possible sites of toxic application are:
 the gastro-intestinal system – mainly through the mouth;
 the respiratory system – through the nasal ligament and the respiratory
tract ligament;
 the skin – intact, damaged or wounded surface;
 the conjunctivas – for liquid and gaseous poisons
 the bladder – in instillation of toxic medication;
 the genital ligament in women – in cases of voluntary termination of
pregnancy attempts with toxic substances;
 parenteral site of application – in cases of poisonous animals biting or
stinging, poisonous plant prickles injuries or by injection.
1. Absorption in the gastrointestinal tract, determined by the following
factors:
 Chemical and physical properties of the poison: the lipotropic substances
and the substances which have acidic properties are better absorbed in the stomach,
while the substances of weak alkaline properties are weaker absorbents. In the
intestinal tract it is the other way round. The main mechanism of infiltration of the
poison from the gastrointestinal tract into the blood is simple diffusion, due to which,
non-ionised substances are easier to infiltrate.
 The dose of the poison intake;
 The chemical reaction with the digestion and intestinal fluid;
 The presence of food in the stomach and in the intestines – it slows down
the absorption of the poison or changes its properties;
 Stomach and intestinal wall tonus and intestinal peristalsis: increased
peristalsis, accompanied by vomiting and diarrhoea reduces absorption;
gastrointestinal paresis, accompanied by atony of intestinal walls leads to increased
absorption;
 Permeability of gastrointestinal epithelium;
 Changes in the blood circulation of the gastrointestinal ligament: in
hyperemia and increased blood flow, absorption increases, whereas under shock
conditions, absorption decreases.
2. Respiratory system absorption. It depends on the following factors:
 Physical and chemical properties of the poison: depending on them, there
are two routs of administration of the poison in blood:
 through the ligament of the respiratory tract – it lets through poisons,
which come into contact with trachea secretions and form new chemical compounds,
which pass through the ligament epithelium;

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  through the alveoli walls – they let through chemically neutral toxic
gases in an unchanged state, which after reaching a particular level of saturation in the
alveoli, penetrate through the alveoli epithelium and into the capillary walls by the laws
of osmosis and diffusion.
 Concentration of the toxic substance in the air inhaled – high
concentration suggests increased absorption;
 Volume and intensity of breathing during exposure to toxic gases
/intensive breathing causes increased penetration of the poison from alveolar air
content into the blood/;
 Dispersion properties of toxic gases – they have the capacity to react with
the water content, the proteins and the alkaline elements of the respiratory tract
ligament , thus forming new chemical substances, which act as new agents /for
example in chlorine poisoning, hydrochloric acid is formed/.
3. Absorption through the skin. It depends on the following factors:
 Lipotropic properties and level of ionisation of the poison – poisons with
lipotropic properties and low level of ionisation penetrate epidermal and dermal cells
more intensively, after which they are retained in the subcutaneous fat deposits. Due
to the low vascularisation of those depots the poison slowly moves through the
vascular walls into the blood and thus stays in the fat depots for a long time;
 Volume of subcutaneous fat deposits – in overweight people larger
quantity of the toxic substance is retained in the subcutaneous fat deposits, which
results in a slower process of intoxication;
 Vascularisation of the contact skin area – skin areas which are better
vascularised permeate the poison quicker /the scalp and areas which are
haemorrhagic due to mechanical friction/;
4. Absorption through Ligaments. Toxic substances are absorbed through
the ligament of the vagina, the uterus or the rectum when applied there for medical
purposes or abortion for example. The level of absorption is high due to the good blood
supply of the ligament.
II. Haematogenic stage
It refers to the time the poison stays in the blood and the lymph. During that
stage transition of the poison from the point of administration to humoral environment
takes place, i.e. that stage covers the interaction of the poison with the blood.
Two main processes take place during that stage:
 Transportation and distribution of the poison, which are common for all
types of exogenous toxic noxes;
 Haemotoxic effect – specific only for poisons with particular chemical
properties, with affinity for blood components.
Of great importance to transportation and distribution of poisons in the blood is
the way they combine with blood components.
The following combinations are observed:
 A part of the poison infiltrated remains uncombined with plasma proteins.
It is only that free fraction of the poison that can penetrate capillary walls and get further
distributed;
 Another part of the poison combines with plasma proteins into toxic
protein complexes, which cannot penetrate the capillary walls and the cell membranes.
The chemical bond between the poison and the proteins in these complexes is, to a
different extent, of a labile nature and thus likely to dissociate. Each of the exogenous
toxic noxes combines with a particular type of plasma proteins: for example metals

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combine with globulins; medicaments combine with albumins and fat-soluble poisons
– with lipoproteins.
Poison distribution happens in the following ways:
 Part of the free toxic substance moves through the vascular walls into the
extravascular fluid, so that the quantity of free toxic substance outside and inside the
vascular walls equalises.
 Due to the processes of metabolization and elimination of the poison off
the extravascular space, an imbalance occurs. The equilibrium is then restored by
gradual dissociation of the toxico-protein complexes and release of new quantities of
free toxic substance in the blood.
Some exogenous poisons have been found to have a clear haemotoxic effect.
These are chemical substances of particular chemical properties and a clear affinity
for blood components Hb and Er /СО/. The haemotoxic effect completes the
toxicokinetics of the poison which has entered the blood.
During that stage partial biotransformation of the poison also occurs, as well as
transportation to a particular organ and deposition in different places.
III. Organ and cell absorption stage
This is the stage when metabolic processes take place, i.e. biotransformation;
elimination and cumulation of the exogenous toxic noxes.
The poison transfers from the humoral environment into a particular organ, to
which it shows selective toxicity. It combines with particular parts of the lipoprotein cell
membrane, forming complexes, after which it penetrates into the cell.
In this way imbalance between the quantity of uncombined with serum proteins
poison in the intra- and extra-vascular space occurs, which leads to the degradation of
more toxico-protein complexes in the capillaries. New quantities of poison which is not
combined with plasma proteins is produced. It transfers into the extra-vascular space
and thus leads to further severer damage to organ structures and the organism as a
whole.
During that stage 3 types of processes take place:
 harmful impact processes /toxicodynamics of poisonous substances/;
 biotransformation processes;
 elimination processes.
Toxicodynamics includes different mechanisms of manifestation of the adverse
effects of the poison on the level of affected organ and the effect on the function of the
organism as a whole. Different poisons have different mechanisms of adverse effects
but, in general, the intracellular toxic aggression is due to:
 fixation of the toxic nox to the chemo-receptors of the enzyme groups or
other cytoplasm components and interacting with them;
 breaking of the membranes of cell organelles / mitochondria; lysosomes,
etc/;
 disruption of protein synthesis in the ribosomes;
 disruption of ATP synthesis.
The cell is one of the main spaces where poisons and their metabolites’
aggression takes place. The toxic effect is exercised on the cell membranes; the
organelles; the nucleus and the cytoplasm. All these changes lead to a disruption of
the normal biochemical status and the physiological functions of the cell. Cell
termination is the end-result of chemical damage, whereas tissue damage varies
considerably. It depends on the type of tissue and on the severity of damage
/epithelium tissue and liver tissue have substantial regeneration potential, whereas

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neural tissue has no regeneration properties/. Some chemical effects are revealed in
genetic defects in somatic cells.
Biotransformation of exogenous poisons – a number of processes through
which the exogenous noxes are subjected to chemical changes in the living organism.
The molecule of the metabolites thus formed substantially differ from the starting
substance. The purpose is for the xenobiotics, which have entered the organism, to be
transformed into more hydrophillic metabolites whose capacity to penetrate biological
membranes has been reduced. As a result, their sedimentation in tissues is also
reduced, whereas their excretion in urine and through the intestines is increased.
Only a small number of xenobiotics cannot be transformed, among them noble
gases; strong acids and alkalis, etc., whereas there are chemical substances /aliphatic
alcohols/ which, in the organism, can fully degrade to metabolic end products: water
and carbon dioxide.
There are two types of biotransformation:
 Spontaneous: consisting of spontaneous degradation of the exogenous
nox in physiological conditions. A small number of xenobiotics metabolise
in this way;
 Enzymatic: catalised by different enzymes.
The main phase of biotransformation takes place in specialised cell structures,
as of particular importance are the hepatocytes in the liver, but it can also take place
in other organs as well /kidneys; lungs, intestines/.
Biotransformation decreases the toxic properties of poisons. That is why the
enzymes which are involved in the process are called detoxification enzymes /they
transform exogenous poisons into less harmful metabolites/. Nevertheless, the so
called “lethal synthesis” is also possible, the result of which are metabolic products
which are more toxic than the initial chemical compounds /for example methyl alcohol
metabolizes to the highly toxic formaldehyde and formic acid/.
Enzymatic biotransformation has two phases:
 The first phase includes the chemical reactions of oxidation; reduction
and hydrolysis, during which functional groups are attached to the poison molecule;
 The second phase of biotransformation includes mainly reactions of
conjugation. These are biosynthesis reactions, which need energy consumption. The
enzymes which are involved in the reactions are transferases – they transfer activated
metabolic remains onto the xenobiotic molecule. Conjugation reactions fall into two
groups:
- the first one includes glucuronidation; sulphitation; methylation and
acetylation;
- the second one includes hypuric acid and ornithine synthesis, as well
as glutamine conjugation.
Elimination of exogenous poisons and their metabilites – it is mainly carried out
through the kidney structures and, to a small extent, through the lungs, the
gastrointestinal tract and some other structures in the organism.
 Elimination through the kidneys – done through two types of processes:
 Osmosis and diffusion, which are possible due to the different
concentration levels of the toxic nox in the blood running in the kidney blood vessels
and in the urine contained in the respective nephron structures;
 Elimination made possible by the enzyme systems in the nephron
cell;

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  Elimination through the lungs – mainly toxic substances and their volatile
gas metabolites which remain free in the blood, such as alcohols, are eliminated in that
way. Through the process of diffusion they separate from the alveolar wall because of
the difference in the partial pressure of the poisonous gas in the blood and in the
alveolar air content.
 Elimination through the gastrointestinal tract. It is carried out in two ways:
 The poison and its metabolites are carried over from capillary
blood circulation /via ligament glands and their secretion/ mainly into intestinal lumen
and, to a very small extent, into the stomach;
 passage into the bile, and bile ducts into the intestines;
A part of the poison transmitted is evacuated with the faeces, while another part
gets reabsorbed back in the intestines.
 Other routs of elimination:
 via the skin – in the sweat;
 via the saliva glands – in the saliva;
 via the mammary glands – in breast milk;
 via the placenta, into the fetus – during pregnancy.
Poison cumulation – it refers to the chemical substances’ property to increase
their toxic effect on the organism when administered for a second time. There are two
types of cumulation:
 material – the toxic substance accumulates in particular tissues, forming
depots. This kind of cumulation mainly occurs in the fat tissues, bone marrow, etc.
Under specific conditions the toxic agents contained in those depots enter the
organism causing repeated intoxication /in case of large quantities being released into
the organism/ or damage on particular cell structures and also contribute to the
occurrence of immune components /with smaller quantities being released into the
body/;
 functional – cumulation of the effects of the toxic substance.
The quantity of cumulation is measured by the so called cumulation coefficient:
 under 1 – excessive cumulation;
 from 1 to 3 – clearly expressed cumulation;
 from 3 to 5 – moderate cumulation;
 over 5 – minor cumulation
IV. Recovery Stage
This stage refers to the final elimination of the poison from the body and
restoration of all functional and structural changes. In some cases of poisoning this
stage may continue for months or even years. During this stage, the so called post-
intoxication syndrome can occur, which has different characteristics for each different
type of intoxication, expressed in the functions of the central neural system; the
peripheral neural system; the kidneys; the liver, etc.

MAIN PRINCIPLES OF DIAGNOSTICS AND TREATMENT OF ACUTE

POISONINGS

Acute poisonings are serious medical conditions, which occur suddenly,

develop quickly and have a tendency to deteriorate. It all calls for quick response on
the part of medical professionals, consisting of adequate diagnostic and treatment
procedures.

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 To this end, unified acute intoxication diagnostic and treatment models has been
established.
I. Diagnostic model for acute intoxication
The unified diagnostic programme includes three groups of criteria:
 Criteria for determining acute poisoning;
 Criteria for identifying the type of poisoning;
 Criteria for measuring the severity of damage inflicted.
Acute poisoning diagnostics is built upon three groups of data:
 anamnestic;
 objective tests;
 laboratory tests.
Anamnesis – patients own, their relatives or witnesses’ information about the
patient’s exposure to the toxic agent and the duration of their stay in the toxic
environment.
Objective tests. Main clinical syndromes – determined after a thorough
examination of the patient by means of basic clinical methods:
 Cerebral and neurogenic syndromes – for barbiturate; alcohol; carbon
oxide, etc. intoxications.
 Pulmonary and respiratory syndromes – for phosphorus organic
substances; nitrogen gases; chlorine, etc.
 Cardiovascular syndromes – for extremely severe forms of exogenous
poisonings.
 Gastrointestinal syndromes – for phosphorus organic substances;
cyanides; food and fungi poisonings.
 Haematogenic syndromes – for aminobenzene; nitrobenzene, etc.
poisonings
 Renal syndromes – for mercury; halogenated hydrocarbons, etc.
Laboratory tests /blood; urine; ECG; EEG; EMG; thin-layer chromatography;
gas chromatography; fast result tentative sample tests /.
II. Treatment model for acute poisonings
An unified treatment programme has been developed to include the following
actions:
1. Reanimation:
 Pulmonary resuscitation;
 Cardio-vascular resuscitation;
 Correction and substitution reanimation.
2. Antidote therapy.
3. Detoxification depuration:
 Purification of the entry port:
 skin and ligament;
 gastrointestinal tract;
 respiratory system;
 Purification of the humoral medium:
 forced diuresis;
 dialysis methods;
 massive blood transfusion.
4. Organ protection.
5. Symptom treatment.
6. Early rehabilitation.

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 1. Reanimation
Pulmonary resuscitation. Indications for performing CPR are breathing
difficulty or obstruction and a state of coma.
 Main methods – oxygen or oxygen mixture is delivered into the
respiratory system. Oxygen utilization in the cells is then activated by:
 mouth to mouth ventilation;
 nasal cannula or oxygen mask;
 endotracheal intubation or respiration equipment ventillation
/contraindicated in cases of inhalation intoxication/
 hyperbar oxygen therapy
 Specialised methods:
 restoration/provision of airways passability;
 stimulation of the respiratory centre;
 enzyme activation /in cases of blocked enzyme system in the cell/;
 blood transfusion /in cases of exposure to poisons with hemotoxic
effect/.
 Restoring control on respiratory impairments.
Cardiovascular resuscitation - indicated in cases of different types and
degrees of blood circulation impairments, resulting from the following mechanisms:
suppression or paralysis of the vasomotor centres in the medulla; toxic heart damage;
impairments in the volume of circulating blood or the tone of blood vessels.
 Main anti-shock means and methods:
 Intravenous drip infusion of water solutions of glucocorticoids;
water-saline solutions; monosaccharide and aminoacid preparations and plasma
substitute solutions in 3:1 ratio of lower to higher molecular weight solutions and in
dosage, adequate to the changes of the haemodynamic parameters;
 Cardioprotective drugs – cardiac glycosides /if there are no
contraindications for them/; antiarrhythmic drugs;
 Cardiac massage; defibrillation and cardiostimulation in cases of
cardiac arrest and absent breathing;
 Specialised means and methods – application of vasopressor drugs
/in cases of toxic suppression of vasomotor centres in the medulla/, etc.
Correction and Substitution Therapy
This kind of therapy is applied in cases of severe water-electrolytic; acid-
alkaline; homeostatic; protein, etc. imbalance in the organism, resulting from or arising
in the course of poisoning. Intravenous drip infusion of water-saline; alkaline;
monosaccharide; plasma substitute; homeostatic, etc. solutions are introduced
depending on clinical, laboratory and haemodynamic parameters. Of particular
importance in toxicology is the emergent infusion of alkalinizing solutions in cases of
severe acidosis, which can cause a rapid lethal ending in acute methyl alcohol;
methylene-glycol, etc. poisoning.
2. Antidote Therapy
The antidote therapy effect is achieved by different medications which neutralize
exogenous poisons, their metabolites and effects on the organism via different
detoxification mechanisms.
The antidote medicinal product can be mono-medicinal or poly-medicinal
depending on its chemical composition. The latter consists of more than one medicinal
substance, with the result that its detoxification effect expands, to cover the poison
itself, its metabolites and more elements of intoxification pathogenesis.

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 Main principles:
 Antidotes are specific medicinal products, so they can be applied only
after the medical diagnosis has been established;
 They are effective only in the toxigenic stage of intoxification and
contraindicated in the somatogenic stage;
 The antidote therapy can be long-term, when applied against slow
acting poisons, with a longer elimination period, and short-term, when applied against
fast acting poisons with a short period of elimination;
 In cases of severe poisoning antidote substances are combined with
medicinal products which can prevent or correct damage of different bodily organs and
systems.
Mechanisms of the Antidote Effect
Antidotes perform their effect via mechanical, physical and chemical reactions;
via metabolic processes, chelation mechanisms, etc.
Depending on their mechanism of action, antidotes fall in one of the following
categories:
 Physico-chemical antidotes: they come into physical and chemical
interaction with the poison and neutralize it in that way:
 contact antidotes: they have an affect on the entry point / medicinal
charcoal, etc./;
 parenteral: they neutralize the poison in the humoral environment
of the organism;
 Biochemical antidotes: they beneficially change metabolisation of the
poison in the organism, thus speed up its neutralization.
 Antidotes blocking poison biotransformation;
 Antidotes reactivating damaged areas and structures /Toxogonin/;
 Antidotes forming new chemical compounds in the organism, with
increased poison affinity;
 Pharmaco-antagonists: they neutralize the effect of poisons, due to their
strong antagonism against it /Atropine/;
 Immunological antidotes: different serums containing antioxidants;
 Combined antidotes: contain two or more antidotes of the same or
different groups /Orocetam; Vtapiracen/;
3. Detoxifying Depuration
The main purpose of the process is to, as fast as possible, eliminate the poison
and its metabolites from the organism, before it has carried out its full aggression on
the organism. Detoxifying depuration is applied on three main levels:
 entry point;
 blood;
 intra- and extracellular liquid medium.
The following methods are applied for detoxifying depuration of the
gastrointestinal tract:
 Mechanical vomiting.
 Stomach flushing: It should be performed as early as possible for
better effect. A nasogastric tube and funnels are used to introduce fluid into the
stomach and then remove it. Large syringes are used for very young babies. In some
cases of poisoning, antidote medical products are introduced before flushing the
stomach.

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  Purgatives:
 saline purgatives: magnesium sulfate or sodium sulfate;
 commercial paraffin oil: it is not absorbed; restricts absorption of
the poison in the intestines and has a purgatory effect;
 castor oil.
 Physiological saline solution enemas: at the end of the first 24 hours
but in some cases of intoxication /morphine intoxication, etc./, several times, 2-3 days
apart, enemas are given with medical products which stay longer in the colon.
Detoxifying depuration of the respiratory system.
It is performed in cases of inhaling toxicants in the form of gases or powder and
when eliminating toxic substances through the lungs (such as chloroform; alcohols;
trichloroethylene, etc.). The following actions must be taken:
 Immediate evacuation from the toxic environment;
 Deep active inhalation and exhalation of fresh air;
 Hyperventilation after intubation (tracheotomy) with oxygen spray or
oxygen spray tracheotomy without intubation if the patient is conscious:
‘gas flushing’ with 15-20ml / min;
Detoxifying depuration of the skin and ligaments: purification with the most
commonly used cleaners, such as alcohol; sodium bicarbonate; potassium
permanganate, etc.
 partial sanitary treatment: - cleaning of affected areas with gauze or
cotton swabs; washing and wiping parts of the body with water; soap water or special
neutralizing solutions (degasifiers);
 full sanitary treatment – thorough body wash with soap and water (the
clothes taken off are packed in suitable packaging);
 eye – thorough rinsing with plenty of running water or with
physiological saline solution for 5-15minutes;
 mouth – rinse thoroughly with water or specialised solutions, such as
sodium bicarbonate; weak acidic or alkaline solutions, used as neutralisers;
 vagina – gynecological examination and poison rinsing with
physiological saline solution, etc. flush
 rectum - purgative enema
Detoxifying depuration of blood and other types of humoral media
 Forced diuresis. It increases the excretion of toxic substances through
the kidneys, by increasing the volume of circulating blood mass, after introducing more
liquids into the organism per orally or intravenously. Specific light- and heavy-
molecular mass solutions are used, at regular intervals combined with diuretics.
 Dialysis methods. Commonly applied are: hemodialysis; peritoneal
dialysis; hemosorption; lymphosorption; plasma exchange and ultrafiltration. Medical
indications for the application of the above listed methods are: intoxication with
dialysable poisons (type and concentration in the blood); severe and extremely severe
case of poisoning. Of particular importance are the following two of these dialysis
methods:
 Peritoneal dialysis, which can only be applied if the patient is in a state
of shock;
 Hemosorption, which is particularly effective in cases of combined
poisoning.

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 4. Organ Protection Treatment
It is carried out with medical products which are aimed to prevent or restore
damage inflicted on different organs and body structures by the poison.
5. Symptom Treatment
The procedure is aimed to restore changes in the organism inflicted by the
poison, which make the patient’s condition worse, such as high temperature; seizures;
strong pain, etc. Commonly used in contemporary medicine medical products for the
above mentioned indications are applied.
6. Early Rehabilitation
The procedure includes means and methods aimed at restricting the possibility
of organ damage and failure: Vibrothorax for patients in toxic coma; inhalation of
broncholytic and anti-oedema aerosols; passive physiotherapeutic procedures, etc.
Each of these methods can be applied if there are no contraindications.

ACUTE POISONING WITH ASPHYXIATING POISONOUS SUBSTANCES

Asphyxiating poisonous substances cause pulmotoxic intoxications. This group

includes a large number of toxic substances but in terms of the mass poisoning, the
most important are:

 Chlorine
 Phosgene
 Ammonia
 Nitrogen oxides

ACUTE POISONING WITH CHLORINE

Chlorine gas is a pulmonary irritant with intermediate water solubility that causes
acute damage in the upper and lower respiratory tract. Chlorine gas was first used as
a chemical weapon at Ypres, France, in 1915. Of the 70,552 American soldiers
poisoned with various gases in World War I, 1843 were exposed to chlorine gas.
Physicochemical properties of chlorine
Chlorine is a yellow-green gas with a specific irritating odour, 2.5 times heavier
than air; it is a chemically active element. Chlorine is a member of the halogen series
that forms the group 7 of the periodic table. Chlorine forms compounds with almost all
of the elements to give compounds that are usually called chlorides. Chlorine gas
reacts with most organic compounds, and will even sluggishly support the combustion
of hydrocarbons. The intermediate water solubility of chlorine accounts for its effect on
the upper airway and the lower respiratory tract. Exposure to chlorine gas may be
prolonged because its moderate water solubility may not cause upper airway
symptoms for several minutes. In addition, the density of the gas is greater than that
of air, causing it to remain near ground level and increasing exposure time. The odor
threshold for chlorine is approximately 0.3-0.5 parts per million (ppm); however,
distinguishing toxic air levels from permissible air levels may be difficult until irritative
symptoms are present.
Plications and uses
1. Production of industrial and consumer products. Principal applications of
chlorine are in the production of a wide range of industrial and consumer products. For

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example, it is used in making plastics, solvents for dry cleaning and metal degreasing,
textiles, agrochemicals and pharmaceuticals, insecticides, dyestuffs, etc.
2. Purification and disinfection. Chlorine is an important chemical for water
purification (such as water treatment plants), in disinfectants, and in bleach. Chlorine
is usually used (in the form of hypochlorous acid) to kill bacteria and other microbes in
drinking water supplies and public swimming pools.
3. Use as a weapon. Chlorine gas, also known as bertholite, was first used as a
weapon in World War I by Germany on April 22, 1915.
Quantitatively, about 63% and 18% of all elemental chlorine produced is used
in the manufacture of organic and inorganic chlorine compounds, respectively. About
15,000 chlorine compounds are being used commercially. The remaining 19% is used
for bleaches and disinfection products.
Toxicity and ways of penetration. Chlorine penetrates through the respiratory
system. The toxic chlorine concentration is 0.2 mg/l, life-endangering in case of 30 to
60 minutes exposure. The lethal chlorine concentration is from 2 g/l.
Mechanism of action of chlorine
The mechanisms of the biological activity are poorly understood and the
predominant anatomic site of injury may vary, depending on the chemical species
produced. At contact with the liquid body environment, hydrogen chloride and
hydrochloric acid are formed; these substances have irritative and corrosive effects
upon the tissues. Cellular injury is believed to result from the oxidation of functional
groups in cell components and from the generation of free oxygen radicals. Although
the idea that chlorine causes direct tissue damage by generating free oxygen radicals
was once accepted, this idea is now controversial.
Solubility effects. Hydrochloric acid is highly soluble in water. The predominant
targets of the acid are the epithelia of the ocular conjunctivae and upper respiratory
mucus membranes. Hypochlorous acid is also highly water soluble with an injury
pattern similar to hydrochloric acid. Hypochlorous acid may account for the toxicity of
elemental chlorine + hydrochloric acid to the human body.
Effects of chlorine on human health depend on how the amount of chlorine that
is present, and the length and frequency of exposure. Effects also depend on the health
of a person or condition of the environment when exposure occurs.
Chlorine irritates the skin, the eyes, and the respiratory system.
Pathologoanatomic changes: hyperemia, bronchorrhea, green colouring of
necrotic areas on the affected mucous membranes of the respiratory system and the
lungs as a consequence of the so called chemical burning, pulmonary edema, changes
of the skin colour, hyperemia of parenchymatous organs, dystrophic changes in the
myocardium, etc. A chemical burn occurs when living tissue is exposed to a corrosive
substance. Chemical burns follow standard burn classification and may cause
extensive tissue damage.
Chemical burns may:
- need no source of heat,
- occur immediately on contact,
- be extremely painful, or
- not be immediately evident or noticeable
- diffuse into tissue and damage structures under skin without
immediately apparent damage to skin surface.
Clinical picture. The immediate effects of chlorine gas toxicity include acute
inflammation of the conjunctivae, nose, pharynx, larynx, trachea, and bronchi. Irritation
of the airway mucosa leads to local edema secondary to active arterial and capillary

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hyperemia. Plasma exudation results in filling the alveoli with edema fluid, resulting in
pulmonary congestion.
1. Fulminant form: at air concentrations exceeding several times the lethal
concentration, there is abrupt irritation and chemical burning of the mucous
membranes of the respiratory tracts, spasm of the vocal cords and the bronchial
muscles, reflexive reactions, and death with signs of shock.
2. Severe form: its course is relatively slower and leads to death in 30 to 40
minutes; superficial, accelerated and irregular breathing, dyspnea, loss of vigilance,
accelerated pulse rate; termination of breathing and cardiac activity 1 to 2 minutes
later.
3. Common form: 1st phase: reflexive reactions against the irritation of the
upper and medium respiratory tracts (burning and irritation of the pharynx and trachea,
pain behind the sternum, watering eyes); 2nd phase: short latent period; 3rd phase:
pulmonary edema, suffocation, cough with abundant foamy hemorrhagic
expectoration, with percussion and auscultatory findings for pulmonary edema,
cyanosis, acute emphysema of the lungs; diffuse bronchitis and broinchiolitis. Duration
in mild cases: 3 to 4 days.
Symptoms
Airways and lungs
• Breathing difficulty (from breathing in the chlorine)
• Shortness of breath (20-51%)
• Throat swelling (may also cause breathing difficulty)
• Water filling the lungs (pulmonary edema)
• Cough (52-80%)
• Chest pain (33%)
Blood
• Severe change in acid levels of the blood (pH balance), which leads to
damage in all of the body organs
Eyes, ears, nose, and throat
• Loss of vision
• Ocular and nasal irritation (4-6%)
• Burning sensation in the throat and substernal area (14%)
• Severe pain or burning in the nose, eyes, ears, lips, or tongue
Heart and blood vessels
• Collapse
• Choking
• Low blood pressure that develops rapidly
Skin
• Burns
• Holes (necrosis) in the skin or tissues underneath
• Irritation
Others
• Muscle weakness
• Dizziness
• Headache
Clinical findings
Decreased breath sounds
Tachypnea
Tachycardia
Wheezing

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 Nasal flaring
Intercostal and subcostal retractions
Cyanosis
Rhinorrhea
Lacrimation
Hoarseness of the voice or stridor
Rales (acute respiratory distress syndrome, noncardiogenic pulmonary
edema)
Crepitus (associated with pneumomediastinum)
Explanation of the pathologic findings
The pathologic findings are nonspecific. They include severe pulmonary edema,
pneumonia, hyaline membrane formation, multiple pulmonary thromboses, and
ulcerative tracheobronchitis.
The hallmark of pulmonary injury associated with chlorine toxicity is pulmonary
edema, manifested as hypoxia. Noncardiogenic pulmonary edema is thought to occur
when there is a loss of pulmonary capillary integrity, and subsequent transudation of
fluid into the alveolus is present. The onset can occur within minutes or hours,
depending upon severity of exposure. Persistent hypoxemia is associated with a higher
mortality rate.
The eye seldom is damaged severely by chlorine gas toxicity; however, burns
and corneal abrasions have occurred. Acids formed by the chlorine gas reaction with
the conjunctival mucous membranes are buffered, in part, by the tear film and the
proteins present in tears. Consequently, acid burns to the eye typically cause epithelial
and basement membrane damage but rarely damage deep endothelial cells. Acid
burns to the periphery of the cornea and conjunctiva often heal uneventfully, while
burns to the center of the cornea may lead to corneal ulcer formation and subsequent
scarring.
Complications
- Early complications: pneumonia, bronchopneumonia, pleuritis,
thrombosis, infarcts, acute cardiac failure.
- Late complications: chronic injuries of the respiratory system
(bronchitis, bronchoectases, emphysema, etc.)
Diagnosis comes from the anamnesis for contact with chlorine, the acute
tracheobronchitis with painful cough and greenish expectoration.
Treatment
It consists first in taking the patient out of the gassed environment, artificial
respiration with oxygen. Antidote: 2% solution of sodium bicarbonate by inhalation
immediately following poisoning; broncholytic drugs, antitussive drugs; antibiotics,
glucocorticoids; respiratory intensive treatment.
Prevention
Exposure to toxic levels of chlorine can be prevented by using a protective
mask, which will help in avoiding inhaling chlorine gas while working with the chemical.
This is most advantageous for those who are constantly encountering chlorine gas,
such as in an industrial setting or in routine cleaning situations. Protective clothing and
glasses will also prevent liquid chlorine exposure and the corrosive damage that will
occur if it encounters the skin or eyes. Most of all, proper handling of the chlorine-
containing substances will significantly help prevent toxic exposure.

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 ACUTE POISONING WITH PHOSGENE

Phosgene is a highly toxic substance that exists as a gas at room temperature.

Owing to its poor water solubility, one of the hallmarks of phosgene toxicity is an
unpredictable asymptomatic latent phase before the development of noncardiogenic
pulmonary edema.
Physicochemical properties of phosgene
Phosgene is the chemical compound with the formula COCl2. Phosgene is a
colorless gas or very low-boiling, volatile liquid (b.p. 8.3°C, 48°F) with an odor of new-
mown hay or green corn.
The chemical was named by combining the Greek words
"phos" (meaning light) and "genesis" (birth); it does not mean it
contains any phosphorus.

Plications and uses

Phosgene is produced and utilized across numerous industries for chemical
synthetic processes. Phosgene is used chiefly in the production of polymers including
polyurethanes, polycarbonates and polyureas. Phosgene is also used as intermediate
in pharmaceutical industries. Large-scale exposure may occur through industrial
accidents. Small-scale exposures most often occur when phosgene is released by
heating chlorinated hydrocarbons. Phosgene has been used in the past as a chemical
weapon by warring nations and extremist groups. This toxic gas gained infamy as a
chemical weapon during World War I where it was responsible for about 85% of the
100,000 deaths caused by chemical weapons.
Phosgene exposure may result from any of the following:
• Small-scale accidental exposure involving the heating of chlorinated
hydrocarbons
• Fire exposure
• Industrial accident
• Industrial sabotage
• Release as a weapon of mass destruction by extremist groups
Toxicity and ways of penetration. Phosgene penetrates through the
respiratory system. The Occupational Safety and Health Administration permissible
exposure limit (OSHA PEL) for the workplace is 0.1 ppm (0.4 mg/m) as an 8-hour time
weighted average. The level immediately dangerous to life or health (IDLH) is 2 ppm.
Even a short exposure to 50 ppm may result in rapid fatality.
Another means to assess exposure and potential complications is using the
inhaled dose instead of concentration alone. An inhaled dose of greater than 25
ppm/min leads to subclinical biochemical lung alterations, greater than 150 ppm/min
causes overt alveolar edema, greater than 300 ppm/min is possibly lethal, and the level
with 50% mortality is about 500 ppm/min.
Mechanism of action of phosgene
Phosgene is a highly reactive gas capable of damaging a variety of biological
macromolecules in an oxidant-like fashion. This activity potentially results from at least
two separate chemical reactions: acylation and hydrolysis. Acylation, the more
important and rapid mechanism, results from the reaction of phosgene with
nucleophilic moieties, such as the amino, hydroxyl, and sulfhydryl groups of tissue
macromolecules. Acylation causes destruction of proteins and lipids, irreversible
alterations of membrane structures, and disruption of enzyme and other cell functions.
Exposure to phosgene depletes lung nucleophiles, particularly glutathione, and

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restoration of glutathione seems to protect against phosgene-induced injury. For
several days after acute phosgene exposure, tissue levels of antioxidant enzymes,
such as glutathione reductase and superoxide dismutase, increase as part of the lungs'
response to injury. In addition to acylation, phosgene is hydrolyzed to HCl. The
formation of HCl occurs on moist membranes and may cause irritation and tissue
damage. Because of the limited water solubility of phosgene, it is unlikely that large
quantities of HCl could result from the exposure of biological tissues. However, small
amounts do form and may contact moist membranes of the eye, nasopharynx, and
respiratory tract. Hydrolysis to HCl is the probable cause of immediate inflammation
and discomfort after phosgene exposure at concentrations greater than 3 ppm.
Pulmonary cellular glycolysis and oxygen uptake following phosgene exposure are
depressed and, thus, leads to a corresponding decrease in the levels of intracellular
adenosine triphosphate and cyclic adenosine monophosphate. This is associated with
increased water uptake by epithelial, interstitial, and endothelial cells. The
semipermeability of the blood-air barrier becomes gradually compromised as a result
of fluid entering the interstitial and alveolar spaces. Later, the blood-air barrier disrupts,
opening channels for the flooding of alveoli.
Pathologoanatomic changes: hyperemia, bronchorrhea, necrotic areas on the
affected mucous membranes of the respiratory system and the lungs, pulmonary
edema, hyperemia of parenchymatous organs, dystrophic changes in the myocardium,
etc.
The pathology of phosgene poisoning is mainly due to its acylating properties
and not a result of hydrochloric acid generation upon hydrolysis, although hydrochloric
acid production may play a minor role. The production of pulmonary edema following
phosgene exposure has been correlated with reductions in pulmonary ATP levels and
sodium-potassium ATPase activity, as well as inhibition of other pulmonary enzymes.
The role of the nervous system in the toxicity of phosgene is considered to be a
nonspecific effect of irritant gases.
Phosgene is only slightly soluble in water; the small amount of phosgene which
dissolves is immediately hydrolyzed to CO2 and HCl. The concentration of HCl
produced from a lethal dose of phosgene is can be easily buffered by the lung tissue.
The inhalation toxicity of phosgene is enhanced by its low water solubility, which allows
it to penetrate further into the lungs than can more soluble gases. When phosgene
reaches the alveolar region it reacts with NH2-, SH- or OH-groups of the bloood-air
barrier. The acylating reaction of phosgene occurs much more rapidly than the reaction
of phosgene with water.
Clinical picture. Symptoms:
• Lacrimation
• Conjunctival irritation/burning
• Burning sensation in mouth/throat
• Throat swelling/changes in phonation - may reflect laryngeal edema
Respiratory manifestations, which can develop relatively early at greater than
4.8 ppm, usually do not develop until after a latent period lasting 4-24 hours
postexposure. They consist of the following signs and symptoms:
• Cough - initially dry, then increasing frothy white/yellow sputum
• Chest tightness, chest pain, or substernal burning
• Dyspnea - exertional early on, subsequently becomes present at rest
• Altered taste sensation - if the patient is a smoker, metallic or unpleasant
taste to cigarettes

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 Other signs and symptoms of this phase, which result primarily from hypoxemia
or volume depletion, include the following:
• Lightheadedness
• Palpitations
• Angina
• Headache
• Anorexia
• Nausea and vomiting
• Weakness
• Anxiety and sense of impending doom
On physical examination, respiratory findings may include the following:
• Crackles on auscultation - herald the onset of pulmonary edema
• Cyanosis - late finding
• Thin, frothy white/yellow secretions
• Wheezing
• Tachypnea
• Stridor
• Accessory muscle use for respiratory effort
Cardiovascular findings may include the following:
• Tachycardia
• Hypotension - late finding secondary to inflammation-mediated fluid
diversion out of vascular system and into lung interstitium
Skin findings may include the following:
• Cyanosis from pulmonary injury and resultant hypoxemia
• Chemical burns from liquefied phosgene (although it also is considered
a frostbite hazard in the compressed liquid form)
Treatment
Treatment that should be performed in the prehospital setting includes the
following:
• Patients exposed to liquid phosgene: Decontamination
• Patients with ocular exposure: Eye flushes with saline or plain
water for at least 15 minutes
• Patients with dyspnea or chest tightness: Supplemental oxygen,
cardiac monitor, symptomatic therapy, and expeditious
transportation to a healthcare facility
In case of asymptomatic patients with suspected exposure to phosgene,
monitor the patient for a minimum of 8-12 hours (many authors recommend 12-24 h)
because of the potential for delayed-onset pulmonary edema. Reassess patients at
least every 2 hours during the first 6 hours after exposure. Criteria for discharge after
this observation time are as follows:
• No symptoms
• Clear lung ausculatory examination
• Normal respiratory rate
• Normal oxygen saturation
• Normal chest radiograph
Treatment for symptomatic patients is as follows:
• Focus on airway, breathing, and circulation
• Proceed rapidly to intubation if necessary
• Provide supplemental oxygen for dyspnea, hypoxia, or crackles
• Provide positive-pressure ventilation

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 • Treat bronchospasm with standard doses of inhaled
bronchodilators and inhaled anticholinergic agents such as
albuterol and ipratropium bromide
Corticosteroids have been studied in various animal models and human cases,
and no clear-cut evidence shows they are advantageous to the patient.

ACUTE POISONING WITH AMMONIA

Physicochemical properties of ammonia

Ammonia is a compound with the formula NH3. It is a colorless gas with a
characteristic pungent smell. It is lighter than air, its density being 0.589 times that of
air. It is easily liquefied due to the strong hydrogen bonding between molecules. The
liquid boils at -33.3 °C, and solidifies at -77.7 °C to white crystals. It is miscible with
water.
Ammonia in an aqueous solution can be expelled by boiling. The aqueous
solution of ammonia is basic. Ammonia does not burn readily or sustain combustion,
except under narrow fuel-to-air mixtures of 15-25% air.
Plications and uses
About 80% of the ammonia produced by industry is used in agriculture as
fertilizer. Ammonia is also used as a refrigerant gas, for purification of water supplies,
and in the manufacture of plastics, explosives, textiles, pesticides, dyes and other
chemicals. It is found in many household and industrial-strength cleaning solutions.
Household ammonia cleaning solutions are manufactured by adding ammonia gas to
water and can be between 5 and 10% ammonia. Ammonia solutions for industrial use
may be concentrations of 25% or higher and are corrosive.
Toxicity and ways of penetration. Ammonia can penetrate into the body by
inhalation, ingestion, skin or eye contact.
Permissible levels of exposure to toxic gases are defined as follows:
 Time-weighted average (TWA)
 Short-term exposure limit (STEL)
 Concentration at which toxic gases are immediately dangerous to
life or health (IDLH)
The TWA is defined as the concentration for an 8-hour workday of a 40-hour
workweek that nearly all workers can be exposed to without adverse effects. The STEL
is the concentration at which an exposure of longer than 15 minutes is potentially
dangerous and may produce immediate or chronic compromise to health. Anhydrous
ammonia has a TWA of 25 parts per million (ppm), a STEL of 35 ppm, and an IDLH of
500 ppm.
Mechanism of action of phosgene
Ammonia most commonly causes damage when anhydrous ammonia (liquid or
gas) reacts with tissue water to form the strongly alkaline solution, ammonium
hydroxide. The formula for this is as follows:

NH3 + H2 O ⇒ NH4 OH

This reaction is exothermic and capable of causing significant thermal injury.

Ammonium hydroxide can cause severe alkaline chemical burns to skin, eyes,
and especially the respiratory system. Mild exposures primarily affect the upper

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respiratory tract, while more severe exposures tend to affect the entire respiratory
system (see Presentation). The gastrointestinal tract also may be affected if ammonia
is ingested.
Tissue damage from alkali is caused by liquefaction necrosis and theoretically
can penetrate deeper than that caused by an equipotent acid. In the case of ammonium
hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of
ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction
of cilia and the mucosa, eliminating the barrier to infection. Furthermore, secretions,
sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction
cause significant airway obstruction.
Airway epithelium can regain barrier integrity within 6 hours after exposure if the
basal cell layer remains intact. However, damaged epithelium often is replaced by
granular tissue, which may be one of the causes of chronic lung disease following
ammonia inhalation injury.
Clinical picture
Injury from ammonia most commonly is caused by inhalation, but it also may
follow ingestion or direct contact with eyes or skin.
Symptoms of exposure to gaseous ammonia include the following:
 Rhinorrhea
 Scratchy throat
 Chest tightness
 Cough
 Dyspnea
 Eye irritation
Symptoms usually subside within 24-48 hours. Absence of symptoms following
inhalational exposure to ammonia essentially rules out significant injury.
Ingestion of ammonia can produce the following symptoms:
 Oropharyngeal, epigastric, and retrosternal pain
 Abdominal pain and other gastrointestinal symptoms, with viscus
perforation (perforation may occur up to 24-72 hours post
ingestion)
 Respiratory symptoms, if aspiration pneumonia or pneumonitis
complicates ingestion
On physical examination, inhalation injury from ammonia is marked by the
following findings:
 Head, ears, eyes, nose, throat - Facial and oral burns and
ulcerations
 Respiration - Tachypnea, oxygen desaturation, stridor, drooling,
cough, wheezing, rhonchi, and decreased air entry
 Central nervous system (CNS) - Loss of consciousness (if
exposure is massive)
Alkali burns to the skin from ammonia are yellow, soapy, and soft in texture; with
severe burns, skin turns black and leathery.
Manifestations of ocular toxicity from ammonia include the following:
 Iritis
 Corneal edema
 Semi-dilated fixed pupil
 Eventual cataract formation
 Hepatic encephalopathy

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 Inhalation: Ammonia is irritating and corrosive. Exposure to high
concentrations of ammonia in air causes immediate burning of the nose, throat and
respiratory tract. This can cause bronchiolar and alveolar edema, and airway
destruction resulting in respiratory distress or failure. Inhalation of lower concentrations
can cause coughing, and nose and throat irritation. Ammonia's odor provides adequate
early warning of its presence, but ammonia also causes olfactory fatigue or adaptation,
reducing awareness of one's prolonged exposure at low concentrations.
Children exposed to the same concentrations of ammonia vapor as adults may
receive a larger dose because they have greater lung surface area-to-body weight
ratios and increased minute volumes-to-weight ratios. In addition, they may be
exposed to higher concentrations than adults in the same location because of their
shorter height and the higher concentrations of ammonia vapor initially found near the
ground.
Skin or eye contact: Exposure to low concentrations of ammonia in air or
solution may produce rapid skin or eye irritation. Higher concentrations of ammonia
may cause severe injury and burns. Contact with concentrated ammonia solutions
such as industrial cleaners may cause corrosive injury including skin burns, permanent
eye damage or blindness. The full extent of eye injury may not be apparent for up to a
week after the exposure. Contact with liquefied ammonia can also cause frostbite
injury.
Ingestion: Exposure to high concentrations of ammonia from swallowing
ammonia solution results in corrosive damage to the mouth, throat and stomach.
Ingestion of ammonia does not normally result in systemic poisoning.
Treatment
Management of toxic exposure to ammonia is largely supportive, as follows:
 Decontaminate the patient (if that was not done at the site of exposure)
 Support the ABCs as necessary
 Provide warmed humidified oxygen
Indications for tracheal intubation include the following:
 Severe respiratory distress (hypoxemia, hypercapnia)
 Stridor
 Hoarseness
 Deep facial burns
 Burns identified by bronchoscopy or endoscopy
 Depressed mental status
Treat ingestions using the following steps:
 Rinse mouth and dilute ingestion with approximately 250 ml of water or
milk
 Do not induce emesis, so as not to worsen injury with a second pass of
toxin
 Promptly arrange a gastroenterology consultation for subsequent
endoscopic evaluation (not often performed before 12 hours post
ingestion)
Corticosteroids are controversial therapies for ammonia toxicity, and should be
used only after appropriate expert consultation. Accepted indications include the
following:
 Acute bronchospasm in patients with underlying reactive airways disease
 Chronic respiratory complications from acute inhalation injury
 Symptomatic airway edema after caustic exposure

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 ACUTE POISONING WITH NITROGEN OXIDES

Physicochemical properties of nitrogen oxides

Nitrogen oxides represent a mixture of gases designated by the formula NOx.
The mixture includes nitric oxide (NO), nitrogen dioxide (NO2), nitrogen trioxide (N2O3),
nitrogen tetroxide (N2O4), and nitrogen pentoxide (N2O5). The toxicity of nitrous oxide
(N2O) or laughing gas, which is used as an anesthetic, is different from that of the other
nitrogen oxides and is not discussed in this protocol.
The most hazardous of the nitrogen oxides are nitric oxide and nitrogen dioxide;
the latter exists in equilibrium with its dimer, nitrogen tetroxide. Nitric oxide is a
colorless gas at room temperature, very sparingly soluble in water. Nitrogen dioxide is
a colorless to brown liquid at room temperature and a reddish-brown gas above 70°F
poorly soluble in water. Nitric oxide is rapidly oxidized in air at high concentrations to
form nitrogen dioxide.
Plications and uses
Nitrogen oxides form naturally during the oxidation of nitrogen-containing
compounds such as coal, diesel fuel, and silage. Nitrogen oxides are also formed
during arc welding, electroplating, engraving, dynamite blasting, as components of
rocket fuel, and nitration reactions such as in the production of nitro-explosives,
including gun-cotton, dynamite and TNT. They are produced commercially, usually as
the first step in the production of nitric acid, either by the direct oxidation of atmospheric
nitrogen in the electric arc or by the catalytic oxidation of anhydrous ammonia. Trace
metal impurities most likely cause nitrogen oxides to form in nitric acid and its solutions.
Nitrogen oxides are intermediates in the production of lacquers, dyes, and other
chemicals and are important components of photo-oxidant smog.
Toxicity and ways of penetration. Nitrogen oxides penetrates through the
respiratory system. Nitrogen oxides are irritating to the upper respiratory tract and
lungs even at low concentrations. Only one or two breaths of a very high concentration
can cause severe toxicity. Odor is generally an adequate warning property for acute
exposures. Nitrogen dioxide is heavier than air, such that exposure in poorly ventilated,
enclosed, or low-lying areas can result in asphyxiation.
Children exposed to the same levels of nitrogen oxides as adults may receive
larger doses because they have greater lung surface area: body weight ratios and
increased minute volumes: weight ratios. In addition, they may be exposed to higher
levels of nitrogen dioxide than adults in the same location because of their short stature
and the higher levels of nitrogen dioxide found nearer to the ground.
Nitric Oxide:
 OSHA PEL (permissible exposure limit) = 25 ppm (averaged over an 8-
hour workshift)
 NIOSH IDLH (immediately dangerous to life or health) = 100 ppm
Nitrogen Dioxide:
 OSHA PEL (permissible exposure limit) = 5 ppm (Ceiling)
 NIOSH IDLH (immediately dangerous to life or health) = 20 ppm
Mechanism of action of nitrogen oxides
Nitrogen oxides are thought to damage lungs in three ways: (1) it is converted
to nitric and nitrous acids in the distal airways, which directly damages certain structural
and functional lung cells; (2) it initiates free radical generation, which results in protein
oxidation, lipid peroxidation, and cell membrane damage; and (3) it reduces resistance
to infection by altering macrophage and immune function.

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 Pathologoanatomic changes:
Clinical picture. Symptoms:
Respiratory. The higher nitrogen oxides are respiratory irritants. The primary
site of toxicity is the lower respiratory tract. Low concentrations initially may cause mild
shortness of breath and cough, fatigue, nausea, headache, abdominal pain. A
symptom-free period of 3 to 30 hours may then be followed by the onset of pulmonary
edema with bronchospasm, anxiety, mental confusion, lethargy, and loss of
consciousness. Inhalation of very high concentrations can rapidly cause burns,
spasms, swelling of tissues in the throat, upper airway obstruction, and death. If
survived, this episode may be followed by bronchiolitis obliterans (fibrous obstruction
of the bronchioles) several weeks later. Any of these phases can be fatal.
Cardiovascular. Absorption of nitrogen oxides can lead to a weak rapid pulse,
dilated heart, chest congestion, and circulatory collapse.
Hematologic. High-dose exposure may convert Fe+2 in hemoglobin to Fe+3, by
virtue of the presence of nitric oxide (NO), causing methemoglobinemia and impaired
oxygen transport.
Dermal. Higher nitrogen oxides are skin irritants and corrosives. Skin moisture
in contact with liquid nitrogen dioxide or high concentrations of its vapor can result in
nitric acid formation, which may lead to second-and third-degree skin burns. Nitric acid
may also cause yellowing of the skin and erosion of dental enamel.
Ocular. Liquid nitrogen oxides cause severe eye burns after brief contact. High
concentrations of the gas cause irritation and, after prolonged exposure, may cause
clouding of the eye surface and blindness.
Potential sequelae
Obstruction of the bronchioles may develop days to weeks after severe
exposure. Patients suffer malaise, weakness, fever, chills, progressive shortness of
breath, cough, hemorrhage of the lungs or bronchioles, blue or purple coloring of the
skin, and respiratory failure. This condition may be confused with the adult respiratory
distress syndrome secondary to infectious diseases such as miliary tuberculosis.
Victims of inhalation exposure may suffer reactive airways dysfunction
syndrome (RADS) after a single acute, high-dose exposure.
Treatment
Victims exposed only to nitrogen oxide gases do not pose risks of secondary
contamination to rescuers. Victims whose clothing or skin is contaminated with liquid
nitrogen oxides or nitric acid can secondarily contaminate response personnel by direct
contact or through off-gassing vapors.
Most of the higher nitrogen oxides are eye, skin, and respiratory tract irritants.
Initial respiratory symptoms after exposure to nitrogen oxides may be mild, but
progressive inflammation of the lungs may develop several hours to days after
exposure. Noncardiogenic pulmonary edema may develop even if initial pulmonary
signs were minimal. Exposures may result in methemoglobinemia, depending upon
the presence of nitric oxide (NO) in the gas mixture.
There is no antidote for nitrogen oxides. Primary treatment consists of
respiratory and cardiovascular support. Methylene blue may be necessary to treat
methemoglobinemia.
Respiratory Protection: Positive-pressure, self-contained breathing apparatus is
recommended in response situations that involve exposure to potentially unsafe levels
of nitrogen oxides.

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 Skin Protection: Chemical-protective clothing is recommended when repeated
or prolonged contact with liquids of nitrogen oxides or with high concentrations of
nitrogen oxide vapors is anticipated because skin irritation or burns may occur.
ABC Reminders: Quickly access for a patent airway, ensure adequate
respiration and pulse. If trauma is suspected, maintain cervical immobilization
manually and apply a cervical collar and a backboard when feasible.
Victim Removal: If victims can walk, lead them out of the Hot Zone to the
Decontamination Zone. Victims who are unable to walk may be removed on
backboards or gurneys; if these are not available, carefully carry or drag victims to
safety.
Decontamination Zone: Victims exposed only to nitrogen oxide gases may
appear to have no skin or eye irritation. However, they should still be decontaminated
as described below as irritation may not become evident until washing commences.
Basic Decontamination: Victims who are able may assist with their own
decontamination. Remove and double-bag contaminated clothing and personal
belongings. Flush exposed skin and hair with water for 20 minutes.
Administer supplemental oxygen by mask to patients who have respiratory
symptoms. Treat patients who have bronchospasm with aerosolized bronchodilators.
Cardiac sensitizing agents may be appropriate. Some clinicians recommend high
doses of corticosteroids for seriously symptomatic patients, especially with severe
bronchospasm. In patients with acute respiratory failure without bronchospasm, the
value of steroids is unproven.

ACUTE POISONING WITH OVERALL TOXIC POISONOUS SUBSTANCES

(HYDROGEN CYANIDE AND CARBON MONOXIDE)

ACUTE POISONING WITH HYDROGEN CYANIDE

Cyanide is often perceived as the archetypal poison, with accidental and

intentional ingestions since ancient times. It is associated with the Jonestown mass-
murder suicides and the Tylenol poisonings in Chicago in 1982. It was used as a
military weapon in World War I and in the Nazi gas chambers during World War II.
More recently cyanide-based weapons have been used during wars in the Middle East.
In the last ten years, cyanide has been used by terrorists in Tokyo subways and by al
Qaeda.
Physicochemical properties of hydrogen cyanide.
At temperatures below 78ºF, hydrogen cyanide is a colorless or pale-blue liquid
(hydrocyanic acid); at higher temperatures, it is a colorless gas. Hydrogen cyanide is
very volatile, producing potentially lethal concentrations at room temperature. The
vapor is flammable and potentially explosive. Hydrogen cyanide has a faint, bitter
almond odor and a bitter, burning taste. It is soluble in water and is often used as a
96% aqueous solution.
Plications and uses
Hydrogen cyanide is manufactured by oxidation of ammonia-methane mixtures
under controlled conditions and by the catalytic decomposition of formamide. It may
be generated by treating cyanide salts with acid, and it is a combustion by-product of
nitrogen-containing materials such as wool, silk, and plastics. It is also produced by

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enzymatic hydrolysis of nitriles and related chemicals. Hydrogen cyanide gas is a by-
product of coke-oven and blast-furnace operations.
Hydrogen cyanide is used in fumigating, electroplating, mining, and in producing
synthetic fibers, plastics, dyes, and pesticides. It also is used as an intermediate in
chemical syntheses.
Exogenous sources of cyanide include food exposures (bitter almonds,
cassava, various fruit seeds/pits), medicines, and industrial exposures (e.g.,
electroplating, mining, plastic manufacturing, fumigation). Smoke inhalation in building
fires produces cyanide secondary to combustion of natural (e.g., wool, silk) and
synthetic (e.g., polyurethane, plastic) materials. Tobacco smoke is also a source of
cyanide. As military and terrorist weapons, the compounds of interest are volatile liquid
hydrogen cyanide and cyanogen chloride.
Toxicity and ways of penetration.
Inhalation. Hydrogen cyanide is readily absorbed from the lungs; symptoms of
poisoning begin within seconds to minutes. The odor of hydrogen cyanide is detectable
at 2-10 ppm, but does not provide adequate warning of hazardous concentrations.
Perception of the odor is a genetic trait (20% to 40% of the general population cannot
detect hydrogen cyanide). Also, rapid olfactory fatigue can occur. Hydrogen cyanide is
lighter than air.
Children exposed to the same levels of hydrogen cyanide as adults may receive
larger doses because they have greater lung surface area: body weight ratios and
increased minute volumes: weight ratios.
Skin/Eye Contact. Exposure to hydrogen cyanide can cause skin and eye
irritation. More importantly, skin or eye absorption is rapid and contributes to systemic
poisoning. After skin exposure, onset of symptoms may be immediate or delayed for
30 to 60 minutes. Most cases of toxicity from dermal exposure have been from
industrial accidents involving partial immersion in liquid cyanide or cyanide solutions
or from contact with molten cyanide salts, resulting in large surface-area burns.
Children are more vulnerable to toxicants absorbed through the skin because of
their relatively larger surface area: body weight ratio.
Ingestion. Ingestion of hydrogen cyanide solutions or cyanide salts can be
rapidly fatal.
Toxicity:
OSHA PEL (permissible exposure limit) (ceiling) = 10 ppm (skin) (averaged over
15 minutes)
NIOSH IDLH (immediately dangerous to life or health) = 50 ppm
AIHA ERPG (emergency response planning guideline) (maximum airborne
concentration below which it is believed that nearly all individuals could be exposed for
up to 1 hour without experiencing or developing irreversible or other serious health
effects or symptoms which could impair an individual's ability to take protective action)
= 10 ppm
Mechanism of action of hydrogen cyanide
The cyanide anion is an inhibitor of the enzyme cytochrome c oxidase in the
fourth complex of the electron transport chain (found in the membrane of the
mitochondria of eukaryotic cells). It attaches to the iron within this protein. The binding
of cyanide to this enzyme prevents transport of electrons from cytochrome c to oxygen.
As a result, the electron transport chain is disrupted, meaning that the cell can no
longer aerobically produce ATP for energy. Tissues that depend highly on aerobic
respiration, such as the central nervous system and the heart, are particularly affected.
This is an example of histotoxic hypoxia.

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 Pathologoanatomic changes
There are no specific pathologic changes that characterize cyanide toxicity.
Evidence of tissue hypoxia may be seen, most notably CNS changes including
necrosis and demyelination.
Clinical picture
Hydrogen cyanide is highly toxic by all routes of exposure and may cause abrupt
onset of profound CNS, cardiovascular, and respiratory effects, leading to death within
minutes.
Exposure to lower concentrations of hydrogen cyanide may produce eye
irritation, headache, confusion, nausea, and vomiting followed in some cases by coma
and death.
Acute Exposure
In humans, cyanide combines with the ferric ion in mitochondrial cytochrome
oxidase, preventing electron transport in the cytochrome system and bringing oxidative
phosphorylation and ATP production to a halt. The inhibition of oxidative metabolism
puts increased demands on anaerobic glycolysis, which results in lactic acid production
and may produce severe acid-base imbalance. The CNS is particularly sensitive to the
toxic effects of cyanide, and exposure to hydrogen cyanide generally produces
symptoms within a short period of time.
Children do not always respond to chemicals in the same way that adults do.
Different protocols for managing their care may be needed.
CNS. CNS signs and symptoms usually develop rapidly. Initial symptoms are
nonspecific and include excitement, dizziness, nausea, vomiting, headache, and
weakness. As poisoning progresses, drowsiness, tetanic spasm, lockjaw, convulsions,
hallucinations, loss of consciousness, and coma may occur.
Cardiovascular. Abnormal heartbeat can occur in cases of severe poisoning.
Slow heartbeat, intractable low blood pressure, and death may result. High blood
pressure and a rapid heartbeat may be early, transient findings.
Respiratory. After systemic poisoning begins, victims may complain of
shortness of breath and chest tightness. Pulmonary findings may include rapid
breathing and increased depth of respirations. As poisoning progresses, respirations
become slow and gasping; a bluish skin color may or may not be present.
Accumulation of fluid in the lungs may develop. Children may be more vulnerable to
gas exposure because of relatively increased minute ventilation per kg and failure to
evacuate an area promptly when exposed.
Metabolic. An anion-gap, metabolic acidosis occurs in severe poisoning from
increased blood levels of lactic acid.
Dermal. Dermal absorption can occur, leading to systemic toxicity. Absorption
occurs more readily at high ambient temperature and relative humidity.
Ocular. When splashed in the eye, hydrogen cyanide can cause eye irritation
and swelling. Eye contact with cyanide salts has produced systemic symptoms in
experimental animals.
Potential sequelae. Survivors of severe exposure may suffer brain damage
due to a direct action on neurons, or to lack of oxygen, or possibly due to insufficient
blood circulation. Cases of neurologic sequelae such as personality changes, memory
deficits, disturbances in voluntary muscle movements, and the appearance of
involuntary movements (i.e., extrapyramidal syndromes) have been reported.
Diagnosis. The diagnosis of cyanide toxicity is challenging because of a lack
of pathognomonic signs. The clinical toxidrome of bright red venous blood, profound
metabolic acidosis, and bitter almond breath is only rarely present. Blood cyanide

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levels are useful in confirming toxicity; however, acute management should begin
before laboratory confirmation is available.
Laboratory
Cyanide levels can be measured directly. Normal plasma cyanide levels are <
0.004 g/ml, but may be higher in smokers. Whole blood levels are higher because
cyanide concentrates in red blood cells. Levels correlate with degree of symptoms.
Rapid tests have been developed, including a paper test that has been shown
to detect levels over 0.5 mg/liter, and a rapid whole blood assay which may become
more available in the future.
Treatment
 Victims exposed only to hydrogen cyanide gas do not pose secondary
contamination risks to rescuers, but do not attempt resuscitation without a barrier.
Victims whose clothing or skin is contaminated with hydrogen cyanide liquid or solution
can secondarily contaminate response personnel by direct contact or through off-
gassing vapor. Avoid dermal contact with cyanide-contaminated victims or with gastric
contents of victims who may have ingested cyanide-containing materials.
 Quickly access for a patent airway, ensure adequate respiration and
pulse. Stabilize the cervical spine with a collar and a backboard if trauma is suspected.
Administer supplemental oxygen as required. Assist ventilation with a bag-valve-mask
device if necessary.
 Speed is critical. For symptomatic victims, provide treatment with 100%
oxygen and specific antidotes as needed. Treatment should be given simultaneously
with decontamination procedures. Victims who are able may assist with their own
decontamination. Rapidly remove contaminated clothing while flushing exposed skin
and hair with plain water for 2 to 3 minutes, then wash twice with mild soap. Rinse
thoroughly with water. Double-bag contaminated clothing and personal belongings.
Irrigate exposed or irritated eyes with plain water or saline for 5 minutes. Continue eye
irrigation during other basic care or transport. In cases of ingestion, do not induce
emesis. If the victim is alert, asymptomatic, and has a gag reflex, administer a slurry of
activated charcoal (administer at 1 gm/kg, usual adult dose 60-90 g, child dose 25-50
g). If the victim is symptomatic, immediately institute emergency life support measures
including the use of the cyanide antidote kit.
 Victims exposed to hydrogen cyanide require supportive care and rapid
administration of specific antidotes.
Antidotes
When possible, treatment with cyanide antidotes should be given under medical
supervision to unconscious victims who have known or strongly suspected cyanide
poisoning. Cyanide antidotes-amyl nitrite perles and intravenous infusions of sodium
nitrite and sodium thiosulfate-are packaged in the cyanide antidote kit.
Amyl nitrite perles should be broken onto a gauze pad and held under the nose,
over the Ambu-valve intake, or placed under the lip of the face mask. Inhale for 30
seconds every minute and use a new perle every 3 minutes if sodium nitrite infusions
will be delayed.
If the patient has not responded to oxygen and amyl nitrite treatment, infuse
sodium nitrite intravenously as soon as possible. The usual adult dose is 10 mL of a
3% solution (300 mg) infused over absolutely no less than 5 minutes.
Next, infuse sodium thiosulfate intravenously. The usual adult dose is 50 mL of
a 25% solution (12.5 g) infused over 10 to 20 minutes. Repeat one-half of the initial
dose 30 minutes later if there is an inadequate clinical response.

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 Prevention
Removal from continued exposure is the key to preventing toxicity. Evacuation
with gaseous exposures and topical decontamination for liquid exposures by removal
of clothing and copious skin washing are paramount.

ACUTE POISONING WITH CARBON MONOXIDE

Physicochemical properties of carbon monoxide (CO)

CO is a colorless, odorless gas that results from incomplete combustion of
hydrocarbons.
Plications and uses
CO is formed as a by-product of burning organic compounds. Many cases of
CO exposure occur in private residences. CO toxicity is especially common during
power outages due to storms, as a result of the improper use of gasoline-powered
portable generators to provide electricity and indoor use of charcoal briquettes for
cooking and heating. Exhaust from generators and propulsion engines on houseboats
has also been linked to CO poisoning.
Most fatalities from CO toxicity result from fires, but stoves, portable heaters,
and automobile exhaust cause approximately one third of deaths. These often are
associated with malfunctioning or obstructed exhaust systems and suicide attempts.
Cigarette smoke is a significant source of CO. Other sources of CO exposure include
the following:
• Propane-fueled forklifts
• Gas-powered concrete saws
• Inhaling spray paint
• Indoor tractor pulls
• Swimming behind a motorboat
Toxicity and ways of penetration. Carbon monoxide penetrates through the
respiratory system. Different people and populations may have different carbon
monoxide tolerance levels. On average, exposures at 100 ppm or greater is dangerous
to human health. In the United States, the OSHA limits long-term workplace exposure
levels to less than 50 ppm averaged over an 8-hour period. In addition, employees are
to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is
reached. Carbon monoxide exposure may lead to a significantly shorter life span due
to heart damage. The carbon monoxide tolerance level for any person is altered by
several factors, including activity level, rate of ventilation, a pre-existing cerebral or
cardiovascular disease, cardiac output, anemia, sickle cell disease and other
hematological disorders, barometric pressure, and metabolic rate.
Mechanism of action of carbon monoxide
CO toxicity causes impaired oxygen delivery and utilization at the cellular level.
CO affects several different sites within the body but has its most profound impact on
the organs (brain, heart) with the highest oxygen requirement.
The mechanisms of action include carbon monoxide binding to hemoglobin,
myoglobin and mitochondrial cytochrome oxidase and restricting oxygen supply, and
carbon monoxide causing brain lipid peroxidation:
1. Hemoglobin
Carbon monoxide shifts the oxygen-dissociation curve to the left. Carbon
monoxide has a higher diffusion coefficient compared to oxygen and the only enzyme

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in the human body that produces carbon monoxide is heme oxygenase which is
located in all cells and breaks down heme. Under normal conditions carbon monoxide
levels in the plasma are approximately 0 mmHg because it has a higher diffusion
coefficient and the body easily gets rid of any CO made. When CO is not ventilated it
binds to hemoglobin, which is the principal oxygen-carrying compound in blood; this
produces a compound known as carboxyhemoglobin. The traditional belief is that
carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which
decreases the oxygen-carrying capacity of the blood and inhibits the transport,
delivery, and utilization of oxygen by the body. The affinity between hemoglobin and
carbon monoxide is approximately 230 times stronger than the affinity between
hemoglobin and oxygen so hemoglobin binds to carbon monoxide in preference to
oxygen.
Hemoglobin is a tetramer with four oxygen binding sites. The binding of carbon
monoxide at one of these sites increases the oxygen affinity of the remaining three
sites, which causes the hemoglobin molecule to retain oxygen that would otherwise be
delivered to the tissue. This situation is described as carbon monoxide shifting the
oxygen dissociation curve to the left. Because of the increased affinity between
hemoglobin and oxygen during carbon monoxide poisoning, little oxygen will actually
be released in the tissues. This causes hypoxic tissue injury. Hemoglobin acquires a
bright red color when converted into carboxyhemoglobin, so poisoned cadavers and
even commercial meats treated with carbon monoxide acquire an unnatural reddish
hue.
2. Myoglobin
Carbon monoxide also binds to the hemeprotein myoglobin. It has a high affinity
for myoglobin, about 60 times greater than that of oxygen. Carbon monoxide bound to
myoglobin may impair its ability to utilize oxygen. This causes reduced cardiac output
and hypotension, which may result in brain ischemia. A delayed return of symptoms
have been reported. This results following a recurrence of increased
carboxyhemoglobin levels; this effect may be due to a late release of carbon monoxide
from myoglobin, which subsequently binds to hemoglobin.
3. Cytochrome oxidase
Another mechanism involves effects on the mitochondrial respiratory enzyme
chain that is responsible for effective tissue utilization of oxygen. Carbon monoxide
binds to cytochrome oxidase with less affinity than oxygen, so it is possible that it
requires significant intracellular hypoxia before binding. This binding interferes with
aerobic metabolism and efficient adenosine triphosphate synthesis. Cells respond by
switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell
death. The rate of dissociation between carbon monoxide and cytochrome oxidase is
slow, causing a relatively prolonged impairment of oxidative metabolism.
4. Central nervous system effects
The mechanism that is thought to have a significant influence on delayed effects
involves formed blood cells and chemical mediators, which cause brain lipid
peroxidation (degradation of unsaturated fatty acids). Carbon monoxide causes
endothelial cell and platelet release of nitric oxide, and the formation of oxygen free
radicals including peroxynitrite. In the brain this causes further mitochondrial
dysfunction, capillary leakage, leukocyte sequestration, and apoptosis. The result of
these effects is lipid peroxidation, which causes delayed reversible demyelinization of
white matter in the central nervous system known as Grinker myelinopathy, which can
lead to edema and necrosis within the brain. This brain damage occurs mainly during
the recovery period. This may result in cognitive defects, especially affecting memory

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and learning, and movement disorders. These disorders are typically related to
damage to the cerebral white matter and basal ganglia. Hallmark pathological changes
following poisoning are bilateral necrosis of the white matter, globus pallidus,
cerebellum, hippocampus and the cerebral cortex.
Clinical picture. The main manifestations of carbon monoxide poisoning
develop in the organ systems most dependent on oxygen use, the central nervous
system and the heart. The initial symptoms of acute carbon monoxide poisoning
include headache, nausea, malaise, and fatigue. These symptoms are often mistaken
for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis.
Headache is the most common symptom of acute carbon monoxide poisoning. It is
often described as dull, frontal, and continuous. Increasing exposure produces cardiac
abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia.
Central nervous system symptoms include delirium, hallucinations, dizziness,
unsteady gait, confusion, seizures, central nervous system depression,
unconsciousness, respiratory arrest, and death. Less common symptoms of acute
carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia,
pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney
failure, skin lesions, and visual and auditory problems.
One of the major concerns following acute carbon monoxide poisoning is the
severe delayed neurological manifestations that may occur. Problems may include
difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia,
psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like
syndromes, cortical blindness, and a depressed mood. Depression may occur in those
who did not have pre-existing depression. These delayed neurological sequelae may
occur in up to 50% of poisoned people after 2 to 40 days. It is difficult to predict who
will develop delayed sequelae. However, advanced age, loss of consciousness while
poisoned, and initial neurological abnormalities may increase the chance of developing
delayed symptoms.
One classic sign of carbon monoxide poisoning is more often seen in the dead
rather than the living – people have been described as looking red-cheeked and
healthy. However, since this "cherry-red" appearance is common only in the deceased,
and is unusual in living people, it is not considered a useful diagnostic sign in clinical
medicine. In pathological (autopsy) examination the ruddy appearance of carbon
monoxide poisoning is notable because unembalmed dead persons are normally
bluish and pale, whereas dead carbon-monoxide poisoned persons may simply appear
unusually lifelike in coloration.
CO poisoning symptoms tend to correlate well with the patient’s peak blood
carboxyhemoglobin levels. Many symptoms are nonspecific.
• Headache and nausea can begin when levels are 10 to 20%.
• Levels > 20% commonly cause vague dizziness, generalized weakness,
difficulty concentrating, and impaired judgment.
• Levels > 30% commonly cause dyspnea during exertion, chest pain (in
patients with coronary artery disease), and confusion.
• Higher levels can cause syncope, seizures, and obtundation.
• Hypotension, coma, respiratory failure, and death may occur, usually
when levels are > 60%.

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 Diagnosis
• Diagnosis considered when patients at risk have nonspecific symptoms
or metabolic acidosis
• Venous carboxyhemoglobin level
Because symptoms can be vague, nonspecific, and variable, the diagnosis
of CO poisoning is easily missed. Many cases of mild poisoning with nonspecific
symptoms are mistaken for viral syndromes. Physicians must maintain a high level of
suspicion. If people from the same dwelling, particularly a heated dwelling, experience
nonspecific flu-like symptoms, CO exposure should be considered.
If CO poisoning is suspected, the carboxyhemoglobin level is measured with
a CO-oximeter.
Treatment
Prehospital care includes the following:
• Promptly remove the patient from continued exposure and immediately
institute oxygen therapy with a nonrebreather mask.
• Perform intubation for the comatose patient or, if necessary for airway
protection, and provide 100% oxygen therapy.
• If possible, obtain ambient CO measurements from fire department or
utility company personnel, when present.
• Early blood samples may provide much more accurate correlation
between HbCO and clinical status; however, do not delay oxygen administration to
acquire them.
• Obtain an estimate of exposure time, if possible.
• Avoid exertion to limit tissue oxygen demand.
Hospital care includes the following:
• 100% O2
• Hyperbaric oxygen therapy (HBO)
Patients should be removed from the source of CO and stabilized as necessary.
They are given 100% O2 and treated supportively. Although its use is becoming

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increasingly controversial, hyperbaric O2 therapy (in a chamber at 2 to 3 atmospheres
of 100% O2) typically should be considered for patients who have any of the following:
• Life-threatening cardiopulmonary complications
• Ongoing chest pain
• Altered consciousness
• Loss of consciousness (no matter how brief)
• A carboxyhemoglobin level > 25%
Hyperbaric O2 therapy should also be considered for pregnant patients, possibly
at lower serum CO levels than in nonpregnant patients.
Hyperbaric O2 therapy may decrease the incidence of delayed neuropsychiatric
symptoms.
Chambers are small monoplace
hulls, allowing space for a single patient in
a supine position who can be viewed
through a window at the head, or they are
acrylic walled and allow full visualization.
Many of these monoplace chambers allow
for care of critically ill patients, including
intravenous lines, arterial lines, and
ventilator. Others are large multiplace
chambers that permit ventilation equipment
and allow medical teams to accompany the
patient.

Prevention
Prevention involves checking sources of indoor combustion to make sure they
are correctly installed and vented to the outdoors. Exhaust pipes should be inspected
periodically for leaks. Cars should never be left running in an enclosed garage. CO
detectors should be installed because they provide early warning that CO is free in a
dwelling’s atmosphere. If CO is suspected in a dwelling, windows should be opened,
and the dwelling should be evacuated and evaluated for the source of CO.

ACUTE POISONING WITH ORGANOPHOSPHATE NERVE AGENTS

Chemical weapons were first used on a large scale by Germany in World War
I. The atrocities witnessed on the battlefield prompted a worldwide convention
prohibiting the use of chemical weapons following World War I. Despite this sanction,
dozens of countries have chosen to develop and deploy nerve agents, as they are
relatively inexpensive to manufacture and raw materials are readily available. Nerve
agents are derivatives of the organophosphate insecticides first synthesized in the
1930. Although initially intended to be more potent insecticides, German scientists
quickly recognized the compounds as potential weapons. Weaponized
organophosphates are known by common chemical names and two letter
designations. The German agents are given a designation of "G" followed by a letter,
which denotes their order of discovery. During the Second World War, Nazi Germany
manufactured and stockpiled thousands of tons of the agents Tabun (GA) and Sarin
(GB). Although the weapons were never used, the Germans continued to develop more
lethal agents such as Soman (GD), which was only made in small quantities. Seizing
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upon this work, British and American scientists continued to refine nerve agents as
weapons through the 1950s, resulting in the Viper series of nerve agents, the most
common of which is VX. Although little is known about their manufacture, it is thought
that the former Soviet Union had produced large quantities of even newer agents.
The first documented use of nerve agents in combat was not until the Iran-Iraq
war of the 1980s, when Iraq used combinations of nerve and blister agents against
Iranian troops. It is also thought that the Soviets may have used nerve agents in a
limited fashion in Afghanistan, while the Serbs allegedly employed them in Bosnia.
Most recently, nerve agents have been considered a potential threat from
terrorists and other extremist groups, as they are relatively inexpensive and require
only rudimentary scientific expertise to produce. More importantly, many of the
precursors necessary for their production can be purchased from reputable sources
such as chemical and agricultural companies. In 1994 and 1995 the Aum Shinrikyo
cult in Japan exploited these circumstances, producing small quantities of liquid
containing Sarin (GB). Members then released the liquid in an apartment complex and
later into crowded subway terminals, killing 19 and injuring over 1300. Despite these
relatively small events, the cult members were able to cause significant disruption and
strike fear into hearts of millions of Japanese citizens.
Agents. Physicochemical properties.
There are two main classes of nerve agents:
G-series nerve agents:
 Tabun (GA);
 Sarin (GB);
 Soman (GD);
 Cyclosarin (GF)

V-series nerve agents:

Code
Chemical Name
Name
VX O-Ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothioate
VE O-Ethyl-S-[2-(diethylamino)ethyl] ethylphosphonothioate
VG O,O-Diethyl-S-[2-(diethylamino)ethyl] phosphorothioate
VM O-Ethyl-S-[2-(diethylamino)ethyl] methylphosphonothioate
V-gas Russian equivalent of VX

The organophosphate nerve agents tabun (GA), sarin (GB), soman (GD), and
cyclosarin (GF) are among the most toxic chemical warfare agents known. Together
they comprise the G-series nerve agents, thus named because German scientists first
synthesized them, beginning with GA in 1936. GB was discovered next in 1938,
followed by GD in 1944 and finally the more obscure GF in 1949.
G-series nerve agents share a number of common physical and chemical properties.
At room temperature, the G-series nerve agents are volatile liquids, making them a
serious risk for exposure from dermal contact with liquid nerve agent or inhalation of
nerve agent vapor.
GB is the most volatile of these agents and evaporates at the same rate as
water. GD is the next most volatile. Dispersal devices or an explosive blast also can

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aerosolize nerve agents. Nerve agent vapors are denser than air, making them
particularly hazardous for persons in low areas or underground shelters. GB and GD
are colorless, while GA ranges from colorless to brown. GB is odorless, while GA and
GD smell fruity.
In 1954, the British first synthesized O-ethyl S-(2-diisopropylaminoethyl)
methylphosphonothioate, the most important agent in the V series and coded in the
United States as "VX". The V-series weapons, including VX, are among the most highly
toxic chemical warfare nerve agents ("V" stands for venomous). The V agents are
approximately 10-fold more poisonous than sarin (GB).
The V-series agents are part of the group of persistent agents, which are nerve
agents that can remain on skin, clothes, and other surfaces for long periods of time
due to low volatility characteristics. The consistency of these agents is similar to oil.
Thus, the inhalation hazard is less than with the G agents. This consistency thus
renders them toxic mainly by dermal exposures.
The other agents in the V series are less known, and the information available
about their characteristics is fairly limited in the open, unclassified literature. The other
agents also have coded names, including VE, V-gas, VG, and VM.

Tabun Sarin VX

Toxicity and ways of penetration.

 Inhalation.
 Skin/Eye Contact.
 Ingestion.
Because nerve agents are soluble in fat and water, they are absorbed readily
through the eyes, respiratory tract, and skin. Vapor agents penetrate the eyes first,
producing localized effects, then pass into the respiratory tract, with more generalized
effects when the exposure is greater. Liquid agents penetrate the skin at the point of

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contact, producing localized effects followed by deeper penetration and generalized
effects if the dose is large enough.
Toxicity:
Accordingly, the lethality of these agents varies with the route of exposure.
For inhalational exposures to tabun, the lethal concentration time product in
50% of the exposed population (LC50) is about 400 mg/min/m3.
For inhalational exposures to sarin, LC50 is 75-100 mg/min/m3. For dermal
exposures, the lethal dose in 50% of the exposed population is 1700 mg.
The LC50 of soman in air is estimated to be 50 mg/min/m3.
VX is the most toxic nerve agent ever synthesized for which activity has been
independently confirmed. The LD50 for humans is estimated to be about 10 mg through
skin contact and the LC50 for inhalation is estimated to be 30–50 mg/min/m3.
Mechanism of action
As their name suggests, nerve agents attack the nervous system of the human
body.
When a normally functioning motor nerve is stimulated, it releases the
neurotransmitter acetylcholine (ACh), which transmits the impulse to a muscle or
organ. ACh is an important neurotransmitter of the peripheral nervous system. It
activates 2 types of receptors, muscarinic and nicotinic. Nicotinic ACh receptors are
found at the skeletal muscle and at the preganglionic autonomic fibers. Muscarinic ACh
receptors are found mainly in the postganglionic parasympathetic fibers. In addition,
ACh is believed to mediate neurotransmission in the central nervous system (CNS).
ACh is released when an electrical impulse reaches the presynaptic neuron. It
travels in the synaptic cleft and reaches the postsynaptic membrane, where it binds to
its receptor (muscarinic or nicotinic). This activates the ACh receptor and results in a
new action potential, transmitting the signal down the neuron. Normally, after this
interaction between ACh and its receptor, ACh detaches from its receptor and is
degraded (hydrolyzed) into choline and acetic acid by the enzyme acetylcholinesterase
(AChE). AChE is the enzyme that mediates the degradation of acetylcholine (ACh).
This regenerates the receptor and renders it active again, and allows the muscle or
organ to relaxes.
Nerve agents disrupt the nervous system by inhibiting the function of the
enzyme acetylcholinesterase. Nerve agents bind to the active site of AChE, rendering
it incapable of deactivating ACh. Any ACh that is not hydrolyzed still can interact with
the receptor, resulting in persistent and uncontrolled stimulation of that receptor. After
persistent activation of the receptor, fatigue occurs. Thus, the clinical effects of nerve
agent poisoning are the result of this persistent stimulation and subsequent fatigue at
the muscarinic and nicotinic ACh receptors.
Acetylcholine thus builds up and continues to act so that any nerve impulses
are continually transmitted and muscle contractions do not stop. This same action also
occurs at the gland and organ levels, resulting in uncontrolled drooling, tearing of the
eyes (lacrimation) and excess production of mucus from the nose (rhinorrhea).
For all nerve agents inactivation of AChE eventually becomes permanent
(irreversible). This phenomenon of irreversible inactivation of AChE is known as aging.
Aging represents the formation of a covalent bond between the nerve agent and the
AChE. Once aging occurs, the AChE enzyme cannot be reactivated, and new AChE
must be produced in order for the clinical effect of the nerve agent to be reversed. This
new enzyme production is a very slow process.

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 Clinical picture
Low doses of nerve agent may cause nonfatal poisoning, which can present as
increased production of saliva, rhinorrhea, and a feeling of pressure on the chest. The
pupil becomes contracted (miosis), and accommodation is reduced so that short-range
vision deteriorates. Higher doses cause the symptoms described below plus
bronchoconstriction and secretion of mucus in the respiratory system with breathing
difficulty. The gastrointestinal cramping and vomiting occur. Muscular weakness,
twitching, and convulsions occur due to the effect on the neuromuscular junction by
excess acetylcholine. If the dose is high, muscle paralysis occurs. Death is by
suffocation due to paralysis of the muscles of respiration.
Patients often present with evidence of a cholinergic toxic syndrome, or
toxidrome. It is useful to remember the toxidrome in terms of the 3 clinical effects on
nerve endings: nicotinic effects at neuromuscular junctions and autonomic ganglia,
CNS effects, and muscarinic effects. Nicotinic signs and symptoms include weakness,
fasciculations, and paralysis, whereas CNS effects may lead to seizures and CNS
depression. Two common mnemonics to remember the muscarinic signs and
symptoms of the cholinergic toxidrome are SLUDGE/BBB and DUMBELS, as follows:
SLUDGE/BBB mnemonic
S = Salivation
L = Lacrimation
U = Urination
D = Defecation
G = Gastrointestinal symptoms
E = Emesis
B = Bronchorrhea
B = Bronchospasm
B = Bradycardia

DUMBELS mnemonic
D = Diarrhea and diaphoresis
U = Urination
M = Miosis
B = Bronchorrhea, bronchospasm, and bradycardia
E = Emesis
L = Lacrimation
S = Salivation

Eyes. The most common effects of nerve agents on the eyes are conjunctival
injection and pupillary constriction, known as miosis. The patient complains of eye pain,
dim vision, and blurred vision. This is most likely from direct contact between the agent
and eye.
Miosis may persist for long periods and may be unilateral. Severe miosis results
in the complaint of dim vision. Ciliary spasm also may cause eye pain.
Patients exposed to VX may not have miosis. This is most likely because the
eye usually is not exposed directly to the agent, unlike with the G-series agents. Miosis
may be a delayed sign of VX exposure.
Nose. Rhinorrhea is most common after a vapor exposure but also can be
observed with exposures by other routes.
Lungs. Shortness of breath is an important complaint. Patients may describe
chest tightness, respiratory distress, or gasping and even may present in apnea.

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Bronchoconstriction and excessive bronchial secretions cause these important life-
threatening symptoms.
With severe exposures, death may result from central respiratory depression
and/or complete paralysis of the muscles of respiration. Respiratory failure is the major
cause of death in nerve agent poisoning.
Skeletal muscle. Fasciculations are the most specific identifiable
manifestations of intoxication with these agents. Upon initial exposure, they can be
localized, but they then spread to cause generalized involvement of the entire
musculature (after severe exposures). Myoclonic jerks (twitches) may be observed.
Eventually, muscles fatigue and a flaccid paralysis ensues.
Skin. With small liquid exposures, localized sweating can be observed along
with the fasciculations. Generalized diaphoresis can occur with larger exposures.
Gastrointestinal. Abdominal cramping can be present. With larger exposures,
nausea, vomiting, and diarrhea are more prominent.
Heart. The patient may present with either bradycardia or tachycardia. Heart
rate depends on the predominance of sympathetic stimulation (resulting in tachycardia)
or of the parasympathetic tone (causing bradycardia via vagal stimulation). Hypoxemia
also increases adrenergic tone, which also manifests itself with tachycardia. Heart rate
is thus an unreliable sign of nerve agent poisoning.
Central nervous system. Smaller exposures to nerve agents may result in
behavioral changes such as anxiety, psychomotor depression, intellectual impairment,
and unusual dreams. Large exposures to nerve agents result in altered mentation, loss
of consciousness, and seizures.
Diagnosis. The diagnosis of nerve agent exposure is largely based on the
history of exposure and clinical findings. It is most important that physicians obtain
historical information regarding exposure to unknown substances or unusual odors
(most nerve agents smell like fruity camphor). The history of the event also provides
important information about the type of exposure. The ideal method for assessing
nerve agent intoxication is to assay tissue cholinesterase levels. As this is not possible,
plasma and erythrocyte cholinesterase levels can be used as surrogates. Erythrocyte
cholinesterase (RBC-ChE) activity can be assessed in some hospital laboratories and
is the best means for diagnosis. Inhibition of 50-90% of the enzyme activity is indicative
of significant intoxication. This test is limited, however, by its availability, turnaround
time, and variations in individual levels of cholinesterase.
Treatment
 Airway, breathing, and circulation (ABCs): Care of the ABCs should be
initiated first because intubation may be necessary in cases of severe
poisoning.
 The patient's clothes must be removed and isolated, and his or her body
washed with soap and water.
 Gastrointestinal decontamination:
• Oral administration of activated charcoal is a reasonable
intervention after ingestion of the poisons. However, as with any poisoned patient, the
risks and benefits must be weighed.
• While a recent systematic review did not find any clear evidence
supporting gastric lavage, the authors recommend it in patients who present early after
ingestion and have no vomiting and in patients who require intubation due to acute
ingestion of a nerve agents.
 Antidotes

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  Anticholinergic. Atropine - antagonizes ACh at the
muscarinic receptor. Nerve agents have a rapid effect, so that treatment must be
immediate. The action of excess acetylcholine at the muscarinic receptor level can be
reversed by atropine, which occupies the muscarinic sites and blocks the action of
acetylcholine. However, atropine will not have any action at the nicotinic receptors such
as the neuromuscular junction. Atropine will improve the effects of excessive
parasympathetic stimulation (the gastrointestinal hyperactivity, bronchospasm,
excessive glandular secretion and rhinorrhea) but will not reverse the flaccid paralysis
seen with toxic doses of nerve agent. Assisted ventilation will be required for patients
having such severe muscular weakness that they cannot oxygenate themselves.
 Reactivators of AChE. Pralidoxime chloride (2-PAM) is the
mostly widely available drug that can reactivate the organophosphate inhibited
cholinesterases by removing the organophosphoryl moiety. Although the nerve agent
initially binds reversibly to acetylcholinesterase, the binding becomes irreversible
within a few minutes to several hours depending on the agent. Once "aging" has
occurred, displacement of the nerve agent with drugs such as 2-PAM will not occur.
Armed forces operating in potential chemical warfare environments carry Mark I
autoinjectors (containing pralidoxime chloride (500 mg) and atropine (2 mg), which can
be immediately used if a nerve agent is encountered).
Minimal Exposure
Symptoms. With mild exposure the patient may have miosis, headache,
rhinorrhea, and salivation, and complain of tightness in the chest.
Treatment. These patients may be managed by removing them from the source of
exposure and that may require removal of their clothes. During the subway Sarin attack
in Tokyo, patients' clothing continued to "off gas," which resulted in continued exposure
of patients plus exposure to medical personnel. Most patients with mild exposure will
not require treatment. If eye pain is severe, topical atropine can be administered in the
eye.
Moderate Exposure
Symptoms. These patients will exhibit all of the signs and symptoms seen with
mild exposure plus increased breathing difficulty, muscular fasciculations, and severe
rhinorrhea. The rhinorrhea in these patients may be so severe as to fill their gas mask
if they are wearing one.
Treatment. These patients usually require atropine and pralidoxime. The atropine and
pralidoxime are dosed to clinical effect with a maximum of 1500 mg of pralidoxime
being used, and the atropine dosing is administered until the patient's secretions are
controlled. This will usually require 2 to 6 mg of atropine. If they were exposed to vapor,
decontamination can usually be accomplished by removal of clothes. If they were
exposed to liquid agent, they will require full liquid decontamination.
Severe Exposure
Symptoms. These patients will exhibit all of the signs listed above plus profound
rhinorrhea, severe respiratory difficulty/arrest, flaccid paralysis, and convulsions.
Treatment. Aggressive airway management, including intubation may be warranted.
Immediate antidotal therapy should be initiated using 4-6 mg atropine, 1-2 g
pralidoxime, and 10 mg diazepam. Supportive ventilatory therapy may need to be
maintained for a period of hours after administration of antidotal therapy. This group of
patients will require full liquid decontamination.
Prognosis
The prognosis of untreated nerve agent casualties varies with the severity of
their exposure. However, those with severe exposures will die from respiratory arrest

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secondary to airway obstruction and diaphragmatic paralysis within minutes.
Conversely, even patients in cardiopulmonary arrest should be treated if resources
permit, because they can survive with adequate antidotal and supportive therapy.
Patients with less severe exposures may survive delayed treatment but many have
noted enduring neurological sequelae.
Prevention
The most effective prevention for nerve agent casualties occurs before the
event. Few emergency responders have the proper training and equipment to deal with
such a crisis. As a result, the best way of preventing casualties is to enforce bans on
their manufacture and use and provide adequate intelligence and surveillance to
prevent their use by rogue organizations. Other means of prevention include personal
protec-tive equipment, patient decontamination, and chemoprophylaxis. Current
means of personal protection revolve around the use of protective suits and respiratory
equipment. Both are necessary because of the potential hazards associated with
inhalation of the vapor and skin absorption of the liquid.
Chemoprophylaxis against nerve agents consists of administering reversible
cholinesterase inhibitors prior to exposure to prevent binding of the irreversible
inhibitors (nerve agents). This is particularly useful if the nerve agent threat is Soman
(GD) or another rapidly aging agent. Chemoprophylaxis is fraught with complications,
as it must be administered over a period of several hours prior to the exposure with the
nerve agent and is not useful against agents with long aging times such as VX and
Tabun (GA). Physostigmine and pyridostigmine bromide were both studied for their
potential use as nerve agent chemoprophylaxis, but pyridostigmine is the agent of
choice as it has fewer side effects. Chemoprophylaxis is of very limited utility given its
side effects, its indication only for a limited number of agents, and the need to
administer it prior to exposure.

TOXICOLOGY OF PSYCHOTOMIMETIC POISONOUS SUBSTANCES AND

PHYSICAL INCAPACITY

I. Toxicology of psychotomimetic poisons

1. General characteristics
The psychotoxic poisonous substances (psychotomimetics; mental
incapacitating agents) belong to the group of temporarily incapacitating (non-lethal)
chemical warfare agents. Their effect is similar to endogenous psychoses. In low
concentrations they have an effect on human psychic, change the emotional sphere
and lead to inadequate respect and response to the surrounding world.
The difference between the effective and lethal doses is very big /over 1000
times/, which means that human life is not at risk.
In 1938 Hofmann and Stoll synthesised the dimethylamid of lysergic acid (DLA,
LSD-25). In 1943 Hofmann discovered the hallucinogenic effect of LSD-25 and in
1947, while studying its psychotomimetic effect in detail, called it “fantasticum”. In 1950
3- hynuklydilbenzolate (BZ) was synthesised and in 1967 it was used by American
troops during the war in Vietnam.
2. Classification
Classification of psychotomimetic agents based on their chemical structure.

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 Group Examples

Lysergic acid derivatives Lysergic acid diethylamid;

Lysergic acid morpholyd;
Lysergic acid ethylamid
Triptamin derivatives Buphotenine
Psylocine
Psylocibine
Pheniletilamin derivatives Mescaline

Glycol acid derivatives Ditrane (JB – 329)

N-metil-3 – piperidilbenzilat (JB –336)
Вz
Others 1(1-phenyl-cyclohexyle ) piperidinehydrochloride
(sernile)

Classification of psychotomimetic agents depending on similarity of their

chemical structures to those of the main mediators in the organism and to their action
mechanism.

Chemical Typical Psychotoxic doses for Latent period of Duration of

structure representatives people in mg. action in min. psychotoxic
similarity effect in hours

Serotonin LSD-25 Psylocibine 0.07-0.15 30-40 4-8

relatives 10-30 20-30 3-4
Adrenalin Mescaline 0.4-0.7 60-20 4-8
relatives
Acetylcholine Ditrane 10-20 15-30 10-36
relatives
Glycol acid BZ 0.01-0.1 6-10 200
relatives
Others Sernile 0.25-1 10-15 48

Classification of psychotomimetic agents depending on the effect they cause.

Prime toxic effect groups Examples

Marcilides (with predominant aggressive effect JB -336
component) ВZ
Hallucinogenic poisonous substances LSD-25
Mescaline
Buphotenine
Depression agents Phenilcyclidine
Sernile
Ketimines (ketalar)

3. Physical and chemical characteristics of psychotomimetic poisons

The psychotomimetic agents are solid, crystal structure substances, without
colour, scent or taste. They are administered in form of aerosols and are dispersed by
means of aerosol generators, bombs, land mines, etc. Their are active in very small
dosed and have specific effects.

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 4. Entry routes and toxicity
The psychotomimetic agents enter the organism through the respiratory and the
gastrointestinal systems. A disadvantage of their warfare characteristics is the fact that
they cannot be absorbed through the skin.
The doses which cause mental disorders and the duration of that effect are
different for each psychotomimetic agent. LSD administered in a dose of 0,001 mg/kg
of body mass causes psychosis for a period of 5-10 hours; Mescalin in a dose of 5-10
mg/kg – for a period of 10-12 hours and Ditrane in a dose of 0.05 – 0.20 gr/kg – for a
period of 10-36 hours.
5. Action mechanism
The exact mechanism which triggers mental disorders when a psychotomimetic
agent enters the organism is a complex one, not entirely understood yet. Each of these
chemical substances has a specific effect of the functions of the central neural system.
There are different theories but they give only one-sided explanation. What is certain
is the fact that their effect is a result of their complex impact on brain structures:
 Direct effect on specific morphine receptors for morphine;
benzodiazepines; neuroleptics and Imipramine;
 Direct effect on the synapses in the central neural system;
 Destruction of mediators metabolism in the organism – serotonin;
noradrenalin; adrenalin and acetylcholine;
 Direct effect on monoaminooxydation (МАО), etc.
BZ is one of the most active central cholinolitics. Psychoses caused by BZ
intoxication are due to acetylcholine function disorder in the central neural system,
which is a result of that mediator’s cholinoreceptors being blocked. The normal balance
between the adrenergic and cholinergic functions of the central neural system is
disturbed, with adrenomimetic effects occurring instead.
One theory explaining the mechanism of action of LSD is the serotonin theory.
According to that theory, LSD blocks the serotonin receptors in the CNS. On the other
hand it also inhibits MAO, which plays a role in serotonin metabolism. In that way
excess quantities of serotonin amass in the CNS, which cannot perform its function of
a mediator because its specific receptors are blocked. This is what causes mental
disorders. According to some authors the psychoses caused by LSD intoxication are
the result of catecholamine metabolism disturbance, leading to excess quantities of
adrenalin degradation products like adrenoxan; adrenolutin and adrenochromium
quantities in the organism, which themselves have psychotomimetic effects.
6. Morbid anatomy
Data concerning pathological changes in human anatomy in psychotomimetic
poisonings are scarce. Some of those substances are known to possess cytotoxic
effect on the central neural system. It is expressed in dystrophic changes in the
neurons /pycknosis and nucleus swelling, thickening or lysis of the tigroid substance,
cytoplasm vacuolization, etc./ with no disturbance of blood circulation.
7. Clinical picture
The clinical picture of psychotomimetic poisoning reveals in three stages: latent
stage, of average duration of 0.5 – hour; manifestation stage, lasting between some
hours and a few days and recovery stage, which also lasts a few days. The duration
of these stages is different for the different substances and the different individuals.
What is common for all cases of psychotomimetic substance poisonings, apart
from the disturbed psychic syndrome is the manifestation of other states, collectively
referred to as somatic syndrome / neurological and vegetative/.

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 The latent stage is the period of time between the administration of the toxic
substance into the organism and the first revelation of symptoms of intoxication.
The manifestation stage differs largely for the different toxic substances. In
cases of hallucinogenic agent poisoning, hallucinations prevail, which reflects on the
clinical picture of the poisoning. Hallucinations can be visual, auditory, taste, etc. In
depressants poisoning the disturbed psychic syndrome develops against the
background of marked depression and apathy, sometimes reaching the stage of
somnolence or even narcosis. With marcilides it is just the opposite – psychoses
develop against the background of marked agitation, rage reaching the level of
aggression.
Clinical picture of BZ (3-hinuclidilbenzilat) intoxication.
The clinical signs of intoxication reveal after a latent period of 6-10 minutes and
persist for 96 hours, as the following clearly distinguished periods are observed:
1. Primarily vegetative period: characterised by dizziness, nausea, vomiting,
dryness in the mouth, dilated pupils, tachycardia reaching 100-150 beats per minute
and in more severe cases – to 180 beats per minute. The skin and ligaments are dry,
body temperature rises to 37.5-38.5°С. The duration of that period is from 1 to 4 hours
post intoxication.
2. Primarily psychogenic period: characterised by apathy, incapability of
adequate reactions. BZ belongs to the group of marcilides and thus causes aggressive
reactions. In more severe cases abrupt psychomotor agitation occurs, accompanied
by anxiety, fear, aggression, resistance at attempts to be given aid, self-injury infliction
is also possible, etc. The duration of this period is from 4 to 12 hours.
3. Recovery period (12 to 96 hours): it is characterised by hyperactivity,
unpredictable reactions and aggressive behaviour. The symptoms gradialy weaken. In
cases of minor intoxications vegetative symptoms prevail.
Clinical picture of LSD intoxication.
1. Somatic syndromes:
- Neurological syndrome – dizziness, paresthesia, drowsiness, hands and
eye lids tremour, dysarthria. In many cases of LSD intoxication ataxia, deep live
reflexes, uncoordinated movements, movement difficulty, etc. are observed.
- Vegetative syndrome – palpitation, hyperemia of the face, increased
salivation, lacrimation, increased sweating, mydriasis, nausea, vomiting, etc.
2. Disturbed psychic syndrome
- perception symptoms: distortion of shape and colour perception.
Perception disturbance is expressed in highly enhanced brightness of colour of
surrounding objects, which constantly change shapes, become raised in parts and
moving.
- mental: sudden mood changes; distorted sense of space and time;
scytzophrenic reactions; depersonalisation; sound and vision hallucinations; suddenly
arising feeling of panic; run away or suicide inclination. The process of thinking slows
down and gets difficult. LSD intoxications are euphoric and hypomaniac. Derealisation
and depersonalisation disorders are observed. Consciousness and attention
disturbance occur. Intoxicated patients often have strong subjective, tormenting
experiences, feel strong fear and suffer from persecution mania.
Mescaline poisoning: starts with fever; headache; nausea; parenthesis,
mainly in the limbs, which are aching. Intoxicated patients become jolly, hilarious,
loquatious, fussy, their sensitivity to light increases. They lose sense of space and time,
have hallucinations, more often visual than auditory.

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 Sernyl intoxication: develops by manifestation of depersonalisation;
derealisation, distortion in thinking, low spirits, depression and drowsiness. In rare
cases intoxicated patients make grimaces or repetitive movements.
8. Diagnosis and differential diagnosis
Establishing diagnosis is difficult because of the diverse clinical symptoms, the
different chemical structure of the different psychochemical warfare agents and the
different individual sensitivity to them. Of major importance is the characteristic
disturbed psychic disorder, which prevails in the clinical picture. Typical for such
intoxications are the presence of a latent stage, relatively fast transitional character of
psychic disturbance and the mass effect of intoxication. The diagnosis is determined
by information given by chemical intelligence units and laboratory tests.
Differential diagnosis during wartime or in cases of terrorist attacks is made with
psychoses which occur as a result of the use of nuclear weapons, some other chemical
warfare agent like organophosphates, etc. Schysophrenia, as well as other reactive
psychoses should also be considered.
9. Protection, first aid and treatment
Protection is ensured by timely use gas masks. Protection against BZ also
includes skin protection measures. Partial sanitary treatment is necessary.
First aid. First aid in the affected zone consists in administration of sedatives to
violently behaving patients, their demobilisation the by means of straps and evacuation
from the affected zone.
Treatment. Treatment should be provided in specialised hospitals /therapy and
neurology clinics/, where conditions are similar to those in psychiatric hospitals. No
specific antidotes have been developed since psychotomimetic agents of different
chemical structure and different mechanism of action cause intoxications with similar
clinical picture. Depending on the stage of intoxication and the clinical picture, symptom
treatment medical products are applied (such as sedatives; analeptics; glucose;
vitamins, etc.).
Upon achievement of symptoms control, intoxicated patients should be put
under active supervision for 12-24 hours and due to the possibility of developing short-
term psychoses, they need to be kept monitored for a few more days.
II. Toxicology of physically incapacitating agents
Physically incapacitating agents belong to the group of chemical warfare agents
of temporary incapacitating effect. They are divided in two groups:
1. Physically incapacitating agents with irritating effect (harassing agents)
/poisons used by the police or riot control agents/.
2. Physically incapacitating agents disturbing motor functions, sensory
perceptions, etc.

1. Physically incapacitating agents with irritating effect (harassing agents)

General characteristics
The definition refers to chemical compounds with marked lachrymatory effect
/lachrymatory agents/ and chemical agents causing heavy sneezing and coughing
/sternites/. They are hard, crystal structure substances, used as aerosols or smoke,
produced in special generators, grenades, bombs, missiles, etc.
In peacetime such agents are used by the police to drive away rioters or
demonstrators, thus they are also called “police poisons”.
Harassing agents have a quick selective effect on the ligament of the upper
respiratory tract and the eyes. The aerosols or the hard smoke particles fall on the
ligaments, causing a very high, above norm concentration, which produces the highly

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irritating effect. Only a few particles are enough to cause heavy lachrymation and
uncontrollable sneezing. The mechanism of action is the same for all harassing
agents, expressed in strong irritation of the relevant neuro-receptors in the ligaments.
The impulses are transmitted along the branches of n. trigeminus и n. vagus to the
central neural system and the reflector response is manifested in sneezing and
lachrymation.
Poisonous substances with lachrymatory effect
Representatives:
 Ortochlorbenzalmalondinitrile /СS/: It is a colourless crystal substance
with a boiling point of 310°С. It badly dissolves in water but well in organic solvents
and in oils. Synthesized by Korean and Settern in 1923, it was widely used in the
Vietnam war during the period 1956-1970.
 Chloracetophenon: It is a colourless crystal substance with a faint scent
of violets. Its boiling point is 245°С. It badly dissolves in eater but well in organic
solvents and in oils.
 Brombenzilcianide: It is a colourless chemical compound with a scent of
bitter almonds. Its boiling point is 242°С. Its solubility characteristics are the same as
for the other representatives.
Entry routes and toxicity. Lachrymatory chemical warfare agents have a strong
irritating effect on the eyes, a slightly less irritating effect on the ligament of the upper
respiratory tract, as well as a minor irritating effect on the skin. Chloracetophenon and
brombenzilcianide have a lachrymatory effect in concentrations of 0.0003 mg/l, while
the concentration for CS is 0.001-0.005 mg/l. In very high concentrations these
chemical warfare agents, similarly to suffocating chemical warfare agents can cause
lung edema.
Mechanism of action and pathogenesis of poisoning. The irritating effects of
chemical warfare agents are of reflex character with an afferent part, starting mainly
from the eye conjunctiva, where the trigeminal nerve endings are located and also from
the ligaments of the nose, the pharynx and the bronchial tubes, on the fibers of the
trigeminal and the vagus nerve. Next to the terminal cores of the trigeminal nerve in
the central neural system are located the motor and the parasympathetic cores of the
facial nerve, which play a role in closing the reflex arc. An impulse starting from the
motor core of the facial nerve causes eyelid closing /blepharospasm/, while starting
from the parasympathetic core causes irritation of the tear gland and thus produces
profuse lachrymation. These protective reflexes are activated to prevent further
quantities of poison getting into the eyes /blepharospasm/, as well as to eliminate the
poison which has already affected the eyes /lachrymation/. In the eventual case of
pulmonary edema the neurogenic theory should be considered.
Clinical picture. Depending on the concentration of the poisonous substance
and the impact time, the following symptoms can be observed:
 Minor form: characterisied by fast occurring burning in the eyes,
lachrymation and fast blinking; moderate hyperemia of the eye conjunctive;
 Moderately severe form: to the above mentioned symptoms
blepharospasm, a feeling of sand in the eyes, photophobia and sometimes pain in the
eye orbits;
 Severe form: the above mentioned symptoms are accompanied by
sneezing, coughing with copious secretion, hoarse voice, severe headache, dizziness,
fatigue, nausea, vomiting.

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 The symptoms weaken and disappear in a few hours after leaving the
contaminated atmosphere, while in cases of moderately severe and severe forms of
intoxication they continue for about 2-3 and 5-6 days respectively.
In rare cases, when a large quantity of a lachrymatory warfare agent enters the
organism, lung edema can be developed, as well as sudden death which is of reflex
genesis. Lachrymatory warfare agents can cause skin irritation with a burning
sensation, minor redness and, in extreme cases, skin blisters on tender naked skin.
Protection, first aid and treatment. Protection against lachrymatory warfare
agents is possible by use of gas masks. First aid: first aid consists in placing a gas
mask, fast evacuation from the contaminated zone and rinsing the ayes with water.
Treatment: in cases of minor impact careful eyewash with cold water is enough to
weaken and eliminate the symptoms, while in more severe cases, eyewash with 2%
solution of sodium hydrogencarbonate or thorough rinsing with water. Eye pain is
treated with 1-2 drops of 1% solution of Dicain and cocaine. Dark sunglasses are worn
if photophobia is developed.Rubbing the eyes is contraindicated, since it can cause
hard smoke particles to get into the eye conjunctive. Only a few cases are referred to
hospitals, where they get symptom treatment.
Poisonous substances with sneezing effect
Representatives.All representatives of the group are arsenic derivatives, due to
which they are also known as arsenites or as sternites because of the characteristic
strong pain they cause behind the sternum. They are divided in two groups: fat line
chemicals, which are liquids and aromatic line chemicals, which are solids.
 Fat line representatives:
 Methyldichloroarsine
 Ethyldichloroarsine;
 Representatives of aromatic order:
 Diphenylchloroarsine;
 Diphenylcianoarsine;
 Diphenylaminochloroarsine /adamsite/.
Physicochemical characteristics. Methyldichloroarsine is a colourless liquid. It
hydrolyses in water forming a poisonous mixture of methylarsine and hydrochloric acid.
Ethyldichloroarsine is also a colourless liquid with a typical smell of onion. Both of these
liquids cause skin damage. Diphenylchloroarsine is either colourless or dark brown
crystal substance, which badly dissolves in water. Diphenylcianoarsine is a colourless
crystal substance with a smell of bitter almonds, badly water soluble. Adamsite is also
a crystal chemical compound, yellowish or green in colour. It does not dissolve in water
and does not hydrolyse. All arsenites are good organic solvents and oil solubles.
Entry routes and toxicity. Chemical warfare agents with sneezing effect enter
the organism mainly through inhalation of contaminated air. They have a strong
irritating effect on the nasal ligament and the ligament of the upper respiratory tract, a
slighter effect on the eyes and only minor effect on the skin. The irritating effect of
diphenylchloroarsine exhibits at concentration of 0.005 mg/l; while for
diphenylcianoarsine the irritating effect concentration is 0.00015 mg/l and for adamsite
it is 0.00038 mg/l. At larger concentrations, which are difficult to create in the open,
and in cases of explosions, these chemical warfare agents can be deadly. In such
cases their effects are similar to those caused by skin damaging chemical warfare
agent and more specifically to the effects of lewisite, which also belongs to the group
of arsenites.
Mechanism of action and pathogenesis of poisoning. The impulses created by
the irritation effect on the neural endings of the olfactory, the upper laryngeal and the

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trigeminal nerves are transmitted into the central neural system, where sneezing,
coughing and secretion of the upper respiratory tract ligament reflexes are triggered.
These protective reflexes are the organism’s elimination response to noxious stimulus,
affecting the respiratory system.
Clinical picture. There are three forms of intoxication: minor; moderately severe
and severe intoxication, all developing very quickly, almost without a latent period.
 Minor form: manifestation of uncontrollable sneezing, coughing and a
burning sensation in the pharynx.
 Moderately severe form: a burning pain behind the sternum, a headache,
pain in the sinuses, coughing and tearing eyes are added to the above mentioned
symptoms.
 Severe form: the above mentioned symptoms are accompanied by pain
in the jaws, which gradually engulfs the whole head. General intoxication develops
manifested in slow, shallow breathing; fatigue; facial cyanosis; cold limbs. In rare cases
pulmonary edema can also develop.
In all these forms of intoxication hyperemia of the nasal, the pharynx and the
eye ligaments is observed.
When the poisonous substance falls on the skin, redness appears after a short
latent period, followed by slight infiltration, sometimes small blisters and, rarely, surface
ulcers. The damage is temporary. Swallowing sneezing warfare agents causes severe
vomiting, that way throwing away a big part of the poisonous substance, so no severer
damage is observed.
Protection, first aid and treatment. Protection can be ensured by wearing a gas
mask. Usually, soon after leaving the contaminated atmosphere, the symptoms
weaken and disappear quickly. First aid. First aid consists in placing a gas mask, quick
evacuation from the contaminated area and eyewash with cold water. Treatment. It is
necessary to thoroughly wash the eyes, the nose and the rhinopharynx with water or
2% solution of sodium hydrogen carbonate. Rinsing the mouth with 1-2% solution of
tannin is also beneficial. A good effect against the irritating action of the poison has the
inhalation of a mixture of 40 gr. of chloroform; 20 gr. of wine alcohol and ether and 5-
10 drops of ammonia, which is popularly known as “antismoke mixture”. Ampoules
containing 1 sm3, of that mixture, wrapped in gauze tissue are available in the first aid
kit. When necessary, the content of the ampoules shall be put on the tissue and inside
the gas mask for inhalation. Headache is treated with analgesics /Analgin, Acetysal,
etc./. Stomach damage is treated by gastric lavage and symptomatic medicines. In
most cases hospitalisation is not necessary.
2. Physically incapacitating agents disturbing motor functions and sense
perceptions.
This kind of poisonous substances cause temporary destruction of the motor
functions in people, make them feel physically weak, destruct the analytic brain
functions and movement coordination, cause generated tremour, ascending spine
paralysis, etc.
Poisonous substances with a temporary destructive effect on the motor
functions of the organism cause extreme agitation /convulsions, cramps/ or
suppression /pareses, paralyses/ of the motor activity. Their mechanism of action is
not yet clearly known but the pathogenesis of poisoning is linked to their manipulation
of the sub-cortex centres and over-agitation of the parasympathicus.
Representatives:
1. Tremorine. It was first introduced in 1956 by Everett, who examined more
than 10,000 substances with a similar effect. Tremorine intoxication develops with a

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tremour which starts from the fingers and gradually overtakes the limbs and whole
body and, at times deteriorate to seizures. Miosis and increases salivation are
observed. The clinical picture is similar to the one of Parkinson disease and can
continue for more than 24 hours in cases of acute intoxication. Intoxicated patients feel
helpless, they are terrified of their condition and feel fear of nearing death. Due to these
effects tremorine and oxitremorine are also known as “fear gases”.
2. Oxytremorine. The clinical picture is similar to the one of tremorine but its
toxicity is 10 times stronger.
3. IDPN (iminodipropionitrile). Its effects were described as early as 1958 by
Lohs. It causes a constantly recurrent flexion of the head in the same direction and
circular movement. The mechanism of action is not yet fully known. It is curious that in
specialised literature there is no information of specific changes in the cerebrum. The
condition created in irreversible. It has a degree of skin absorption property.
4. Chemical compounds, similar to scutamil and carisoprodol, which cause
ascending spinal paralysis. It starts with a paralysis of the lower limbs, followed by
paralysis of the torso, the shoulder girdle, and finally, of the neck. Respiratory muscles
and the diaphragm remain unaffected. The paralysis lasts for about 24 hours, gradually
disappearing in reverse order.
Due to scarcity of information concerning these poisonous substances, there
are no specific protection measures and treatment prescribed.

ORGANISATION OF CIVIL PROTECTION IN EMERGENCY SITUATIONS –

PREVENTION AND GENERAL RESCUE MEASURES

The emergence of a challenging general and medical situation in the event of

disaster requires the rapid organisation and conduct of complex rescue and disaster
recovery measures in the affected areas, so as to prevent or mitigate the impact of the
devastation factors.
I. Civil protection
Definition
Civil Protection is an element of the National Security of the Republic of
Bulgaria. It constitutes a system of humanitarian activities with social, organisational,
economic and technoscientific nature, aimed at protecting the population and property
in case of disaster.
Main objectives
 Prevention or mitigation of the losses and negative impact of devastation
factors in case of disaster.
 Conduct of rescue and emergency operations.
 Provision of survival conditions for the population.
Means
 Education and training of the population to react to different types of
disaster situations.
 Conduct of prevention activities.
 Coordination of the operations of the Integrated Rescue System.
 Informing the population about the current situation in the disaster area
and the undertaken measures.
 Resourcing of the measures for handling emergencies.
 Providing individual and collective protective equipment.

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  Organising and conducting evacuation of people from the disaster area.
 Receiving aid from neighboring regions and other countries.
 Disaster support and recovery.
Principles
 The tasks, organisation and structures of civil protection are formed
based upon a scientifically-grounded concept and the forecasted situation in the event
of disaster on a national and local level.
 Civil protection is organised on a territorial-production basis; the
organisational development is carried out in accordance with the administrative and
economic structure of the country.
 Reasonable sufficiency in establishing the forces and means of protective
action, resources, etc; the recruitment of the main units is currently performed on a full-
time professional and voluntary basis, allowing a highly competent reaction in disaster
areas.
 Decentralisation of tasks. Nowadays, the establishment of a civil
protection system relies on the principle of decentralisation, regarding both
management and responsibilities.
Tasks. Depending on the timing and nature of the tasks they are divided into
three groups:
First group – tasks covering preventive measures and preparation for dealing
with disasters:
 Establishment and maintenance of governing bodies as well as action
forces and means in case of disaster;
 Study of the factors, conditions and probabilities of disaster outbreak in
the country;
 Forecast and assessment of the general and medical situation in different
types of disasters;
 Forecast-based emergency rescue planning ;
 Provision of individual and collective protective equipment;
 Population training;
 Organisation of the evacuation of the population to low-risk areas;
Second group – includes tasks that are performed when a state of emergency
has been announced, i.e. after the disaster has struck. The state of emergency is
declared by the Council of Ministers following a proposal put forward by the Minister of
the Interior. This group of tasks includes:
 Implementation of a National Programme for Protection in Case of
Disasters and action plans of the local units;
 Bringing the governing bodies and units of Directorate-General "Fire
Safety and Civil Protection" into a state of continuous readiness;
determining the degree of interaction and cooperation with the armed
forces;
 Assessment of the situation as well as the needs to conduct rescue
operations and provide volunteers and if necessary foreign forces;

 Constant submission of reliable information to the governmental

authorities about the current situation and the reaction of the population;
 Distribution of humanitarian aid;
Third group – includes tasks related to the organisation and management of the
rescue operations. The nature and scale of these activities depend on the information

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obtained in the assessment of the general and medical situation regarding the nature
and severity of the disaster, the size of the affected areas, the number of victims and
deaths. Based on the conclusions drawn after this assessment, forces and resources
of Derectorate-General "Fire Safety and Civil Protection“ are brought to the disaster
area, having the following tasks:
 Clearing debris, opening rescue passages, digging up buried shelters,
fire fighting;
 Searching for trapped survivors, extracting them and providing first aid;
 Body extraction and burial;
 Evacuation of the unaffected population to disaster-free areas and
organising its provisioning;
The whole complex of rescue and emergency measures is subject to one main
task: saving the lives of people caught in the disaster area.
Organisational Structure and Management of the Civil Protection System.
The Civil protection system includes central and local executive authorities and
organisations which manage, conduct and coordinate the activities related to the
protection of the population and the national economy.
The National Assembly carries out the legislative organisation of the civil
protection system safeguarding the population and the national economy in emergency
situations. The Council of Ministers (CoM) defines the state disaster policies and
exercises overall directioning and control of disaster management and recovery
measures. Given the established EU legal framework and following the changes to the
Disaster Protection Act in 2007, an Interdepartmental Commission for Recovery and
Assistance was established by the Council of Ministers. It organises, coordinates and
manages preventive activity nationwide. In case of emergency, the Commission shall
exercise overall guidance and control of the Rescue and Urgent Emergency and
Restoration Works (RUERW) across the country.
In case of disaster, a headquarters for coordination and control will be
established with the competent ministry administration taking into account the
character of the disaster.
For the successful realisation of civil protection objectives on the territory of the
Republic of Bulgaria, an Integrated Rescue System has been established, which
allows a stepwise approach to the involvement of forces and means in accordance with
the development of the emergency situation. The core mission of the System is the
organisation, coordination and management of the activity of the units, services and
structures in the preparation of disaster response and when rescue, emergency and
restoration works need to be carried out simultaneously.
The key components of the Integrated Rescue System are:
 Directorate –General “Fire Safety and Civil Protection” at the Ministry of
the Interior;
 Centers for Emergency Medical Care at the Ministry of Health.
Among the other constituent parts of the Integrated Rescue System are the
Police and the Armed Forces. The civil protection activities are implemented by units,
services and other operative structures of ministries, administrations and
municipalities, medical and health institutes, etc.
In case of disaster, the constituent parts of the Integrated Rescue System
perform their functions according to the district plans for implementation of rescue and
emergency recovery activities. The cooperation and coordination between the
components of the Integrated Rescue System, which take part in the rescue and
urgent emergency and restoration works in the disaster area, are organised and

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managed by the district governor of the Directorate-General “Fire Safety and Civil
Protection” at the Ministry of the Interior.
The Directorate "National Emergency 112 System" at the Ministry of Interior
plays an important role in initiating the actions of the components of the Integrated
Rescue System. This specialised unit includes emergency call centers, receiving calls
to the European Emergency Number – 112 (EEN) and the national emergency services
– DG "Fire Safety and Civil Protection” at the Ministry of the Interior, the Police and
Centers for Emergency Medical Care. The calls are related to the provision of help and
rapid response services in disaster situations, criminal acts, terrorist acts and medical
emergencies.
The overall management of civil protection in emergency situations is performed
by the Council of Ministers (CoM), directly by the Ministry of the Interior (MoI). On a
permanent basis and operationally it is conducted by Directorate-General “Fire Safety
and Civil Protection” (DG FSCP).
Organisational structure of Directorate–General “Fire Safety and Civil
Protection”
The DG “Fire Safety and Civil Protection” is a national specialised structure of
the Ministry of the Interior. It is a key component of the Integrated Rescue System of
the country. It includes a Headquarters, ministerial administration units, action forces
and volunteers. The Directorate – General "Fire Safety and Civil Protection” includes
28 Fire Safety and Civil Protection regional administrations.
The regional administrations operate 28 professional rescue teams, provided
with modern specialised equipment, off-road vehicles, etc. The directorate has two
rescue teams prepared for immediate involvement in humanitarian missions abroad.
Action Forces:
 Rescue teams – permanent structures for carrying out rescue and urgent
emergency and restoration works in case of peacetime and wartime disasters;
 Mixed rescue teams – established on a territorial-production basis when
potentially dangerous sites for the occurrence of a disaster situation are present; they
are staffed by DG "Fire Safety and Civil Protection" and the municipal administrations;
 Voluntary formations – formed on a voluntary (unremunerated) principle
or under contract to local administrations against payment for work completed;
 Non-military formations – established on а territorial-production basis and
intended to participate in rescue and urgent emergency and restoration works when
the situation requires an increase in the forces and means in the heart of the disaster
area.
II. Means of Civil Protection in Case of Disaster
The means of civil protection against the devastation factors of disasters include
technical instruments, equipment, heavy earthmoving equipment, chemical and
biological agents. They can be classified as:
1. Individual means of protection:
a) protection means for the face and the respiratory system:
- filtering gas masks;
- rebreathers;
b) skin protection equipment;
c) medical protection:
- antidotes;
- radioprotectants;
- vaccines;
- serums;

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 2. Collective means of protection:
a) blast shelters;
b) fallout shelters.
Individual Means of Protection
The individual means of protection are stored in the warehouses of the
Directorate – General "Fire Safety and Civil Protection" on the territory of the respective
districts and municipalities.
In the event of emergency, on instructions of the Permanent district or municipal
commissions, these means are distributed to the population by rescue teams of DG
"Fire Safety and Civil Protection".
The individual means of civil protection are intended to secure the personal
safety of people.
 Individual Protection Means for the Face and the Respiratory System
 Filtering gas mask. The filtering mask provides protection from
airborne toxic substances as well as from radioactive dust and bacterial aerosols. Many
variations of filtering masks have been developed /military, civil, industrial, children’s/
which differ in their structure, but share the same principles of construction. The main
protective function of the mask is performed by the cartridge (canister), which purifies
inhaled air of harmful substances. It is esentially a metal container enclosing:
a) A smoke filter – It purifies the inhaled air from smoke, radioactive
and bacterial aerosols by means of mechanical filtration;
b) Activated charcoal – It purifies the inhaled air from gaseous and
vapory pollutants through the adsorption mechanism;
c) A chemical absorber – It purifies the inhaled air from harmful
chemicals by means of chemical neutralisation.

DETERMINING THE SIZE OF THE FRONTAL PART OF

A CIVIL GAS MASK

Two measurements are to be performed:

- Measuring the loop which encircles the crown, cheeks and chin;
- Measuring the line connecting the ear canals and passing over the eyebrows.
The results of the two measurements are then summed.

Sum of the two measurements in Size of the frontal part

centimetres
Up to 92 cm 0

From 92 to 95,5 cm 1

From 95,6 to 99 cm 2

From 99,1 to 102,5 cm 3

Over 102,5 cm 4

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 THE IMPACT OF THE GAS MASK ON THE PHYSIOLOGICAL FUNCTIONS
OF THE BODY
The prolonged use of a gas mask negatively affects the functioning of various
organs and body systems:
 Mechanical compression of the face.
 Pain and swelling caused by incorrect size or misplacement.
 Limiting the field of vision.
 Reduction of visual acuity.
 Hearing loss.
 Speech difficulties.
 Respiratory failure. It is caused by the presence of the so-called
“dead space” and increased airway resistance. Breathing becomes irregular, shallow
and rapid. This leads to dysfunctions of the cardiovascular, nervous and other systems.
There are absolute and relative contraindications to wearing a gas mask. The
absolute ones include severe damage to the cardiovascular system /sub- and
decompensation/ and to the respiratory system /emphysema, pneumosclerosis, etc./.
Relative contraindications are acute respiratory disease / pneumonia, pleurisy, etc./,
facial dermatologic disorders /furuncles, eczema, etc./.
 Rebreathers / Rebreather-46, Oxygen rebreathers, etc/. Rebreathers
completely insulate the respiratory organs from the external environment. They sustain
breathing entirely with internally stored oxygen.
 Respirators.
 Other means of respiratory protection.
a) dust masks;
b) cotton gauze masks – they serve to protect the respiratory tract
in case of radioactive contamination and if soaked with a solution of sodium
bicarbonate (baking soda) they offer protection against chlorine gas air poisoning. If
large amounts of ammonia are contained in the air, the cotton gauze mask has to be
soaked with acetic or citric acid. The cotton gauze mask is made of a piece of gauze,
measuring 100 x 50 cm, and a piece of absorbent cotton wool. Cotton wool with uniform
thickness of 1-2 cm and size 30 x 20 cm is layered in the middle of one side of the
gauze bandage. The gauze is folded lengthwise in the middle and sewn at the edges.
Then an incision measuring 30-35 cm in length is made on both sides, so as to create
ties. The mask should cover the chin, the mouth and the nose up to the eye orbits. It
is tied crosswise: the lower ties are fastened at the crown while the upper – at the back
of the neck.
 Individual Skin Protection Equipment. These include means which
protect the body from radioactive and chemical substances and biological agents –
protective suits, cloaks, gloves, boots, etc.
1. Depending on the degree of skin protection which the individual means
offer, they are divided into:
 Insulating protective equipment – made of airproof materials;
 Filtering protective equipment - impregnated with special
substances.
2. Depending on their purpose, protective suits are divided into:
 nuclear protective suits;
 chemical protective suits;
 biological protective suits;

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 The prolonged use of protective suits can lead to serious disturbances in the
thermoregulation of the body - high temperatures can lead to overheating, and low
temperatures - to frostbite.
 Medical Protection
1. Radioprotectants.
2. Antidotes.
3. Other types of medication – painkillers, antibiotics, antiemetics.
They are assembled into:
 Individual protective kits.
 Individual First Aid Kits /IFAK-1/.
Collective Protection Means
The facilities of Directorate–General "Fire Safety and Civil Protection“ for
collective sheltering of the population (protective facilities) in the Republic of Bulgaria
are:
1. Blast Shelters – buildings and facilities that provide protection against the
shock wave, light radiation and ionizing radiation in case of a nuclear explosion.
2. Fallout Shelters – the most reliable type of protective facilities against
conventional weapons, chemical weapons, industrial poisons and radioactive
contamination. Two main types of fallout shelters exist:
 Urban fallout shelters:
 dedicated – monolithic, assembled, etc .;
 dual-purpose – in residential buildings, basements, cellars,
etc .;
 Field-type fallout shelters – specially designed for military purposes.
Fallout shelters have different capacities and levels of protection which
determine their categorisation. The most important characteristic is the manner in
which air is supplied into the shelter. According to this criterion shelters are divided
into:
 Unventilated shelters – completely hermetically sealed, they do no allow
additional air in; intended for a strictly defined number of people and for
a certain period of time;
 Shelters with air regeneration;
 Ventilated shelters – provide the most effective protection; the polluted
atmospheric air is filtered and brought into the shelter.
For the purposes of the effective sheltering of the population, employees are
subjected to preliminary allocation schemes, devised by the municipalities, according
to their residence and workplace.
Instruction signs, occupancy schedules and internal rules of conduct for the
people sheltered inside are prepared and kept by the municipal bodies.
If needed (according to the specific situation) the plans of DG "Fire Safety and
Civil Protection" are implemented and the necessary information is provided to the
population.
III. Basic Methods of Protection
1. Sheltering in protective facilities.
2. Carrying out rescue operations.
3. Distribution of personal protective equipment and medical aid.
With the purpose of ensuring disaster protection the following measures are
taken:
4. Emergency response and protection training.
5. Public service announcement.

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 6. Radiological, dosimetric, chemical and biological intelligence and
laboratory control.
7. Food, water and livestock safety.
8. Adherence to a code of conduct in the contaminated area.
9. Sanitary and anti-epidemic measures.
10. Sanitisation of people, clothing, territory.

ORGANIZATION OF THE PROVISION OF MEDICAL CARE FOR THE

POPULATION IN DISASTER SITUATIONS

I. Provision of medical care

1. Definition
The provision of medical care to the population is a complex of interconnected
organizational, treatment-and-evacuation, sanitary-hygienic and anti-epidemic
activities.
2. Goals:
Preserving the health and improving the physical condition and the work
capacity of the population.
Saving the lives of the affected people, reducing mortality and disability rates,
restoring the affected persons’ health and work capacity within the shortest possible
timeframe.
Preventing the emergence and development of infectious diseases.
3. Tasks:
Prior to the emergence of a disaster situation:
 Exploring the impact of different devastation factors in disaster situations
on the population and the means of prevention, diagnosis and treatment;
 Planning of the activities of the healthcare system in connection with the
provision of medical care to the population;
 Establishment of formations and facilities within the healthcare system,
as well as their preparation and arrangement;
 Storing the necessary reserves of medical and sanitary equipment and
supplies;
 Training the general population and the medical personnel;
 Hygiene control of blast and fallout shelters.
When a disaster situation is likely to occur:
 Deploying the formations and facilities in accordance with the operational
plant, maintaining them in operational readiness, organizing actions to
protect them;
 Preparing the system of management for a state of operational
readiness;
 Provision of medical care to the evacuated population;
 Intensification and purposeful focus of the operational and special
training of the staff at the formations and facilities within the healthcare
system;
 Intensification of the epidemiological observation of the area.
Following the occurrence of a disaster situation:
 Medical intelligence;

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  Deployment of formations in the heart of the disaster zone;
 Organization and provision of medical first aid in a timely manner in the
heart of the disaster zone;
 Moving and evacuation of the affected people to receive medical
treatment and aftercare at the medical stations and healthcare
establishments opened for that purpose;
 Conduct of the necessary complex of hygienic and anti-epidemic
activities;
 Constant management and maneuvering of the forces and resources of
the healthcare system for the purposes of their optimal use;
 Issue of forensic and medical certificates to the affected persons for the
purpose of determining their degree of disability and predicted working
capacity.
4. Principles:
 Uniformity in the use of the medical formations.
 Maximally economical use of the available forces and resources.
 Integration of the provision of treatment and evacuation /PTE/ into the
system of the overall organization of rescue operations.
 Unified coordination system for management of the rescue and medical
operations / “unified rescue system”/.
 Unified doctrine for the provision of medical assistance and treatment,
starting from the heart of the disaster zone and ending at the multi-profile
and specialized health facilities until the final outcome of the treatment.
5. Governing bodies.
The governing bodies that manage the provision of medical care in different
types of DS are distributed over several levels. The responsible authorities are: the
Ministry of Health at the national level, the Regional Health Inspectorates /RHI/ at the
regional level, and the health facilities at the municipal level.
In the event of DS, the healthcare leaders at the respective levels also become
leaders of the provision of medical care.
The Minister of Health manages the national healthcare system and the
provision of medical care in DS. The governing bodies of the healthcare system work
in close cooperation with the Ministry of the Interior, the Ministry of Defense, the
Ministry of Transport, Information Technology and Communications, the Ministry of
Justice, the Bulgarian Red Cross, different NGOs and the central and local authorities.
At the national level, the Ministry of Health develops plans for the provision of
medical care in DS, which are sanctioned by the Council of Ministers.
The Minister of Health performs the management of the provision of medical
care by issuing his orders, instructions and ordinances to the Security and Crisis
Management Council and to all other ministries and departments connected with DS.
The Minister of Health is assisted in the performance of his responsibilities by the
Security and Crisis Management Council /it includes the directors of directorates at the
Ministry of Health and the national consultant on disaster medicine/. The Security and
Crisis Management Council performs the direct management of the provision of
medical care to the population through the governing bodies at the regional and
municipals levels.
The Chief State Health Inspector organizes the actions connected with the
hygienic and anti-epidemic provision in the event of DS through:
a/ The Regional Health Inspectorates / RHI/;
b/ The National Centers of:
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  Radiobiology and Radiation Protection /NCRRP/
 Infectious and Parasitic Diseases /NCIPD/
 Public Health and Analyses /NCPHA/
At the regional level, the directors of the Regional Health Inspectorates (RHI)
develop and refine the provision of organization and resources for the plans
implemented in the event of disasters and accidents, and lead their implementation.
For the purposes of organizing the provision of medical care in disaster situations, the
director of the RHI presides over a Council of Directors, consisting of the director of
the RHI, the deputy-directors, the principal secretary, the directors of directorates, as
well as one officer with a law degree and another with a degree in economics.
The director of the RHI conducts the actions connected with the organization
and provision of medical care in disaster situations, accidents and catastrophes on the
territory of the respective region and organizes the conduct of defense and mobilization
preparations and the development of wartime plans for the organization of medical
assistance for the population of the region.
At the regional and municipal levels, the directors /managers/ of health facilities
/HF/ perform their operations in DS through a medical council by:
 Developing specific plans for the preparations and actions of the HF;
 Preparing estimates of the medical losses and the necessary forces and
resources to provide medical assistance to the injured persons;
 Establishing a structure of the bed capacity of the respective HF and
restructuring it if necessary;
 Leading the provision of medical care to the population in DS /health
facilities provide medical first aid and treatment to the injured persons in
the affected area/.
6. Formations.
 Large-Scale Medico-Sanitary Formations /LSMSF/.
The Bulgarian Red Cross (BRC) establishes and trains large-scale medico-
sanitary formations that provide medical first aid in disaster situations:
 National Disaster Response Team (NDRT). It operates on a voluntary
basis and provides assistance in the elimination of the negative impact of disaster
situations.
 Voluntary Disaster Response Team (VDRT). They perform their tasks
prior to, during and following a disaster situation. There are three VDRTs within the
system of the BRC, based in the towns of Dobrich, Pazardzhik and Ruse. Additional
teams are being established in different parts of the country.
 Force of the Mountain Rescue Service /MRS/. It consist of mountain
rescuers and dogs trained to locate buried, missing and injured persons in DS.
 Teams of swift water rescuers. They render aid to people injured in
floods. There is one national swift water rescue team and eight regional ones on the
territory of the country.
 Youth Volunteer Disaster Response Teams. On the territory of the
country there are 17 Youth Disaster Response Teams /YDRT/.
 Teams and specialists that can provide psychological first aid.
 Medical formations.
Medical teams:
 Specialized medical teams. They consist of a medical specialist, a
nurse, a driver and an ambulance. These teams are established to provide specialized
medical assistance in locations where no such specialists are generally available.

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Depending on the need, the teams can include medical specialists in the following
areas: surgery, traumatology, resuscitation, burns, neurosurgery, toxicology,
cardiology, maxillofacial injuries ,etc.;
 General medical team. It includes a therapist or pediatrician, a driver
and an ambulance. The team guides and provides medical assistance, and performs
the triage of the injured persons in peacetime disasters;
 Medical auxiliary teams – a medical auxiliary, a driver and an
ambulance. They render medical first aid;
 Transport teams – a driver with an ambulance. They deliver blood,
blood substitute, etc. for the casualties in the heart of the disaster zone.
Medical formations.
 Medical Provision Force /MPF/. This is a multifunctional formation
based on the multi-profile hospital for active treatment. It is designed to provide medical
first aid and therapeutic and surgical care delivered by qualified medical professionals
on the basis of health indicators in the heart of the disaster zone. It is organized on the
premises of surviving hospitals or public buildings and in accordance with the
established staffing plan. The force consists of 10 doctors, including surgeons and
therapists, over 30 nurses, hospital attendants, recorders, assistant pharmacists,
laboratory technicians, etc. – a total of 108 individuals. It is supplied with medical and
sanitary materials in accordance with the planning tables /medicaments, dosimetric
equipment, plasma substitutes, disinfectants, tools and instruments, wound dressings
and individual means of protection, pharmaceutic, hospital and sanitary-and-
housekeeping materials and equipment/ sufficient for 3 twenty-four-hour periods of
operation.
 Rapid Response Military Medical Team /RRMMT/. This is a moving
military medical formation set up on a functional basis and composed of specialists
from the Military Medical Academy. Its primary function is to perform triage and to
provide specialized medical care. The structure and operational organization of
RRMMT are designed to allow rapid movement and deployment in the field /the team
is equipped with a mobile diagnostic and treatment complex, a sanitary vehicle and
two resuscitation ambulances/. The formation consists of mobile groups and a
permanent component. The permanent component includes the following:
management, diagnostic and treatment complex /admission and triage; intensive care
unit; surgery; postoperative care unit; radiology unit; clinical laboratory; therapy,
gynecology, pediatric and polyclinic units/ and a service segment /pharmacy;
housekeeping, lighting and transportation units/. The module groups include the
following: surgery, radiology and toxicology modules consisting of three groups each;
resuscitation module – two groups; infectious diseases module – one group. If
necessary, it is possible to form additional therapy, pediatrics and obstetrics and
gynecology modules.
 Sanitary Control Stations (SCS). These are either regular or functional
units under the Regional Health Inspectorates. They are established to perform anti-
epidemic control and confinement measures along the main motorways and transport
hubs in order to prevent the importation of infectious diseases from neighboring
countries. The regular SCS are set up at the border crossing points. The Sanitary
Control Stations are staffed by a health inspector, a disinfector and a hospital
attendant. They work in close collaboration with the organs of the Ministry of the
Interior, which set up checkpoints near the stations.
 Sample Collection Teams /SCT/ - they are set up on a functional
principle and composed of health inspectors and sample collectors from the Regional

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Health Inspectorates. They are designed to collect samples from the external
environment in the event of disaster situations. Depending on the category, level of
preparedness and qualification of the personnel, the teams can collect between 260
and 640 samples from food products and drinking water over the course of 10 hours.
 Sanitary Vehicle Convoys /SVC/ - they are mostly used in wartime
situations and utilize the resources of road transport companies. They conduct
evacuation of injured persons from the medical stations to the health facilities. SVC
consist of a command center and four divisions that include sanitary passenger buses,
heavy duty and light duty vehicles, and passenger cars. In theory, it is estimated that
SVC can transport up to 1000 injured people per course and perform four courses over
a 24-hour period.
 Health facilities.
 Individual and group practice facilities, Diagnostic and Consultation
Centers (DCC).
 Health facilities for inpatient care:
o Active treatment hospitals: Multi-profile Hospitals for Active
Treatment /MHAT/, Specialized Hospitals for Active Treatment
/SHAT/;
o Hospitals for further treatment and continuous treatment;
o Rehabilitation hospitals.
 Medical centers. Facilities for medico-social care.
 Centers for Emergency Medical Care (CEMC). CEMC teams provide
the current emergency medical care and are the first to enter the disaster zone.
 Centers for Transfusion Hematology. They are established on the
basis of the existing centers /national and regional centers for transfusion hematology/.
Their purpose is to supply blood and blood products, etc.
II. Systems for the provision of medical care
In the event of disaster, a complex and challenging general and medical
situation emerges in the affected area. In order to achieve the optimal efficiency in the
provision of medical care and treatment to the injured persons, it is necessary to
institute a system for the provision of treatment and evacuation /PTE/. Historically, the
organized provision of medical care in large-scale disasters first took place in wartime
situations. It becomes necessary because the scale of the devastation leads to a
disparity between the resources and the needs for the provision of medical assistance.
Over the years, several types of systems for the provision of treatment and
evacuation in disaster situations have been created and developed:
 On-site treatment system.
 Evacuation system.
 System for “stage-based treatment”.
 System for stage-based treatment and destination-based evacuation.
1. Types of PTE systems
 On-site treatment system. Historically, this is the oldest system used
under wartime conditions. Complete medical care was provided at the health facilities
located in close proximity to the war theatre. The primary drawback of this system is
the low level of medical care provided on the site of the military operations, but it also
has multiple advantages:
o Avoidance of additional transportation-related trauma to the injured
persons;
o Possibility for the provision of exhaustive medical care at the health
facility;
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 o Single surgical intervention.
 Evacuation system. In order to prevent the accumulation of a large
number of injured persons in the proximity of the war theatre, the victims are rapidly
evacuated to the health facilities in the rear of the military operations. No medical care
is provided during the evacuation process, which leads to high mortality rates.
 System for “stage-based” treatment. Medical care is divided into first aid,
primary medical care, etc., and it is rendered in accordance with the respective stage
of the medical evacuation process. The term “medical evacuation stage” refers to the
medical forces and resources /medical stations, health facility, group of health facilities/
deployed in the evacuation process for the purposes of admission of casualties and
provision of medical care, treatment and preparation for further evacuation. Certain
volumes of medical care activities apply to the different stages.
 System for stage-based treatment and destination-based evacuation.
The most modern type of PTE system. Essentially, this is an improved version of the
system for “stage-based treatment” in which the victims are divided into a number of
categories /slightly injured persons, persons suffering from infectious diseases, etc./
and evacuated directly to the respective health facilities without going through all the
stages of medical evacuation.
2. Main principles in the development of a PTE system
 Developing the system based on the administrative and territorial division
of the country.
 Universal character of the system, i.e. the operational possibilities for
different types of disasters.
 Operational independence in emergency situations.
 Universality and uniformity of the principles and methods of prevention,
diagnosis and treatment of injuries.
 Effective management of the system.
3. Structuring of the PTE system
It is structured based on the existing civil healthcare network following functional
principles and is designed to provide:
 Maximum spatial and temporal proximity of the medical care to the
injured persons.
 Close cooperation between the medical teams and the other rescue
groups in the disaster area.
 Early medical triage and evacuation of injured persons.
 Continuous medical assistance provided to casualties from the heart of
the disaster zone to their hospitalization at the health facility.
In disaster situations, the first institutions providing medical assistance are the
CEMCs. In small-scale accident they can manage on their own the organization of
medical care for the injured persons. In case of large-scale devastation, the resources
of CEMC are insufficient, which activates the PTE system. The type of system to use
depends on the assessment of the general and medical situation in the heart of the
disaster zone:
 Nature and scale of the catastrophe;
 Structure and extent of the medical losses;
 Presence of an intact healthcare system or lack thereof;
 State of the personnel and material resources;
 Presence of well-equipped teams and formations;
 Presence of interstate cooperation.

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 The PTE system should be designed in a way that allows it to be adjusted
depending on the specific situation and to alter its foundations /organization, hierarchy,
interaction/.
4. Types of medical assistance provided at different stages in the
organization of the medical provision
 Medical first aid (MFA) – it is rendered in the disaster zone in the form of
individual and mutual medical assistance provided by surviving sanitary teams, civil
protection formations, the medical personnel of the surviving health facilities. MFA is
most effective during the first 30 minutes following the injury.
 Primary medical aid (PMA) – volume of activities:
o Control and continuation of MFA;
o Stopping blood loss;
o Shock prevention and anti-shock measures;
o Prevention of wound infection;
o Surgical and therapeutic aid based on vital signs /tracheotomy,
thoracocentesis, laparocentesis, primary amputation, blood vessel ligation,
venesection, skull trepanation, etc./
PMA is most effective during the first 40 munites – 6 hours, while the surgical
aid based on vital signs – 6-12 hours since the injury has occurred.
 Specializated medical aid– it is provided in specialized health facilities by
medical specialists – neurosurgeons, traumatologists, burns specialists, toxicologists,
radiologists, infectious diseases specialists, etc. It is most effective when rendered
during the first two or three 24-hour periods.
The provision of treatment and evacuation is a system of measures to render
medical aid to injured persons and to provide their evacuation and treatment until the
final outcome of the treatment.
The optimal version is the “two-stage system with destination-based
evacuation”, which includes providing a certain level of medical assistance to injured
persons in the heart of the disaster zone followed by their evacuation to the health
facilities.
The first stage of the system includes medical intelligence, medical triage,
medical evacuation and provision of medical first aid and primary medical aid.
The second stage includes destination-based evacuation, medical triage and
provision of qualified and specialized medical care.
The medical care in DS becomes more exhaustive as the casualties are moved
away from the heart of the devastation.
The purpose of the evacuation is to provide better treatment conditions than
those found in the heart of the disaster zone.

ORGANISATION AND RANGE OF FIRST MEDICAL AID, PRIMARY

MEDICAL AID AND SPECIALIZATED MEDICAL AID IN DISASTER SITUATIONS

I. First Medical Aid

Catastrophes are characterized with sudden occurrence, massive losses, initial
confusion and uncertainty about the current situation. As a result, tension and anxiety
escalate, and healthcare workers face numerous challenges. Immediately provided
first medical aid (FMA) is crucial to saving the lives of the injured, and to prevent any
complications. FMA is a prerequisite for all subsequent treatment.

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 The main goal of first medical aid is to prevent and reduce the severe
consequences of incidents, and in some cases to save the lives of the injured.
First medical aid in such cases is possible only when there is efficient
collaboration and flawless cooperation among healthcare providers and law
enforcement, technical and administrative services, Bulgarian Red Cross organization,
Directorate General “Fire Safety and Protection of the Population”, volunteering
teams, etc.
1. Organisation of First Medical Aid
First aid provision can be divided into three stages:
 Isolation stage
 Rescue stage
 Recovery stage
First stage – Isolation stage. This is the period preceding the intervention of the
relevant authorities for an organized provision of FMA. This stage focuses on the
unexpected and rapid impact of the disaster on some of the defenseless or partially
protected population. At this stage aid provision is impossible. First medical aid is
provided in the form of self-help and mutual help, healthcare and medical sanitary
centers functioning in the area of the disaster. That is why training the population to
provide immediate first medical aid is of great importance.
Second stage – rescue stage. Planned rescue operations are performed in the
area of the disaster by a specially trained team (teams of the Centers for Emergency
Medical Aid, medical teams, medico-sanitary and medical groups, groups of
Directorate General “Fire Safety and Protection of the Population”, police, etc.). The
organization of first medical aid is commissioned to an experienced physician-
organizer. The search, relief and evacuation of the injured from the affected area is
done by the rescue teams of Directorate General “Fire Safety and Protection of the
Population”. They cooperate directly with medical teams and other rescue groups.
Third stage – recovery stage. It includes the determination of the most severe
damages and their triaging, the coordination of medical and technical aid, the
distribution of sanitary materials and equipment, the enforcement of medical centers
and clinics with specialized teams, allocation of transport, the assessment of
epidemiological conditions and holding of relevant events in the area of the incident.
2. Range of First Medical Aid
 Limiting or stopping the continuous action of the damaging factors:
digging and releasing the buried from the pressing pieces, putting out fire
from burning clothes, positioning inhalers, cotton-gauze mask, or gas
mask.
 Temporary withholding of bleeding.
 Initial reanimation of breathing and blood circulation.
 Initial anti-shock activities.
 Immobilization of fractures.
 Administration of primary aseptic dressing and hydration of burnt
wounds.
 Prophylaxis of infectious complications.
 Transportation of the injured in appropriate condition to hospitals.
The temporary withholding of bleeding can be life-saving and it determines the
severity of the duration and outcome in the injured with traumatic damages. Bleeding
can be arterial / throbbing and with bright red blood/, venous /dark blood color and low
pressure flow/, and capillary /drops/. Temporary stopping of blood flow can be
performed by:
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  Pressing with fingers /digital/;
 Swabbing;
 Forced bending of the limb;
 Administering Esmarch dressing, tourniquet or using available means.
The blood –stopping dressing cannot be applied for more than 1 hour in the
winter, and 1,5-2 hours in the summer, because of irreversible necrotic processes.
During transportation with a duration exceeding this limit, a periodical release of
the hold on the dressing is applied for 5-10 minutes, followed by a direct pressing on
the blood vessel.
Primary reanimation of breathing and blood circulation. The primary reanimation
of breathing is performed through artificial respiration, or the following three basic
methods: mouth to nose, mouth to mouth, and through an appliance for artificial
ventilation. The reanimation of blood circulation is performed through extrathoracic
pressure in the heart area / the palm of the hand is placed in the area of the lower third
of sternum, and the other hand envelops the wrist of the latter hand/. The combined
primary reanimation of respiration and heart activity can be performed by one or two
rescuers. If done by only one rescuer, after two breathings, 15-30 extrathoracic
pressings are performed. If done by two rescuers, the ratio is 1:10-15. The primary
reanimation is performed until breathing and cardiac activities are restored. It is
recommended to stop the resuscitation efforts if no signs of life are present after 30-
40 minutes of effective reanimation.
The initial antishock measures, despite being simple, are fundamental for shock
prophylaxis /hemorrhagic, traumatic, thermal/. In order to preserve body temperature,
body warming is recommended (covering with a blanket, warm clothes, etc.), drinking
hot beverages (tea, coffee, sweetened water, stock, etc. through the mouth). If FMA is
provided by qualified medical staff, the fluids must be administered by IV perfusions,
which is a part of the proper treatment for shock victims. Of key importance during
shock prophylaxis is pain alleviation by analgesics /pre-filled syringe with analgin, etc.).
Furthermore, heart stimulating substances can be administered (such as caffeine,
corasol, coramin,etc.), where full rest is required. After anti-shock measures have been
taken, the victims are subjected to emergency transportation to a medical centre for
qualified surgical intervention.
Immobilisation of fractures. Immobilization reduces pain irritation, the risk of
rupture of blood vessels and fat embolism. It is performed in case of fractures /open
and closed/ on the limbs, the vertebral column, and the pelvis. Immobilization is needed
in case of widespread injuries of the soft tissues and widespread burns. Immobilization
in case of limb fracture can be performed by standard splints /Cramer, inflated splints,
etc./, triangular cloths, with available means, or through attachment of the broken limb
to the healthy one. Nevertheless, the requirements for immobilizations must be strictly
followed: two adjacent joints are immobilized; padded means are used; proper fixation
of the limb is provided, without harming major functions. In cranio-cerebral injuries, the
victim is fixed to the stretcher in stable lateral recumbency to avoid additional
complications.
Prophylaxis of infectious complications. In disaster situations prophylaxis is
necessary in cases of burns, injuries of soft tissues, open fractures, facial injuries, ENT
organs, epidemic risk, etc. Different types of sterile dressings are used /gauze, roller
bandage, cloths, special hemostatic and antiseptic dressings – lidocol, gentacol,
gemaspont, etc., personal dressing kit, etc./ Their prophylactic effect lasts for several
hours /6-8 hours/, after which the appropriate antibiotics must be administered. In a
large-scale disaster with numerous victims the surgical treatment of the wounds is

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considerably slowed down, and antibiotic administration as first aid is compulsory for
all traumatic and thermally affected, as well as in the presence of radiation factor
impact.
In order to assess the condition of unconscious victims, the following signs are
checked:
 Papillary reactions;
 The pulse in large blood vessels
 Presence of breathing checked with a smooth surface (mirror, glass,
etc.), movements of the thoracic cavity.
One must keep in mind that providing first medical aid to two or more victims
begins with the injured with strong arterial hemorrhages, then the injured who are in
shock, with signs of aphyxation, as well as children and pregnant women in otherwise
equal conditions.
Priority is given to the severely injured, whose life is under immediate threat.
These are elements of primary triaging, which is always performed together with first
medical aid provision.
Of crucial importance for FMA effectiveness is the rapid transportation of victims
after FMA provision away from the area of the incident.
The injured are separated into:
 Capable of walking independently or with an accompanying human
support;
 Those who are transported on stretchers.
The second group are predominantly severely injured, who must be positioned
properly on the stretcher depending on the character and localization of the injuries, in
order to avoid additional complications. Very often those injured must be reanimated
on the way to the hospital, or they may need close watch, performing a number of
medical manipulations during transportation (artificial ventilation, cardiotonic
measures, respiratory analeptics, etc.)
The effect of first medical aid depends on:
 The span of time from the injury to FMA provision.
 People’s knowledge of how to provide FMA (self-help or helping others)
 The preparedness and speed of the rescue groups for providing FMA.
 The possibilities for providing a certain range of FMA.
 Presence of necessary transportation.
 Presence and immediate delivery of medicines.
The efficiency of first aid is reversely proportional to time. If provided within the
first hour, the percentage of survival is up to 90%. In the following hours – up to 80%,
and for 1-2 circadian periods – up to 37%. A necessary condition for reaching a high
rate of survival is the preliminary training of people to provide first aid to the injured in
such cases. If such training has not been done, 50% of the victims are due to improper
behavior in extreme situations.
3. Specifics of FMA in chemical disaster area
The range of FMA provided to the injured in chemical disaster area /CDA/
includes the following main events:
 Detachment from the contact with the toxic substance: putting a gas
mask on the injured, a respirator, cotton-gauze mask, etc.
 Administration of antidotes or other medicines as anti-toxic measures.
 Partial sanitary treatment
 Rapid evacuation of the injured from the source.

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 FMA must be provided immediately in the form of self –help and mutual help by
the health care units which are located in the vicinity. This is important because the
noxious chemical substances, especially those in gaseous state, must be neutralized
as quickly as possible.
The toxic substances from the neuro-paralitic and general toxic elements have
a deadly effect, and that is why FMA, including antidote administration and evacuation
must be provided immediately.
On entering the CDA the rescue teams must wear a gas mask, and in case of
dermally resorbed and phosphorus organic substances – protective clothing.
The duration of intervention of FMA providers in CDA depends on the protective
power of individual means and the training of the rescuers. After finishing their work,
the rescuers leave the protective means on designated places outside the source and
undergo sanitary treatment.
4. Specifics of First Medical Aid in biological disaster area
All medical teams and centers on the territory of the disaster are used to
organize and take measures to eliminate the occurred biological disaster area /BDA/.
If needed, after a very precise estimation outside human forces can be introduced.
The main medical group which takes part in eliminating the source of biological
infection are the anti-epidemic teams under the Regional Health Inspection. They are
commissioned to organize and perform biological investigation, prophylactic vaccines,
external prophylaxis of people with wide-spectral antibiotics, of control over any
disinfection measures, of quarantine measures, health literacy, etc.
During the crossing of the territory of BDA of the medical forces and means it is
necessary to provide a special regime route service. Those passing along the route
must be immunized against the infection, which has created the source.
After eliminating the threat at the BDA, hospitalization and monitoring of the
people at the BDA are performed.
5. Specifics of First Medical Aid in nuclear disaster area
The character and range of first medical aid provided at a nuclear disaster area
are not substantially different from the aid described in the previous slide. In the region
of the incident itself, especially if it is a result of steam explosion and subsequent fire,
and if the victims have traumatic and thermal injuries, they will need dressings,
immobilization, reanimation, etc.
The Specifics of the situation require the FMA teams to work under a special
regime, radiation control and relevant protection.
Within the range of FMA are included additional measures, such as:
 Partial sanitary disinfection
 Distributing radioprotectors, means for blocking the primary radioreaction
/pirimetin, marofen/;
 Protection of the respiratory pathways and the open body parts until
leaving the affected area, etc.
II. Primary medical aid (PMA)
During a disaster of small to middle size, primary medical aid /surgical and
therapeutic based on vital signs/ is provided in actually existing preserved centers for
treatment and prophylaxis /Centers for emergency medical aid, multi-profile and
specialized hospitals, diagnostic and consultation centers, etc./ of the healthcare
network.
In cases of big disasters and complicated medical conditions, the following
medical groups are used to provide qualified physician aid with high alert:

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  Military Emergency Medical Unit /MEMU/, built on the base of Military
Medical Academy;
 Medical Provision Unit /MPU/
These medical units set up a medical centre for provision of qualified and
specialized emergency medical aid.
The medical centre for provision of qualified and specialized emergency aid is
formed in the following cases:
 Destruction of the roads, absent or insufficient transportation.
 Remote location of other medical centers
 Concurrent occurrence of a large number of injured, who cannot be
treated in the medical centers in the region.
 Difficulties in the availability or additional provision of patient beds in the
health centres.
 During war-time conditions as a first stage of medical evacuation.
A typical characteristic of PMA is the fact that there cannot be drawn a definitive
line between first medical and primary medical aid. The two types of aid overlap and
often at the source of disaster FMA and PMA are simultaneously provided. In general,
PMA is provided by Emergency Medical Aid teams, by already formed and trained
medical teams or by additionally formed teams of physicians.
During peace time catastrophes the first group, which is deployed, is the Military
Emergency Medical Unit.
This mobile unit is capable of providing the movement in the region of the
catastrophe of medical specialists in optimally short terms with the necessary
equipment to perform triaging and provision of qualified and specialized medical aid of
victims. The Military Emergency Medical Unit can divide into five modules / surgical,
radiological, toxicological, reanimation and infectious/ depending on the character of
the catastrophe. These modules can act independently or to support the medical teams
of health centres, which are within the vicinity of the affected region.
Another functional mobile group, characterized by its great maneuverability, is
the Unit for Medical Provision (UMP). The main tasks of the Unit are:
 Performing of medical investigation at the source of the disaster,
organization of search operations, provision of first medical aid and transporting the
injured.
 Forming a medical center for accepting the injured and providing PMA
and qualified therapeutic and surgical emergency aid according to the vital signs.
 Exercising dosimetric control, partial sanitary care for the injured,
decontamination of clothes and shoes.
 Provision with medico-sanitary equipment of the non-qualified groups
working in the source.
The regular staff structure of UMP includes: commanding, main /triage, surgical,
dressing, anti-shock, hospitalization, evacuation/ and auxiliary /medical, stock delivery,
sanitary transport/ units. UMP opens a medical centre on the basis of medical centres
or preserved public buildings /schools, city halls, etc./
Range of Primary medical aid
 Checking and correction of administered dressings and immobilizations
 Fighting asphyxia through artificial ventilation apparatus and
tracheotomy.
 Prophylaxis of the wound infection.
 Fighting shock and blood loss.

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  Novocain blockages and analgesia.
At UMP medical centre the following procedures can also be performed
 Final hemostasis
 Catheterization and urinary bladder puncture.
 Initial amputation of limb.
 Skull trepanation when the intracranial pressure is too high
 Thoracotomy and laparotomy.
 Administration of serums, antidotes and antibiotics.
 Preparation for evacuation.
 Temporary hospital treatment of those incapable of being transported.
The primary medical aid is most effective in the first 40 minutes – 6th hour,
whereas the surgical on vital signs – up to 6-12 hours after the body has been injured.
III. Specializated medical aid
It is provided in specialized health centres by specialists and consultants –
neurosurgeons, traumatologists, specialists in burning, toxicologists, radiologists,
infectious diseases specialists, etc.
It is most effective if provided in the first 48-72 hours after injury.

TRIAGE

I. Definition
Triage is a method of distributing injured persons into groups depending on the
character and severity of the injury and the need for uniform prevention, treatment and
evacuation measures. It becomes especially important in situations where the number
of persons requiring medical assistance /or evacuation/ exceeds the capacity of the
local /territorial/ health facilities.
Triage is used to determine the priorities concerning medical assistance and
evacuation, and the need to maintain or prevent the deterioration of the state of the
injured persons during their transportation. The disproportion between needs and
capacity, the abrupt nature of the losses and the psychological climate caused by the
disaster can lead to changes in the triage principles. Not all casualties can receive the
necessary medical assistance immediately, which means that a certain level of
selection of the injured persons is unavoidable.
The triage principle is often regarded as an inhumane, faceless and typically
military classification, which doctors find difficult to accept. In this type of situation, the
medical doctor is not required to act in accordance with the usual ethical standards –
the tendency to devote oneself completely to saving a patient in a serious condition,
sometimes even a patient who cannot be saved. The significant number of victims and
the limited resources available require the selection of injured persons and the
separation of those, who have the best chances of recovery over the shortest period
and with minimal resources.
Triage gives priority to those casualties who are deemed “savable”, i.e. those
who can survive and recover. The dire situation in the event of a disaster means that
the optimal treatment of all affected persons is practically impossible. When there is
large-scale devastation, doctors are faced with an extremely difficult choice that would
not be required in their regular medical practice.
The guiding principle underlying this action is to save as many human lives as
possible. The choice of selection criteria is made by the medical doctors present in the

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disaster area and is based on the instructions and orders of the leaders of the
respective rescue operations. This leads to a certain degree of variety in the principles
of triage which have to correspond to the actual situation.
The triage of casualties is a dynamic process, which is repeated at every stage
of the provision of medical assistance. It is of prime importance for the effectiveness of
the system of medical provision.
The decision-making process in the triage of victims of catastrophes is
influenced by a number of additional factors: the unfavorable environmental conditions,
the time required to provide the necessary medical assistance, the human resources
available, the provision of material resources, the means of transportation at the
rescuers’ disposal, the health facilities that can admit victims of the disaster, etc.
The methods of triage have to be simple and reliable, to correlate with the results
and the prognosis for the casualties who have sustained any possible type of trauma,
taking into account the polymorphism of the initial injury in different kinds of disaster
situations: traumatic damage and injuries, burns, frostbite, poisoning, psychological
reactions, etc.
Not all injured individuals require surgical intervention. Some need to receive
more or less specific resuscitation and treatment. Care has to be provided to the
uninjured “participants” in the catastrophe as well. Some or them are merely hungry
and thirsty, they demonstrate normal behavior and simply need a shelter. Others
manifest unstable behavior. They could fall into a state of panic accompanied by
prostration or excitement that interfere with the triage process. Such individuals require
isolation.
II.Triage indicators
The distribution of the victims is performed on the basis of the following primary
triage indicators:
 Threat to other people.
 Treatment indicator.
 Evacuation indicator.
Threat to other people. The injured persons who pose a risk to other people
are those contaminated with radioactive and poisonous substances, as well as persons
suffering from infectious diseases, mental health disorders, etc. Because of the danger
they pose to other people, it is necessary to perform sanitary processing of
contaminated individuals and isolation of persons suffering from especially dangerous
infections, mental health disorders, etc.
Treatment indicator.
The need for medical assistance, as well as its urgency, location and duration
determine the treatment indicator, which is used to distribute casualties into the
following categories:
 Individuals that require emergency medical assistance.
 Individuals needing medical assistance that can be postponed for the
following few hours.
 Individuals in terminal condition that need symptom-based treatment.
Evacuation indicator.
The evacuation indicator determines the need for and the order in which the
evacuation is performed, the type of transport and the position of the victims in the
vehicle. The injured persons are divided into the following groups based on this
indicator:
 Individuals to be evacuated to health facilities outside the disaster zone
(neighboring health facility, regional or central treatment center).

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  Individuals to remain in a local health facility temporarily or until the final
outcome of their treatment.
 Individuals to be returned to their place of residence or relocated to
another area for outpatient treatment.
III. Types of triage
1. Medical triage.
2. Evacuation and transportation triage.
3. Intra-station triage.
4. Hospital triage.
5. Inter-hospital triage.
Medical triage
It is conducted in the heart of the disaster zone. Depending on the severity of
their injuries, the victims are distributed into the following main groups:
 Lightly injured individuals /40%/. This group includes persons who have
sustained soft tissue injuries and do not require hospital treatment.
 Individuals who have sustained moderate and severe injuries /60%/.
Victims that require emergency medical assistance and inpatient care. This group is
further divided into four subgroups:
o Group Т1. Individuals who have sustained immediately life-threatening
injuries /20-40%/. This group includes casualties suffering from respiratory failure,
heart failure, hemorrhage, shock, etc. They receive medical first aid to stabilize their
basic vital functions and are given priority in regard to treatment.
o Group Т2. Individuals who need medical assistance that can be
postponed for 6-8 hours /20%/. They are given priority in regard to transportation, but
do not require immediate emergency treatment. This group includes persons who have
sustained thoracic and abdominal injuries, injuries to the genitourinary tract, etc.
o Group Т3. Individuals who have sustained traumatic brain injury,
spinal cord injuries and lightly injured individuals /40%/. These are persons who have
sustained traumatic injuries to the small facial bones, moderate and light soft tissue
injuries, etc.
o Group Т4. Terminally injured and moribund individuals.
When conducting primary medical triage, the doctor has to determine the
following aspects:
 Survival prognosis.
 Priority of the medical assistance based on vital signs and indicators.
 Ways to sustain the functions of vital organs.
 Treatment activities that need to be performed immediately, regardless
of the conditions and circumstances.
The diagnostic algorithm used to determine the type and degree of the damage
by means of observation, palpation, percussion and auscultation is presented below:
 respiratory function: character, rate, type of respiration, mobility of the
thoracic cage;
 cardiovascular system: pulse, rate, rhythm, arterial blood pressure;
 state /integrity/ of blood vessels, presence of external and internal
(arterial or venous) bleeding;
 state of the sense organs: motor and verbal response, pupillary
response.
When there is a significant number of casualties, the answers to these questions
need to be provided within 1-3 minutes in conjunction with the conduct of lifesaving
measures.
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 Evacuation and transportation triage
Medical evacuation from the disaster zone is a constituent component of the
system of emergency medical care and a continuation of primary medical triage.
Evacuation and transportation triage is used to determine the need for
evacuation, the means and conditions of transportation, the time and duration of the
transportation of victims, the type of vehicle used and the health facility which serves
as the destination for the evacuation.
The priority and timeframe of the medical evacuation is determined by the doctor
as s/he performs the primary medical triage. It is also determined by the need for
medical measures to be undertaken during transportation, as well as the type of
transport /road, rail, air, sanitary or adapted/.
Under equal conditions, priority in regard to medical care and medical
evacuation is given to children, pregnant women, elderly and disabled individuals.
Evacuation and transportation triage is used to divide the victims into two main
groups:
 Group of the walking wounded – it includes lightly injured persons who
can walk on their own and can assist the medical teams helping the other casualties.
They can leave the disaster zone on foot or using regular transport /buses, passenger
vehicles/ and do not require medical assistance in the process.
 Group of the victims on the ground /litter-bound/ - it includes all casualties
that require immediate medical aid based on vital signs, others for whom medical
assistance can be postponed and those that are terminally injured. This group is further
divided into two subgroups:
o Individuals that require specialized transport /ambulances, sanitary
aircraft, helicopters, buses, etc./ outfitted with resuscitation equipment if
possible.
o Casualties that can be evacuated using non-specialized transport.
Intra-station triage
It is performed at the station where the Medical Provision Force /MPF/ is based
or at a local health facility. There patients can receive primary medical aid and qualified
/therapeutic and surgical/ medical assistance based on vital signs and indicators.
At the distribution point /DP/, the casualties are subjected to dosimetric control
/if necessary/ and divided into 4 groups:
 Lightly injured.
 Severely injured.
 Radioactively contaminated.
 Persons suffering or suspected of suffering from contagious diseases, as
well as mentally ill individuals.
The following activities take place at the admission and triage department: the
medical documents /admission record, medical card for primary registration, case
history, etc./ are completed, prophylactic serums and antibiotics are administered,
urgent treatment is performed, etc.
After the available medical aid has been provided to the casualties that require
it, the intra-station triage can be initiated. It is conducted on the basis of a medical
examination of the casualties to determine the character and severity of the injury.
When the examination is performed, the diagnosis and distribution of the injured
persons into uniform groups is based on the following indicators:
 Localization of the trauma – head, thorax, abdomen, pelvis, limbs, spine.

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  Character of the trauma – multiple, combined, thermic, hemorrhage,
open or closed, broken bones, compartment syndrome, acute poisoning,
poisoning from smoke inhalation, etc.
 Leading injury /in case of combined injuries/.
 Degree of severity of the condition – consciousness, degree of impaired
consciousness, pupillary response, pulse, blood pressure, respiration,
temperature, color of mucosa and skin, awareness, capability of
independent movement, etc.
 Necessary medical aid – character, time and place to render it: on site by
a doctor or nurse, during the transportation or at the health facility.
Following the triage, the casualties are distributed to the respective departments
of the health facility for further treatment. Triage is performed by triage teams that
include doctors with different specialties and nurses.
Hospital triage
It is conducted at the regional and interregional hospitals and at the Military
Medical Rapid Response Force stations where specialized medical aid is provided.
Specialized medical aid is a continuation of the medical first aid and primary medical
aid and is regarded as the final stage of the hospital treatment until its final outcome.
The triage of casualties and the assessment of their condition is conducted
following the clinical method of diagnosis and prognosis and using auxiliary methods
for determining the prognostic index, point estimate, algorithms, tables, diagrams, etc.
When a catastrophe occurs, the health facility is not always prepared to manage
this situation using its own resources /insufficient number of specialists and limited bed
capacity/, especially in the event of medium- or large-scale disasters. This necessitates
evacuation of some of the casualties to nearby health facilities, specialized clinics and
centers for highly specialized medical care. This in turn requires triage of the admitted
casualties at the respective departments of the health facility based on treatment
indicators and the need for such highly specialized medical care. The main criterion
used in this medical triage is the stability of the general state of health and the
hemodynamics of the casualty in order to prevent the deterioration of the condition of
the injured person and the development of life-threatening complications and the need
for this type of medical assistance.
Inter-hospital triage
It is aimed at providing an even patient load and distribution of the casualties to
the nearest available health facilities in the vicinity of the disaster zone.
It is coordinated by Directorate “Medical Activities” at the Ministry of Health.

ORGANISATION OF HYGIENIC AND ANTI-EPIDEMIC SERVICES TO PEOPLE IN

DISASTER SITUATIONS

I. Specifics of the hygienic and epidemiologic conditions in disaster

situations. The damaging factors of various disasters affect the environment by
creating dire and complicated hygienic and epidemiological conditions.
Damaged and destroyed buildings and shared facilities, fire outbreaks, etc. are
frequent phenmena. This leads to pollution of the inflicted territory, of food products
and tap water, of households and industrial sites with dust, mud, waste water, organic
refuse, etc. Water supply and sewage systems are damaged. There are difficulties in
digging and burying corpses, reconstructing buildings, electricity supply and various

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communication systems. It is necessary to mention the lowering of public and personal
hygiene standards, the lack of water and sanitary units, the disregard for sanitary
requirements during food and water distribution, etc. Frequent phenomenon is the
invasion of rodents and insects, corpse decay, food and agricultural produce
decomposition, etc. A number of authors indicate the increase of populations of
infectious agents, such as those which cause malaria, yellow fever, enteric fever,
tularemia, etc.
The reasons for the appearance of various hygienic and epidemiological
problems are rooted in the increase of general morbidity, the processes of
decentralization, evacuation and transportation of the unaffected population, the
overcrowded temporary living spaces, the lack of clothing, detergents, basic personal
hygiene maintenance, cleaning, etc.
In disaster situations the above- indicated factors create favorable environment
for the appearance and development of epidemic diseases such as enteric fever,
paratyphoid fever, dysentery, salmonelosis, malaria, hepatitis, yellow fever, tularemia,
etc., of different intoxications and radiation damages.
II. Definition
Hygienic and anti-epidemic services are a key branch of healthcare activities in
disaster situations. As a part of medical services, they comprise a system of
organizational, prophylactic, sanitary, hygienic and anti-epidemic measures for the
protection of people from epidemics and harmful factors of various disasters.
The main objectives can be separated into several groups:
 Preserving health and supporting the overall physical condition of people
 Prevention of epidemic outbreaks, radiation and chemical damages
 Elimination of epidemic disaster area
 Provision of active sanitary control over outdoor sites in disaster
situations
The main problems mainly comprise the execution of sanitary and hygienic
and anti-epidemic measures. They can be preventive, protective, control and
eliminatory. Depending on the time of execution, they can be separated into two
groups:
 Problems and measures prior to disaster outbreak – they have
preventive, prophylactic and protective character
 Problems and measures in disaster situations and biological disaster
area (BDA)
III. Hygienic and anti-epidemic measures prior to disaster situations
1. Scientifically proven and specific planning. Plans are drawn by the organs
of the Regional Health Inspection and are part of the overall plan of medical services
within the territorial unit. The prognostic hygienic and epidemiological conditions are
seen as a basis for determining the needs for specific health resources and the ways
to provide them, taking in consideration the state and local health network capabilities.
2. Systemic monitoring and analysis of the health conditions and
specifics of the region:
• Infectious morbidity
• Presence of epidemic and endemic areas
• The state of the collective immunity and environmental conditions
• The spread of insects, rodents, wild animals, etc.
• Impact on the everyday life, chores, customs, health habits of the
population, the geographical specifics of the region, end others, on the development
of the epidemic process;

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 • Analysis on the organizational state of the Regional Health Inspection
and the healthcare centers, of the lab base and anti-epidemic formations, the
possibilities for providing additional beds for infected people, etc. A large number of
these factors change, which requires a constant supervision and immediate correction
of the planning documents and the approaches for action.
3. Immunization of the population. One of the main ways to protect
people from infectious diseases and epidemic outbreaks is to create specific resistance
through active or passive immunization.
• Active immunization is widely applied prior to disaster outbreak and is
performed with vaccines of living or killed microorganisms, or from their byproducts.
The acquired immunity is continuous and allows the creation of immune stratum in the
population against the most threatening infections.
• Passive immunization is performed with the help of serums and gama-
globulins. Immunity is acquired immediately, but has a short-term duration. To avoid
the disadvantages, the two methods are often combined.
4. Provision of stored means to conduct disinfection, disinsectization and
deratization activities.
5. Provision of specific staff and material resources. In general,
specialists in epidemiology, infectious diseases, sanitation, inspection, radiology,
toxicology, etc. are drawn from the staff of the Regional Health Inspection and the
regional health centers. If needed, enforcement with anti-epidemic formations, lab units
and specialized teams from neighboring regions can be provided. It is accepted to
reserve material and technical means and to organize unit formations using pre-
arranged tables.
6. Informing people about health and prophylaxis. The following
preventive measures can be taken: providing good working and household conditions,
physical education and stamina; maintaining good sanitary and hygienic conditions in
settlements, industrial areas and restaurants; provision of water, etc.
7. Educating people and healthcare providers. The systemic preparation
of healthcare providers determines to a large extent the competence and efficiency
during hygienic and anti-epidemic provision. Training people consists of
decontamination methods, care for infected patients, conduct and work at the
biological disaster area, etc.
8. Protection and systemic health control on outdoor sites.
• The protection of food products is maintained through the building of
storehouses which meet the hygienic norms and requirements, positioning the
storehouses in regions which are not exposed to threats; technical protection and
application of progressive technologies for raw resource processing. Special attention
is paid on packaging of food in protective containers, respecting the hygienic norms
and the rules at food storing and preparation sites, of the hygienic control on the
product quality, processing and packaging.
• Water protection. A large part of the settlements are facililtated with
central water supply, which is accepted as protected in disaster situations.
Underground water protection is achieved through hermetic sealing of tube wells, and
protective lids for well pits. Artesian or deep soil water sources are considered as
naturally protected. The hygienic measures include permanent control on the sanitary
state of water sources, water supply system and water quality.
9. Health control on temporary living areas, food and water distribution
sites, etc.

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 IV. Hygienic and anti-epidemic measures in disaster situations and
biological disaster area (BDA)
In disaster situations there are certain conditions which can facilitate the
outbreak and development of various epidemics. In such cases we often use the terms
“biological disaster area” (by particularly dangerous infections) and “epidemic area” (by
other infectious agents).
The measures taken during the outbreak of epidemic area in peace time
disasters and in case of a terrorist attack with a biological weapon have a complex
character and are not radically different from one another. Managers of the activities
during an epidemic area are the director of the Regional Health Inspection and the
specialized structures of the Ministry of Health, the Ministry of Agriculture and Food, or
the manager of the regional Veterinary Medical Services. If needed, the structures of
Directorate General for Fire Safety and Protection of the Population and the police (as
part of the Ministry of the Interior) participate in the anti-epidemic measures together
with the Ministry of the Defense, the Ministry of the Environment and Waters, the Plant
Protection Services, etc.
In case of a signal for the presence, or a suspicion for an outbreak of epidemic
area, biological investigation is immediately launched. The investigation consists of a
combination of measures for continuous and pertinent collection of evidence for the
situation.
Biological investigation is conducted in order to:
 Confirm the use of biological weapon
 Determine the borders of the biological disaster area
 Determine the degree of contamination of the area, air, water, food, etc.
 Determine the number of infected people and the health centres in the
affected region
 Evaluate the epidemiologic conditions
 Determine the type and the specifics of the used bioagent.
It is accepted that all investigation procedures should be conducted by teams of
the Regional Health Inspection and infectious diseases specialists. According to the
investigation results, the range and character of the measures for elimination of the
SBC are determined.
In case of confirmed infection with particularly dangerous infections (PDI) –
plague, cholera, smallpox, yellow fever, tularemia, etc. a quarantine is imposed.
“Quarantine” is the system of anti-epidemic measures in order to isolate
completely the area with the local people, animals, plants, from the surrounding
population and to eliminate the diseases at the very area.
Quarantine is announced by the Director of the Fire Safety and Protection of the
Population of the municipality or the state following a report by the Minister of Health.
In cases when the infectious agents are not part of the PDI, an observation is
ordered. “Observation” is the system of measures for enforced medical observation at
the area, medical and prophylactic activities, isolation and limiting events to stop the
spread of the infection. Observation does not include blocking of the area with armed
guards, however, the entry and exit of the population is limited and controlled.
The limiting measures (quarantine or observation) are valid up to the termination
of the optimal incubation period, typical for the infection and after the last affected
patient has been found.
Quarantine measures
 Isolation of the area with armed police forces

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  Establishing of commanding authorities on the territory of the area by
the Ministry of the Defense.
 The entry and exit of the BDA is strictly regulated. The entry in the area
is permitted only to persons, involved in its elimination, after preliminary immunization,
special protective clothing etc.
 Under no circumstances shall any objects be taken away from the area
without preliminary disinfection.
 The infected patients are hospitalized in infectious units or in opened
or adapted hospitals (units) for particularly dangerous infections.
 In case of mass diseases people are assigned to houses in groups
and enforced medical observation is provided.
 Strict anti-epidemic regime is imposed. The movement of people
within the area is allowed only if the rules for anti-epidemic control are respected.
 Food, water, basic necessities, medicines, etc. are distributed at
special sites at the border of the area.
Anti-epidemic and medical –prophylactic measures during quarantine and
observation
 Early detection of patients with infectious diseases, isolation,
hospitalization and treatment.
 Emergency prophylaxis with wide spectral antibiotics and other
medicines.
 Specific prophylaxis with vaccines, serums, etc.
 Sanitary treatment of the population.
 Large scale disinfection and deratization on the territory of the area,
vehicles, facilities, buildings, etc.
 Health education and training of the population.
 Health control.
For early detection and isolation of the patients a constant medical supervision
on the population on the territory of the BDA is organized. In case of epidemic area
outbreak medical losses are determined by the number of the infected and are
separated into primary and secondary. Primary medical losses are those patients who
get infected through water and food products, while secondary – who contract the
disease from other patients.
The medical and sanitary formations under the supervision of the Regional
Health Inspection survey households, enquire after the presence of typical symptoms
of an infectious disease, and measure body temperature. The persons surveying the
households must wear individual means of protection (masks, eyeglasses, protective
overalls or robes, rubber boots and gloves).
In order to transport the infected patients, vehicles of the Centre for Emergency
Medical Aid and specially adapted buses are used. The vehicle is disinfected, and the
accompanying medical staff is subjected to thorough sanitary treatment.
The infected patients are isolated and treated in the nearest infectious units. In
case of highly contagious diseases the patients are sent to an infectious hospital, which
is opened on the territory of the epidemic area. In case of a lack of necessary beds,
part of the infected are treated at home with respect to the strict rules for their
treatment.
Urgent prophylaxis with wide spectrum antibiotics. It is performed before the
determination of the type of the infectious agent in epidemics spreading with great
dynamics or leading to high mortality. Thus, protection from the disease is provided,

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and the patient can fight the infection more easily. After determining the type of the
agent, urgent prophylaxis can be accompanied by administering medical serums and
gama-globulins.
Specific prophylaxis. It is performed after the determination of the type of the
infectious agent. Here, artificial immunity is created through immunization of the
population. Vaccination is done cutaneously and subcutaneously, which is time-costly.
To speed up the vaccination in an outbreak of BDA it is recommended to use
needleless injection devices and aerosol vaccination methods. For some vulnerable
contingents such as children, managerial and healthcare providers, formation staff, etc.
as well as the area region population (border immunization), vaccination is mandatory.
Sanitary treatment. Sanitary treatment is divided into partial and complete.
Partial sanitary treatment is conducted at the biological disaster area and includes
cleaning the open parts of the body (face, hands, legs, etc.) with 2% solution of
chloramine, alcohol, degasifier from the universal individual protective kit, clean water,
etc. The complete sanitary treatment of the whole body is done outside the area in the
units for special treatment of medical provision teams, at washing stations, in special
baths or in home conditions, where relevant anti-epidemic requirements are met.
Disinfection, disinsectization and deratization. Disinfection, desinsectization and
deratization are conducted to decontaminate outdoor sites (territory, facilities,
buildings, food products, tap water, etc.). During disinfection mechanical, chemical and
physical methods are used, such as washing, wiping, boiling, hot steam treatment,
burning, chemical detergents, etc. To destroy the carriers of the infection insecticides
and deratization chemicals are applied.
Health education. Health education assists the inclusion of the population in the
hygienic and anti-epidemic measures and has a positive moral and psychological
impact. Media such as the radio and TV are used to explain the situation, for behavioral
measures, protection and the means for decontamination, etc.
State health control. Health control as such is the main element of hygienic and
anti-epidemic services and is a continuation of the routine control, performed by the
organs of the Regional Health Inspection.
During elimination of the BDA the following principles are observed:
 The organization of medical services to the affected is conducted
according to the on-site treatment system. Evacuation from BDA is strictly forbidden.
 During the provision of medical services all healthcare personnel,
formations and health centres (Multi-profile Hospitals for Active Treatment, Diagnostic
Consultation Centres, individual and group practices for first medical aid), which are at
the area of biological contamination are involved.
 Regional Health Inspections (RHI) perform active supervision and
investigate thoroughly the epidemiological conditions at the area of biological
contamination.

PLANNING THE MEDICAL CARE

The medical care of the population in disaster situations is a complex of

interrelated organizational, healing, evacuation and sanitary and anti-epidemic
measures.
The main prerequisite for their efficient implementation are both the in-depth
forecasting of the general and medical situation regarding the most possible disasters

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and the detailed preliminary planning of the activities and resource provision of the
health services at the respective level.
I. Nature and importance of planning
Planning during disaster situations is a main task for the governing health bodies
and is a prerequisite for a successful preparation and implementation of healing and
evacuation and sanitary and anti-epidemic measures on the territory of the outbreak.
It is necessary to stress on the significance of the unity of medical and general
saving measures. Providing timely medical assistance to the victims is closely related
to digging up destroyed buildings and shelters, extinguishing fires, recovering the
negotiability of streets and boulevards, etc. This determines the close linking of medical
events to planning that is performed by the commissions for civil protection in case of
disasters and emergencies and by the bodies of DG “Fire safety and civil protection”.
The planning of the medical care is of essential importance for determining and
maintaining the medical teams, formations and institutions in constant readiness as
well as for the provision of the necessary personnel and material and technical
resources. On the other hand, in case of “suddenness” planning allows to reduce the
time for providing different types of medical help and evacuation of the victims.
The plan for medical care in case of emergencies is a operational and staff
document. It is an intrinsic part of the general plan for protection in case of disasters
of the territorial unit.
The plan defines the guidelines, content, scope, order and deadlines of the
events to be undertaken in case of disaster situations.
II. Main goals
 Protecting the health of the population from the impact of the affecting
factors of different disasters during peace and war times.
 Saving life, reducing mortality and disability.
 Recovering the health and the ability to work of the victims.
 Providing the quick enabling of the medical forces and means and
carrying out the specific tasks for medical care for the victims in a certain manner and
scale.
 Organizing the current health care for the population from the region of
the disaster.
III. Main principles
 Territorial principle. All health facilities in the Republic of Bulgaria develop
action plans on territorial principle for undertaking urgent actions in the event of
disasters. Their nature and scope are defined by the place of the respective health
institution in the structure of the national healthcare system. This planning is carried
out at state, regional ad municipal level, by health facilities, etc.
 During planning the general principles for building civil protection and the
adopted systems for healing and evacuation and sanitary and anti-epidemic provision
during disaster situations are followed.
 Close linking to the organizational principles and approaches of current
health provision for the population in times of peace and war.
 Using the current staff structures and facilities of the healthcare system
and establishing functional units – medical teams, etc.
 Maintaining reasonable sufficiency during the planning of the necessary
staff and material and technical resources.
IV. Requirements
 To have a complex character;
 To utilize the available resources to a maximum;
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  The medical care plan should be short and simple, with a graphic and
text part and provide an opportunity to take competent and swift management
decisions on the established medical situation;
 To be realistic and flexible, so that the health care system should be able
to react timely and adequately to disasters of different nature, gravity and scale;
 The planned events should be grouped by periods of operational
readiness and the focus should be on the preparatory measures in case of danger of
disaster situations and when rescue activities are carried out;
 To be agreed with and interrelated with the plans of DG “Fire safety and
civil protection”, BRC, MoI, MoD and other in the respective region. When necessary,
the plan of the territorial unit is agreed with the plans of the neighbouring regions and
clarifies the possibilities of transborder crossing of the harmful events and
contamination of the territories.
V. Methodology of planning the medical care
Planning of the medical care of the territorial units and the health facilities is
done by the respective administrative managers and by experts in separate directions
of the activity: experts from RHI, surgeons, traumatologists, toxicologists, economists,
statisticians, etc. Planning is related to gathering certain data and analyzing a series
of factors.
The plan is developed on the base of:
 forecasting the general and the medical situation during the most
probable disasters;
 researching the medical and geographic peculiarities of the region;
 researching the needs, availability and training of health personnel;
 researching the needs and availability of medical teams and formations
and of medical and sanitary property.
Forecasting the general and medical situation is based on:
 studying and analysis of the data and instructions of the bodies of Fire
safety and civil protection and of the Intradepartmental Commission for Reconstruction
and assistance. They state the forecast of the most possible disasters and the situation
that can occur, as well as the conception and organization of the rescue events.
Information is given on the level of protection and the planned removal of the
population from the endangered or affected region. The instructions define the place
and tasks of the health bodies in planning, give the procedure and manner of
interaction, as well as the material and technical availability (facilities, transport,
technical availability, etc.).
 the methodical guidelines of the Ministry of Health and the superior health
manager on: the organization of the healing and evacuation and sanitary and anti-
epidemic provision; staff, material and technical and transport completion; organization
of blood collection and provision of blood and blood substitutes; principles and means
for managing the medical forces and means, etc.
Evaluation of the local territorial conditions and their influence on the
health condition of the population and the organization of the healing and anti-
epidemic events. To this end a medical and geographic evaluation is carried for:
 Natural factors – topography of the area, meteorological situation, soil,
hydro-geographic and bio-geographic elements, etc.
 Economic-geographic factors – density and migration of the population,
peculiarities of the settlements, number of floors of the buildings, type of the industrial
and agricultural production, the presence of potentially dangerous sites to cause
secondary outbreaks, the density and condition of the roads, etc.
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  Medical and sanitary conditions – morbidity, presence of epidemic and
endemic outbreaks, the sanitary and hygienic condition of the food and water sources,
the health culture of the population, etc.
Organizational condition of the health facilities and the RHI – availability of
medical staff and property, beds and laboratories, etc. The evaluation of these factors
affects the managerial decisions and the main events. The planning preparation pays
special attention to the evacuation peculiarities and the stationary morbidity. This gives
the opportunity to forecast the possibility of discharging a maximum number of ill
people from hospital to continue their recovery at home. Thus the acceptance capacity
of hospital facilities in the condition of disaster situations can be determined. The
transportability of the seriously ill should be determined, as well as the needs for
transportation out of the endangered region.
VI. Content of the medical care plan
Depending on the purpose of the plan (for a region, municipality, settlement or
health facility) it includes topics that are different in nature and scope. The plan consists
of:
 graphic part;
 text part;
 appendices.
The graphic part represents a topographic map or scheme of the region with
printed data about the landscape of the region, the settlements, road infrastructure,
rivers, etc.
By means of symbols the entire complex of data is input, which characterizes
the territorial unit and represents the concept of the rescue activities organization. Thus
outlined are:
1. The boundaries of the territorial unit.
2. The settlements and roads, that are related to the planned events.
3. The location of the medical staff and means – health facilities, RHI,
CEMA, medical teams and formations, warehouses for medical reserves and
pharmaceutical companies, etc.
4. The available epidemic and endemic outsources, etc.
5. The potentially dangerous sites for an outbreak of chemical
contamination outbreaks from industrial and agricultural poisons and the contamination
zones as per the forecast, the possible regions for radioactive contamination in case
of NPP failures.
6. The flooded areas during catastrophic floods.
7. The seismic zones of the forecasted earthquakes and the landslide
areas.
8. The roads for the entry of the medical formations and the points for
opening medical stations, evacuation roads for the victims, etc.
The text part describes:
1. The goals and tasks of the health bodies responsible for the medical
care during disaster situations.
2. The medical and geographic peculiarities of the region and their
influence on the organization of the medical care.
3. The forecasted general and medical situation during possible disasters.
4. Forecasts and estimates of the necessary medical staff and means for
different types of disasters.
5. The organization of the medical and evacuation and sanitary and anti-
epidemic provision of the population.

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 6. The principles and approaches for the medical and sanitary supply.
7. Organization of the messengers, the medical intelligence, the
information, the reports and the management of the medical staff and means.
8. Cooperation with the bodies and offices of MoI /FSCP, police/, MoD,
BRC, the neighbouring regions, etc.
The appendices are given in tables, schemes, etc. These are:
 estimates of the forecasted medical losses among the population,
medical staff and establishments, storages, etc.;
 the necessary, the available and the shortage of medical powers and
means, including beds and medication;
 the necessary quantities of blood, blood substitutes, means for special
treatment, equipment, etc.

MANAGEMENT OF THE MEDICAL CARE OF THE POPULATION IN DISASTER

SITUATIONS

The management of the medical care is defined as a complex activity of the

leading health bodies for assessment of the medical situation, taking managerial
decisions and management of the medical staff and means during rescue events.
The significance of the management constantly increases in the modern
conditions. The presence of a well-structured system for health care management
during disaster situations plays a key role for achieving high efficiency in the activity of
the medical teams, formations and establishments during the medical care for the
population under the difficult work conditions, mass damage and shortage of medical
resources.
I. Management principles
 Management unity and subordination. On the territory of the country, the
region and the municipality the general conception for the organization of rescue works
is determined by the respective territorial commission for civil protection in case of
disasters and emergencies. The considerations and the managerial decisions of the
health manager in medical care are subordinate to the general concept and are
approved by the head of the territorial unit.
 Reasonable combination of the principles of centralization and
decentralization, which is determined by the dynamic and complex nature of the rescue
activities. The centralization and decentralization are developed in manifests of
initiative and creativity by the health manager in conformity with the situation that
occurred.
 Undivided authority, which represents a main and important principle in
taking managerial decisions and in the management of the medical staff and means
during the rescue activities. This, however, does not exclude discussing the occurred
problems, requesting opinion, making proposals and preparing considerations.
 Applying scientifically-based organization approaches, which are used in
the health care system. In addition, into account should be taken the achievements of
the medical science and practice in surgical, therapeutic, toxicological and radiological
help, epidemiology, hygiene, etc.

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 II. Requirements of the management
 Firmness in management – it is manifested in taking swift and competent
decisions and applying certain requirements to their implementation, regardless of the
complexity and difficulties of the situation.
 Flexibility and initiative. The flexible application of the managerial
decisions is necessary because of the complex nature and frequent changes in the
situation. In such cases the initial decision does not meet the actual needs in one way
or another and it is necessary to initiate its adaptation to the actual conditions.
 Continuity in management is a requirement, which is closely related to
the constant following of the changes of the situation, directing the efforts of the
medical units to the areas that need it most, etc.
 The efficiency of the medical care activity is determined to a greater
extend by the business performance and operational preparedness of the managing
bodies. This requirement entails shortening of the periods and increasing the efficiency
of the operational activity.
 The secrecy in management refers to the disaster situations during war.
It is achieved by means of secured connections, cryptographic technical means, strict
following of the requirements for keeping state secrets, etc.
III. Content of the management
The system for medical care management consists of management bodies and
stations and of technical means for reporting and information processing. Management
bodies in health care systems are the respective health managers from all levels –
from the Ministry of Health to the local health establishments.
The management of the health system in the region of the disaster
encompasses various activities, which provide efficient usage of the medical staff and
means included in the rescue activities.
Main elements of the management are:
1. Organizing the activity of the managing health bodies.
2. Maintaining readiness for work of the medical teams, formations and
facilities.
3. Gathering information of the disaster that occurred and of the established
general and medical situation.
4. Clarifying and evaluating the medical situation and the tasks of the
medical bodies.
5. Preparing expedient considerations for the medical care during the
rescue events.
6. Carrying out medical intelligence.
7. Putting into implementation the decisions for medical care.
8. Management of the medical staff and means during the rescue works.
9. Maintaining constant cooperation with Directorate General FSCP and the
police in the MoI, MoD, sections of other Ministries and the departments, participating
in the rescue works, with the neighbouring regions, etc.
10. Organizing the supply of medical staff with medical and sanitary goods.
11. Caring out a maneuver with the medical staff and means.
12. Exercising constant control during the healing and evacuation and
sanitary and anti-epidemic events.
13. Providing the protection, shift work, rest and recovering the work ability
of the medical teams on the territory of the disaster.
14. Following the changes in the general and medical situation and taking
adequate decisions.

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 IV. Technology of the management
In case of a disaster situation the managing health bodies should tackle complex
and difficult tasks. In a short time based on the preliminary planning and the actual
situation considerations for solutions of the medical availability for the rescue works
should be prepared and once they are approved, they should be implemented and
respectively controlled.
The considerations for solution are based on:
 Evaluation of the medical situation.
 Evaluation of the sanitary and epidemiological situation.
 Evaluation of the area.
 Evaluation of the time/weather.
Evaluation of the medical situation
This evaluation includes the following main elements:
 Evaluation of the general situation. It defines the size, area and time of
the disaster. This evaluation clarifies the scope of the damage and their impact on
carrying out the rescue events.
 Evaluation of the quantity and structure of the medical losses. It is done
on the basis of the forecasted and implemented medical intelligence. This evaluation
should summarize the conclusions about the settlements, residential areas or the
specific buildings, towards which the main rescue and medical efforts should be
directed.
 Evaluation of the condition of the medical staff and means. It takes into
account:
o diseased and injured health staff;
o destroyed or subject to expert evaluation for the level of its
contamination medical and sanitary equipment;
o the number of prepared, complete and able to work medical teams,
formations and facilities;
o health facilities, RHI, laboratories, etc., that can participate in the
rescue, medical, evacuation and sanitary and anti-epidemic events;
o the volume of the different types of medical assistance, that can be
given in the health facilities, medical stations, etc.;
o the level of protection of the health staff working in the region of the
disaster, as well as of the ill and injured people.
Evaluation of the sanitary-epidemiological situation
Based on the data of the sanitary and epidemiologic condition of the region and
the situation that occurred during the disaster a conclusion can be made about the
influence of the epidemiologic factors on the organization of the medical help,
evacuation and treatment of the victims, evacuating the population from the region of
the accident, etc. To a great extent, this evaluation determines what anti-epidemic
formations and sanitary bodies should be employed at the outbreak.
A significant importance is also paid to the clarification of the necessary type
and volume of anti-epidemic measures, which need to be undertaken, including the
restricting measures on the roads and at the evacuation and housing sites, to the
introduction of anti-epidemic regime in the medical facilities, opening an infectious
hospital in the outbreak, etc.
Evaluation of the site (the region)
The specific medical and geographic analysis of the region of the disaster and
of the entire territorial unit, as well as the situation of the road network provides the
opportunity to take expedient decisions for the introduction and the activities of the

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medical teams and formations, for the way and roads for evacuation of the victims, for
the conditions and places for opening medical stations, etc.
Evaluation of time and weather
It is done as quantity (astronomic time) and quality (meteorological conditions)
in order to clarify these will affect the organization of the medical provision.
V. Considerations of the medical care
After clarifying and evaluating the situation the managing health body develops
considerations for the organization of the medical assistance to the victims and of the
sanitary and anti-epidemic provision. In its essence the considerations are a proposal
for a decision, and consist of three parts:
• Findings
• Conclusions
• Proposals for a decision
Findings
This part contains a short evaluation of the medical situation and concerns the
forecast of the following issues:
 quantity and structure of the medical loses;
 regions, settlements or residential areas, where the medical situation is
the worst and to which the main efforts of the medical teams and
formations should be directed;
 losses of medical staff and means;
 necessary, available and shortage of teams, formations, beds, medical
and sanitary equipment, blood, blood substitutes, etc.;
 condition of the sanitary and epidemiologic situation;
 physical and psychological condition of the population in the region.
Conclusions
Based on the findings about the medical situation the management draws two
main conclusions:
 is the health care system in the region of the disaster capable to organize
the medical coverage of the rescue works with its own powers and
means;
 will the sanitary and epidemiologic situation in the region and the moral
and psychological condition of the population influence the rescue works.
Proposal for a decision
In this part are proposed the main measures that need to be undertaken and
their resource provision:
 the necessary medical staff and means;
 the order and scope of providing medical help to the victims;
 the specific tasks of each medical team and formation;
 the places for opening temporary medical and loading stations;
 the roads for evacuation and the medical facilities to host the victims;
 the duration of the working hours and the places for rest;
 the орorganization of the medical and sanitary supply at the outbreak;
 the cooperation with the other parts of the Unified rescue system, the
neighbouring regions, etc.;
 the place and time for reporting the condition and the changes in the
situation and in the measures undertaken.
After being formed, the considerations are being reported to and deliberated by
the respective commission for civil protection in case of disasters and emergencies

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and are approved by the chairperson of the commission – the regional governor or the
chairperson of the municipal council. Thus the considerations become a decision for
implementing the tasks of the medical bodies during the disaster situation that has
occurred.
V. Enforcement of the decisions
This is the next responsible activity, which is realized through the so called
“private instructions”. Before them, in order to speed the rescue works up, the
managing body can issue “preliminary instructions”. Both of them are a main form of
management for the management staff of the medical facilities, formations and teams.
The managerial body uses them to define:
1. The specific task for each unit.
2. The scope of the help that needs to be provided.
3. The duration of the working hours, the way shifts are formed and
providing rest for the personnel.
4. The roads for leaving and the work places, the places to open medical
stations, temporary loading points, etc.
5. The places for evacuation, for providing specialized medical help and
treatment of the victims.
6. The beginning and the end of the rescue work.
7. The places and the way to supplement the used materials.
8. The efforts put and the reciprocal action that they should entail.
9. The requirements for the protection of the personnel, the ways for
establishing connection, the requirements about information and reporting on the
situation and the work done.
10. The place, where the managing health body is located, etc.
VI. Control over the course of the rescue works
It gives opportunity to actually assess the adequacy of the medical measures
compared to the established situation, for quick reaction to its changes, for maneuver
with the available medical forces and means, etc. The control is active and is carried
out through:
1. Immediate observation and interference in the course of the events held.
2. By means of reports.
3. Maintaining a constant contact with the people working in the region of
the outbreak, etc.

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