Health Service Support in a Nuclear, Biological, and Chemical Environment

Chapter XIV: Appendix: A

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MEDICAL EFFECTS OF NUCLEAR, BIOLOGICAL, AND CHEMICAL WEAPONS AND TOXIC INDUSTRIAL MATERIAL

A-1. General

Biological and chemical weapons/agents may be employed by assassins, terrorists, rebels, and insurgents, as well as well-formed battle organizations, across the continuum of operations. In addition, nuclear weapons will remain a threat on the future battlefield. Another weapon that may be used is the RDD. The RDD can cause significant damage and present health hazards to fighting forces by exposing them to radiation without the thermal and full blast effects of nuclear weapons. The RDD can disperse radioactive material over an area of the battlefield; the area covered is dependent upon the amount of radioactive and explosive material used. In order to detonate a nuclear weapon, an adversary must first obtain access to the appropriate weapons-grade material. However, an RDD can be produced and used by anyone with access to industrial or medical radioisotopes and explosives. Biological agents are easy to disperse on the battlefield without immediate detection; however, their effects on exposed troops can change the course of the battle. Some nations consider chemical weapons as a component of their munitions for the battlefield. As more nations enter the arena of developing biological and chemical weapons, their potential effects on our troops will increase. The enemy's use of TIMs as weapons or collateral damage to TIM storage faculties can severely affect the unit personnel's ability to continue the mission. The signs and symptoms of some TIM exposure can be the same as those presented from exposure to NBC weapons. Considerations of both the physical and biological effects of these weapons are required for HSS operations. Field Manual 4-02.283 provides additional information on nuclear and radiological effects; FM 8-284 provides additional information on biological agent effects; FM 8-285 provides additional information on CW effects; FM 8-500 provides detailed information on hazardous material (TIM) effects.

A-2. Physical Effects of Nuclear Weapons

_a._ The principal physical effects of nuclear weapons are blast, thermal radiation (heat), and nuclear radiation. These effects are dependent upon the yield (or size) of the weapon expressed in kilotons (KT), the physical design of the weapon (such as conventional and enhanced), and the method of employment. The distribution of energy (Figure A-1) from the detonation of a moderate-sized (3 to 10 KT) weapon is as follows:

(1) Fifty percent as blast.

(2) Thirty-five percent as thermal radiation; made up of a wide
spectrum of electromagnetic radiation, including infrared,
visible, and ultraviolet light and some soft x-ray radiation.

(3) Fourteen percent as nuclear radiation, 4 percent as initial
ionizing radiation composed of neutrons and gamma rays emitted
within the first minute after detonation, and 10 percent as
residual nuclear radiation (fallout).

(4) One percent as EMP.

_b._ Larger weapons are more destructive than smaller weapons, but the destructive effect is not linear. Table A-1 presents a comparison of three aspects of nuclear weapons effects with yield.

_c._ The altitude at which the weapon is detonated determines the blast, thermal, and nuclear radiation effects. Nuclear blasts are classified as air, surface, or subsurface bursts.

(1) An airburst is a detonation in air at an altitude below
30,000 meters, but high enough that the fireball does not touch
the land or water surface. The altitude is varied to obtain
the desired tactical effects. Initial radiation will be a
significant hazard, but there is essentially no local fallout.
However, the ground immediately below the airburst may have a
small area of neutron-induced radioactivity. This may pose a
hazard to troops passing through the area.

(2) A surface burst is a detonation in which the fireball
actually touches and vaporizes the land or water surface. In
this case, the area affected by blast, thermal radiation, and
initial nuclear radiation will be smaller than for an airburst
of comparable yield. However, in the region around ground
zero, the destruction will be much greater and a crater is
often produced. Additionally, all the material that was within
the fireball becomes fallout and will be a hazard downwind. A
surface burst is the most likely type of terrorist detonation.

(3) A subsurface burst is an explosion in which the detonation
is below the surface of land or water. Cratering usually
results. If the burst does not penetrate the surface, the
only hazard is from the ground or water shock. If the burst
penetrates the surface, blast, thermal, and initial nuclear
radiation will be present, though less than for a surface burst
of comparable yield. Local fallout will be heavy over a small
area.

(4) A high altitude burst occurs above 30,000 meters. Radiation
and physical effects do not reach the ground and there is no
local fallout. This is the only detonation where the effects
of the EMP are significant. Nonhardened electronic equipment
including many medical devices may become inoperative. The EMP
damage is a moot point with other types of detonations, as its
range is primarily limited to the area of intense physical
destruction.

_Table A-1. Comparison of Weapons Effects (Radii of Effects in Kilometers--Airburst)_

==============================================================
1 KT 20 KT 100 KT 1 MT 10 MT
--------------------------------------------------------------
NUCLEAR
RADIATION 0.71 1.3 1.6 2.3 3.7
(1,000 cGy)
--------------------------------------------------------------
BLAST (50% INCIDENCE
OF TRANSLATION WITH
SUBSEQUENT IMPACT 0.28 1.0 1.4 3.8 11.7
WITH A NON-YIELDING
SURFACE)
--------------------------------------------------------------
THERMAL (50% INCIDENCE
OF 2ND-DEGREE BURNS TO 0.77 1.8 3.2 4.8 14.5
BARE SKIN, 10 KM
VISIBILITY)
==============================================================

A-3. Physiological Effects of Nuclear Weapons

The physiological effects of nuclear weapons are the result of exposure to the blast; thermal radiation; ionizing radiation (initial or residual) effects; or a combination of these. For smaller weapons (less than 10 KT), ionizing radiation is the primary creator of casualties requiring medical care, while for larger weapons (greater than 10 KT), thermal radiation is the primary creator of casualties.

_a._ The rapid compression and decompression of blast waves on the human body results in transmission of pressure waves through the tissues. Resulting damage is primarily at junctions between tissues of different densities (bone and muscle), or at the interface between tissue and airspace. Lung tissue and the gastrointestinal system (both contain air) are particularly susceptible to injury. The tissue disruptions can lead to severe hemorrhage or to an air embolism; either can be rapidly fatal. Direct overpressure effects do not extend out as far from the point of detonation as the drag force and are often masked by the drag force effects. A typical range of probability of lethality, with variations in overpressure for a 1 KT weapon, is shown in Table A-2.

_Table A-2. Range of Lethality of Peak Overpressure_

==============================================================
LETHALITY PEAK OVERPRESSURE DISTANCE FROM
(APPROXIMATE %) (ATMOSPHERES) GROUND ZERO; METERS
--------------------------------------------------------------
1 2.3-2.9 150
50 2.9-4.1 123
100 4.1+ 110
==============================================================

(1) The significance of the data is that the human body is
relatively resistant to static overpressure compared to rigid
structures such as buildings. For example, an unreinforced
cinder block panel will shatter at 0.1 to 0.2 atmospheres.

(2) Overpressure lower than those in Table A-2 can cause
nonlethal injuries such as lung damage and eardrum rupture.
Lung damage is a relatively serious injury, usually requiring
hospitalization, even if not fatal; whereas eardrum rupture is
a minor injury, often requiring no treatment at all.

(_a_) The threshold level of overpressure for an unreinforced
unreflected blast wave that can cause lung-damage is about 1.0
atmosphere.

(_b_) The threshold level for eardrum rupture is around 0.2
atmospheres; the overpressure associated with a 50 percent
probability of eardrum rupture is about 1.1 atmospheres.

(3) Casualties requiring medical treatment from direct blast
effects are produced by overpressure between 1.0 and 3.5
atmospheres. However, other effects (such as indirect blast
injuries and thermal injuries) are so predominate that patients
with only direct blast injuries make up a small part of the
patient workload.

_b._ The drag forces (indirect blast) of the blast winds are proportional to the velocities and duration of the winds. The winds are relatively short in duration, but can reach velocities of several hundred km per hour. Injury can result from missiles impacting on the body or from the physical displacement of the body against objects and structures.

(1) The distance from the point of detonation at which severe
indirect injury occurs is greater than that for equally serious
direct blast injuries. A high probability of serious indirect
injury can occur when the peak overpressure is about 0.2
atmospheres. This range will increase with the increased size
of the weapon; for a 1 KT weapon, the range is 0.22 km, whereas
for a 20 KT weapon, the range is 0.76 km. At greater ranges
injuries will occur and casualties will be generated, but not
consistently.

(2) The drag forces of the blast winds produced by a nuclear
detonation are so great that almost any form of vegetation or
structure will be broken up or fragmented into missiles. Thus,
multiple, varied missile injuries will be common, increasing
their overall severity and significance. Table A-3 lists ranges
at which significant missile injuries can be expected.

_Table A-3. Ranges for Probabilities of Serious Injury from Small Missiles_

=================================================================
RANGES (km)
-----------------------------------------------------------------
YIELD 1% PROBABILITY OF 50% PROBABILITY OF 99% PROBABILITY OF
(KT) SERIOUS INJURY SERIOUS INJURY SERIOUS INJURY
-----------------------------------------------------------------
1 0.28 0.22 0.17
10 0.73 0.57 0.44
20 0.98 0.76 0.58
50 1.4 1.1 0.84
100 1.9 1.5 1.1
200 2.5 1.9 1.5
500 3.6 2.7 2.1
1,000 4.8 3.6 2.7
-----------------------------------------------------------------
1 INCIDENCE OF INJURY BASED ON SKIN AND TISSUE PERFORATION.
2 MISSILES USED WERE 10 GRAM (gm) IN WEIGHT.
=================================================================

(3) The velocity to which missiles are accelerated is the major
factor in causing injury. The probability of a penetration
injury increases with increasing velocity, particularly for
small, sharp missiles such as glass fragments. Small, light
objects are accelerated to speeds approaching the maximum
(wind) velocity. Table A-4 shows data for probability of
penetration related to size and velocity of glass fragments.

_Table A-4. Probability of Glass Fragments Penetrating the Abdominal Cavity_

=======================================================
MASS OF GLASS 1% 50% 99%
FRAGMENTS (gm) IMPACT VELOCITY (METERS PER SECOND)
-------------------------------------------------------
0.1 78 136 243
0.6 53 91 161
1.0 46 82 143
10.0 38 60 118
=======================================================

(4) Heavy, blunt missiles may not penetrate, but can result
in significant injury, particularly fractures. The threshold
velocity for skull fractures from a 4.5 milligram (mg) missile
is about 4.6 meters per second (m/sec).

(5) The drag forces of the blast winds are strong enough to
displace large objects (such as vehicles), or cause large
structures to collapse (such as buildings) resulting in serious
crushing injuries. Man himself can become a missile resulting
in injuries (called translational injuries). The velocity at
which the body is displaced will determine the probability and
the severity of injury. Assuming a displacement of 3.0 meters,
the impact velocity associated with various degrees of injury
is shown in Table A-5. The velocities in Table A-5 can be
correlated against yield. The ranges at which such velocities
can occur and the probability of injury are given in Table A-6.

_Table A-5. Translational Injuries_

================================================
A. BLUNT INJURIES AND FRACTURES
PROBABILITY OF INJURY VELOCITY (m/sec)
------------------------------------------------
1% 2.6
50% 6.6
99% 16.5
------------------------------------------------
B. FATAL INJURIES
PROBABILITY OF FATALITY VELOCITY (m/sec)
------------------------------------------------
1% 6.6
50% 17.0
99% 39.7
================================================

_Table A-6. Ranges for Selected Impact Velocities of a 70-Kilogram Human Body Displaced by Blast Wind Drag Forces for Different Yield Weapons_

==============================================
WEAPON YIELD VELOCITIES (m/sec)
(KT) 2.6 6.6 17.0
----------------------------------------------
RANGES (km)
----------------------------------------------
1 0.38 0.27 0.19
10 1.0 0.75 0.53
20 1.3 0.99 0.71
50 1.9 1.4 1.0
100 2.5 1.9 1.4
200 3.2 2.5 1.9
500 4.6 3.6 2.7
1,000 5.9 4.8 3.6
===============================================

A-4. Biological Effects of Thermal Radiation

The thermal radiation emitted by a nuclear detonation causes burns in two ways--by direct absorption of the thermal energy through exposed surfaces (flash burns); or by the indirect action of fires in the environment (flame burns). Indirect flame burns can easily outnumber all other types of injury.

_a._ Thermal radiation travels outward from the fireball in a straight line; therefore, the amount of energy available to cause flash burns decreases rapidly with distance. Close to the fireball all objects will be incinerated. The range for 100 percent lethality will vary with yield, height of burst, weather, environment, and immediacy of treatment. The critical factors determining the degree of burn injury are the flux (calories per square centimeter/second [cal/cm^2/sec]) and the duration of the thermal pulse. The total amount of thermal radiation needed to cause a flash partial thickness burn on exposed skin will vary with the yield of the weapon and the nature of the pulse (Table A-7). Most burn patients will come from the zones where partial thickness burns occur. In areas where radiation, blast, and thermal intensity are highest, burn victims surviving long enough to reach medical care will be rare.

NOTE

The battle dress uniform (BDU), MOPP gear, or any other
clothing will provide additional protection against flash
burns. The airspace between the clothing significantly impedes
heat transfer and may prevent or reduce the severity of burns,
depending on the magnitude of the thermal flux.

_Table A-7. Factors for Determining the Probability of Partial Thickness Burns_

==================================================================
YIELD OF WEAPON 1 KT 10 KT 100 KT 1 MT 10 MT
------------------------------------------------------------------
RANGE (km) FOR PRODUCTION
OF PARTIAL THICKNESS BURNS 0.78 2.1 4.8 9.1 14.5
ON EXPOSED SKIN
------------------------------------------------------------------
DURATION OF THERMAL
PULSE IN SECONDS 0.12 0.32 0.9 2.4 6.4
------------------------------------------------------------------
Cal/cm^2/sec REQUIRED TO
PRODUCE PARTIAL THICKNESS 4.0 4.5 5.3 6.3 7.0
BURNS ON EXPOSED SKIN
==================================================================

_b._ Indirect (flame) burns result from exposure to fires caused by the thermal effects in the environment, particularly from ignition of clothing. The larger-yield weapons are more likely to cause firestorms over extensive areas. There are too many variables in the environment to predict either incidence or severity of casualties. Expect the burns to be far less uniform (in degree) and not limited to exposed surfaces. For example, the respiratory system may be exposed to the effects of hot gases produced by extensive fires. Respiratory system burns cause high morbidity and high mortality rates.

_c._ The initial pulse of radiation in the optical and thermal bands can cause injuries in the forms of flash blindness and retinal scarring. The initial brilliant flash of light produced by the nuclear detonation causes flash blindness. This flash swamps the retina, bleaching out the visual pigments and producing temporary blindness. During daylight hours, this temporary effect may last for about 2 minutes. At night, with the pupil dilated for dark adaptation, flash blindness will affect personnel at greater ranges and for greater durations. Partial recovery can be expected in 3 to 10 minutes, though it may require 15 to 35 minutes for full night adaptation recovery. Retinal scarring is the permanent damage from a retinal burn. It will occur only when the fireball is actually in the individual's field of view and should be a relatively uncommon injury. The location of the scar will determine the degree of interference with vision. Because night vision apparatus electronically amplifies an image, it cannot transmit the flash intensity and will not cause eye injury.

A-5. Physiological Effects of Ionizing Radiation

A nuclear burst results in four types of ionizing radiation: neutrons, gamma rays, beta, and alpha radiation. The initial burst is characterized by neutrons and gamma rays while the residual radiation is primarily alpha, beta, and gamma rays. The effect of radiation on a living organism varies greatly by the type of radiation to which the organism is exposed. See Table A-8 for characteristics of nuclear radiation.

_a._ Alpha particles are extremely massive, charged particles (four times the mass of a neutron); they are a fallout hazard. Because of their size, alpha particles cannot travel far and are fully stopped by the dead layers of the skin or by the uniform. Alpha particles are a negligible external hazard, but if inhaled or ingested, can cause significant internal damage.

_Table A-8. Characteristics of Nuclear Radiation_

_b._ Beta particles are very light, charged particles that are found primarily in fallout radiation. These particles can travel a short distance in tissue; if large quantities are involved, they can produce damage to the basal stratum of the skin. The lesion produced is similar to a thermal burn (called a beta burn).

_c._ Gamma rays, emitted during the nuclear detonation and in fallout, are uncharged radiation similar to X rays. They are highly energetic and pass through matter easily. Because of its high penetrability, radiation can be distributed throughout the body, resulting in whole body exposure.

_d._ Neutrons, like gamma rays, are uncharged, are only emitted during the nuclear detonation, and are not a fallout hazard. However, neutrons have significant mass and interact with the nuclei of atoms, severely disrupting atomic structures. Compared to gamma rays, they can cause 20 times more damage to tissue.

_e._ When radiation interacts with atoms, energy is deposited resulting in ionization (electron excitation). This ionization may involve certain critical molecules or structures in a cell, producing its characteristic damage. Two modes of action in the cell are direct and indirect action. The radiation may directly hit a particularly sensitive atom or molecule in the cell. The damage from this is irreparable; the cell either dies or is caused to malfunction. The radiation can also damage a cell indirectly by interacting with water molecules in the body. The energy deposited in the water leads to the creation of toxic molecules; the damage is transferred to and affects sensitive molecules through this toxicity.

_f._ The most radiosensitive organ systems in the body are the male reproductive, the hematopoietic, and the gastrointestinal systems. The relative sensitivity of an organ to direct radiation injury depends upon its component tissue sensitivities. Cellular effects of radiation, whether due to direct or indirect damage, are basically the same for the different kinds and doses of radiation. The simplest effect is cell death. With this effect, the cell is no longer present to reproduce and perform its primary function. Changes in cellular function can occur at lower radiation doses than those that cause cell death. Changes can include delays in phases of the mitotic cycle, disrupted cell growth, permeability changes, and changes in motility. In general, actively dividing cells are most sensitive to radiation. Additionally, radiosensitivity tends to vary inversely with the degree of differentiation of the cell.

_g._ Predicting radiation effects is difficult because often it is unknown which organs were exposed. Thus, most predictions are based on whole body irradiation. Partial body and specific organ irradiation will occur due to shielding by equipment, from fallout particles, or from internal deposition. Depending upon the organ system, the irradiation can be severe. The severe radiation sickness resulting from external, whole body irradiation and its consequent organ effects is a primary medical concern. The median lethal dose (LD) of radiation that will kill 50 percent of the exposed persons within a period of 60 days (designated as LD50/60) is estimated to be approximately 4.5 gray (Gy) if appropriate medical care is not provided to the casualties. Medical intervention should raise this figure to approximately 10 Gy. This larger figure includes most of the casualties who would be actually capable of reaching medical care following a nuclear detonation, and nearly all those who could be exposed to a RDD. For acute effects of single high dose rate exposures of whole-body irradiation to healthy adults see Table A-9.

_h._ Recovery of a particular cell system will occur if a sufficient fraction of a given stem cell population remains after radiation injury and appropriate stimulation and protection are received. Complete recovery may appear to occur; however, the immune system may repair incompletely with consequent greater susceptibility to future insult from a variety of agents. It is possible for late somatic effects to have a higher probability of occurring because of the radiation damage. Efficacy of both prior and future immunization in this group is not adequately understood.

_i._ Interactions between radiological injury and chemical or biological agents appear to be synergistic. Insult by these agents in radiologically injured personnel, even in individually subclinical dosages, may result in significant clinical illness.

A-6. Handling and Managing Radiologically Contaminated Patients

_a._ _Radiologically Contaminated Patients._ Personnel from contaminated areas may have fallout on their skin and clothing. Although the individual will not be radioactive, he may suffer radiation injury from the contamination. Removal of the contamination should be accomplished as soon as possible; definitely before admission into a clean treatment area. The distinction must be made between a radiation-injured soldier and one who is radiologically contaminated. Although personnel may have received substantial radiation exposure, this exposure alone does not result in the individual being contaminated. Contaminated personnel do not pose a short-term hazard to the medical staff, rather the contamination is a hazard to the individuals' health. However, without patient decontamination, medical personnel may receive sufficient exposure to create beta burns, especially with extended exposure.

_b._ _Handling Radiologically Contaminated Patients._ To properly handle radiologically contaminated personnel, medical personnel must first detect the contamination. Detectors that may be used are the AN/PDR27 and AN/VDR2 to monitor patients for contamination. Generally, a reading on the meter twice the current background reading indicates that the patient is contaminated. Monitoring is conducted when potentially contaminated personnel arrive at the MTF. This monitoring is conducted at the MTF's receiving point before admitting the patient. Contaminated patients must be decontaminated before admission. Removal of radiological contamination is less important than immediate lifesaving treatment and providing the best possible medical care. Lifesaving care before decontamination is provided outside the MTF.

_c._ _Decontamination._ Removing all outer clothing and a brief washing or brushing of exposed skin will reduce 95 percent of contamination; vigorous bathing or showering is unnecessary. See Appendix G for patient decontamination procedures.

_d._ _Internal Contamination._ Internalization of radioactive isotopes will primarily occur via inhalation, ingestion, and contaminated wounds. Extensive internal decontamination should only be undertaken when individual dose estimates indicate that the individual will benefit from the procedures. Soldiers who wear their protective mask will be adequately protected from inhalation and ingestion of radioactive particulate matter. Internal contamination is considered a delayed problem and does not influence triage categories, as does irradiation injury.

_e._ _Treatment._ Treatment procedures for radiation injuries are described in FM 4-02.283, FM 8-9, and the NATO Handbook, _Emergency War Surgery_. Appropriate medical intervention and bone marrow resuscitation will prevent most deaths secondary to irradiation and infection.

_Table A-9. Acute Clinical Effects of Single High Dose Rate Exposures of Whole-body Irradiation of Healthy Adults_

[Part 1]
-----------------------++-----------+------------+
|| 0-100 cGy |100-1000 cGy|
DOSE (RANGE) || (SUB- | (SUBLETHAL |
|| CLINICAL | RANGE) |
|| RANGE) |------------+
|| |100-200 cGy |
----------+------------++-----------+------------+
|INCIDENCE || | |
|OF NAUSEA || NONE | 5-50% |
|& VOMITING || | |
+------------++-----------+------------+
|TIME OF || ---- | APPROX |
INITIAL |ONSET || | 3-6 HRS |
PHASE +------------++-----------+------------+
|DURATION || ---- | LESS THAN |
| || | 24 HRS |
+------------++-----------+------------+
| || | |
|COMBAT || | |
|EFFECT- || 100% | 100% |
| IVENESS || | |
| || | |
----------+------------++-----------+------------+
LATENT |DURATION || ---- | MORE THAN |
PHASE | || | 2 WEEKS |
----------+------------++-----------+------------+
|SIGNS & || | MODERATE |
|SYMPTOMS || NONE |LEUKOPENIA |
+------------++-----------+------------+
|TIME OF || | |
|ONSET POST || ---- |2 WEEKS OR |
SECONDARY |EXPOSURE || | MORE |
PHASE +------------++-----------+------------+
|CRITICAL || | |
|PERIOD POST || ---- | NONE |
|EXPOSURE || | |
+------------++-----------+------------+
|ORGAN || | |
|SYSTEM || NONE | |
|RESPONSIBLE || | |
----------+------------++-----------+------------+
HOSPITAL- |PERCENTAGE || NONE |LESS THAN 5%|
IZATION +------------++-----------+------------+
|DURATION || ---- | 45-60 DAYS |
----------+------------++------------------------+
INCIDENCE OF DEATH || NONE | NONE |
-----------------------++-----------+------------+
AVERAGE TIME OF DEATH || ---- | ---- |
-----------------------++-----------+------------+
|| | REASSURANCE|
THERAPY || NONE | HEMATOLOGIC|
|| |SURVEILLANCE|
-----------------------++-----------+------------+

[Part 2]
-----------------------++--------------------+--------------------------+
|| 100-1000 cGy (SUBLETHAL RANGE) |
DOSE (RANGE) || |
||--------------------+--------------------------+
|| 200-600 cGy | 600-1000 cGy |
----------+------------++--------------------+--------------------------+
|INCIDENCE || | |
|OF NAUSEA || 50-100% | 75-100% |
|& VOMITING || | |
+------------++--------------------+--------------------------+
|TIME OF || APPROX 2-4 HRS | APPROX 1-2 HRS |
INITIAL |ONSET || | |
PHASE +------------++--------------------+--------------------------+
|DURATION || LESS THAN 24 HRS | LESS THAN 48 HRS |
| || | |
+------------++--------------------+--------------------------+
| ||CAN PERFORM ROUTINE |CAN PERFORM ONLY SIMPLE |
|COMBAT ||TASKS. SUSTAINED |ROUTINE TASKS. SIGNIFICANT|
|EFFECT- ||COMBAT OR COMPARABL |INCAPACITATION IN UPPER |
| IVENESS ||ACTIVITIES HAMPERED |PART OF RANGE. LASTS MORE |
| ||FOR 6-20 HRS. |THAN 24 HRS. |
----------+------------++--------------------+--------------------------+
LATENT |DURATION || APPROX 7-15 DAYS | NONE TO APPROX 7 DAYS |
PHASE | || | |
----------+------------++--------------------+--------------------------+
|SIGNS & || SEVERE LEUKOPENIA; PURPURA, HEMORRHAGE; |
|SYMPTOMS || INFECTION; EPILATION ABOUT 300 cGy. |
+------------++--------------------+--------------------------+
|TIME OF || |
|ONSET POST || SEVERAL DAYS TO 2 WEEKS |
SECONDARY |EXPOSURE || |
PHASE +------------++-----------------------------------------------+
|CRITICAL || |
|PERIOD POST || 4-6 WEEKS |
|EXPOSURE || |
+------------++-----------------------------------------------+
|ORGAN || |
|SYSTEM || HEMATOPOIETIC TISSUE |
|RESPONSIBLE || |
----------+------------++--------------------+--------------------------+
HOSPITAL- |PERCENTAGE || 90% | 100% |
IZATION +------------++--------------------+--------------------------+
|DURATION || 60-90 DAYS | 90-120 DAYS |
----------+------------++--------------------+--------------------------+
INCIDENCE OF DEATH || 0-80% | 90-100% |
-----------------------++--------------------+--------------------------+
AVERAGE TIME OF DEATH || 3 WEEKS TO 2 MONTHS |
-----------------------++-----------------------------------------------+
|| |
THERAPY || BLOOD TRANSFUSION, ANTIBIOTICS |
|| |
-----------------------++-----------------------------------------------+

[Part 3]
-----------------------++------------------------+----------------------+
|| OVER 1000 cGy (LETHAL RANGE) |
DOSE (RANGE) || |
||------------------------+----------------------+
|| 1000-3000 cGy | OVER 3000 cGy |
----------+------------++------------------------+----------------------+
|INCIDENCE || |
|OF NAUSEA || 100% |
|& VOMITING || |
+------------++-----------------------------------------------+
|TIME OF || LESS THAN 1 HR |
INITIAL |ONSET || |
PHASE +------------++------------------------+----------------------+
|DURATION || LESS THAN 48 HRS | APPROX 48 HRS |
| || | |
+------------++-----------------------------------------------+
| ||PROGRESSIVE INCAPACI- |PROGRESSIVE INCAPACI- |
|COMBAT ||TATION FOLLOWING AN |TATION FOLLOWING AN |
|EFFECT- ||EARLY CAPABILITY FOR |EARLY CAPABILITY FOR |
| IVENESS ||INTERMITTENT HEROIC |INTERMITTENT HEROIC |
| ||RESPONSE. |RESPONSE. |
----------+------------++------------------------+----------------------+
LATENT |DURATION || NONE TO APPROX 2 DAYS | NONE |
PHASE | || | |
----------+------------++------------------------+----------------------+
|SIGNS & ||DIARRHEA; FEVER; DISTUR-|CONVULSIONS; TREMOR |
|SYMPTOMS ||BANCE OF ELECTROLYTE |ATAXIA; LETHARGY. |
| ||BALANCE. | |
+------------++------------------------+----------------------+
|TIME OF || | |
|ONSET POST || 2-3 DAYS | |
SECONDARY |EXPOSURE || | |
PHASE +------------++------------------------+----------------------+
|CRITICAL || | |
|PERIOD POST || 5-14 DAYS | 1-48 HR |
|EXPOSURE || | |
+------------++------------------------+----------------------+
|ORGAN || | |
|SYSTEM || GASTROINTESTINAL TRACT |CENTRAL NERVOUS SYSTEM|
|RESPONSIBLE || | |
----------+------------++------------------------+----------------------+
HOSPITAL- |PERCENTAGE || 100% | 100% |
IZATION +------------++------------------------+----------------------+
|DURATION || 2 WEEKS | 2 DAYS |
----------+------------++------------------------+----------------------+
INCIDENCE OF DEATH || 90-100% |
-----------------------++------------------------+----------------------+
AVERAGE TIME OF DEATH || 1-2 WEEKS | 2 DAYS |
-----------------------++------------------------+----------------------+
|| MAINTENANCE OF | |
THERAPY || ELECTROLYTE BALANCE | SEDATIVES |
|| | |
-----------------------++------------------------+----------------------+

A-7. Radiological Patients in Stability Operations and Support Operations

In stability operations and support operations, high levels of environmental contamination and the use of RDD can cause radiological injury to personnel at levels below that necessary to produce performance decrement and traditional casualty status. Treatment and evacuation guidelines will be in accordance with command guidance. Individual physical dosimetry is the most expedient measurement technique for this exposure (see Table A-10). These radiation injuries and effects may also be seen in war; especially, from hostile forces employment of RDDs.

_Table A-10. Stability Operations and Support Operations: Radiation Injuries and Effects of Radiation Exposure of Personnel_

========================================================================
RADIATION TOTAL STOCHASTIC RISK
EXPOSURE CUMULATIVE LONG-TERM MEDICAL NOTE MEDICAL ACTIONS
STATUS DOSE HEALTH EFFECTS
------------------------------------------------------------------------
0 <0.05 cGy NORMAL RISK. US BASELINE 20% RECORD IN EXPOSURE
LIFETIME RISK OF RECORD IF NORMALLY
FATAL CANCER. MONITORED PERSONNEL.
------------------------------------------------------------------------
1A 0.05 TO UP TO 0.04% NONE (0.001 Sv US RECORD AS HISTORY IN
0.5 cGy INCREASED ANNUAL GEN. POP. MEDICAL RECORD--
RISK LIFETIME EXPOSURE LIMIT.) TACTICAL OPERATION
FATAL CANCER. EXPOSURE.
------------------------------------------------------------------------
1B 0.5 TO 5 cGy US RADIATION REASSURANCE RECORD IN MEDICAL
OCCUPATIONAL (0.05 Sv US RECORD--
RISK. ANNUAL TACTICAL OPERATION
0.04%-0.4% OCCUPATIONAL EXPOSURE.
INCREASED RISK LIMIT.)
LIFETIME CANCER.
------------------------------------------------------------------------
1C 5 TO 10 cGy 0.4%-0.8% COUNSEL REGARDING RECORD IN MEDICAL
INCREASED RISK INCREASED LONG- RECORD--
LIFETIME FATAL TERM RISK. TACTICAL OPERATION
CANCER. NO LIVE VIRUS EXPOSURE.
VACCINES X
3 MONTHS.
------------------------------------------------------------------------
1D 10 TO 25 cGy 0.8%-2% POTENTIAL FOR INC- RECORD IN MEDICAL
INCREASED RISK REASED MORBIDITY RECORD--
LIFETIME FATAL OF OTHER INJURIES TACTICAL OPERATION
CANCER. OR INCIDENTAL EXPOSURE. CONSIDER
DISEASE. <2% ROUTINE EVACUATION
INCREASED LIFETIME FROM THEATER IAW
RISK OF FATAL COMMANDER'S OPER-
CANCER. ATIONAL GUIDANCE.
------------------------------------------------------------------------
1E 25 TO 75 cGy 2%-5.6% INCREASED MORBIDITY RECORD IN MEDICAL
INCREASED RISK OF OTHER INJURIES RECORD--
LIFETIME FATAL OR INCIDENTAL TACTICAL OPERATION
CANCER. DISEASE. <6% EXPOSURE. CONSIDER
INCREASED LIFETIME EXPEDITED EVACU-
RISK OF FATAL ATION FROM THEATER
CANCER. IAW COMMANDER'S
OPERATIONAL
GUIDANCE.
========================================================================

A-8. Effects of Biological Weapons

Biological warfare is the intentional use, by an enemy, of live agents or toxins to cause death and disease among personnel, animals, and plants, or to deteriorate materiel.

_a._ _Live Agents._

(1) Live agents are living organisms like viruses, bacteria,
and fungi. They can be delivered directly (artillery or
aircraft spray), or through a vector such as a flea or tick.
Advances in modern weaponizing of biological agents have become
easier.

(2) For some agents, only a few organisms are needed to cause
infection. Live agents are small and light; they can be spread
great distances by the wind and contaminate unfiltered or
nonairtight places.

(3) Aerosolized particles of 1 to 5 micron (μ) size carrying
live agents are small and light. They require time after
they are ingested to multiply enough to overcome the body's
defenses. This incubation period may vary from hours to days or
weeks depending on the type of organism. Thus, to be effective,
a live agent attack would need to be launched well in advance
of a tactical assault.

(4) These agents are sensitive to environmental conditions (for
example humidity and sunlight). Many bacterial agents will not
survive outside the host organism (human and animals).

(5) Live agents are not detectable by any of the five physical
senses; usually the first indication of a biological attack
is the ill personnel. The diseases caused by live agents may
be difficult to control when the aerosol attack is directed
against a large population. Some diseases may be transmitted
from person-to-person after the initial attack; examples
include plague, smallpox, and some viral hemorrhagic fevers.

(6) Because of their incubation period and life cycle, likely
areas for live agent use are in the combat service support
(CSS) area; but attacks in forward areas cannot be ruled out.

_b._ _Spore Forming Biological Agents._ Spore formers such as anthrax can survive for an extended time, even under very adverse environmental conditions (dry, extremes of temperatures, and flooding). Once inhaled, ingested, or injected into the human body, the spores germinate and produce the illness.

_c._ _Toxins._

(1) Toxins are by-products (poisons) produced by plants,
animals, or microorganisms. It is the poisons that harm man,
not the organisms that make the toxins. In the past, the
only way to deliver toxins on a large scale was by using the
organism. With today's technology large quantities of many
toxins can be produced; thus, they can be delivered without the
accompanying organism.

(2) Toxins have several desirable traits. They are poisonous
compounds that do not grow, reproduce, or die after they have
been dispersed; they are more easily controlled than live
organisms. Field monitors capable of providing prompt warning
of a toxin attack are not available; therefore, personnel must
learn to quickly recognize signs of attack, such as observing
unexplained symptoms of victims. Toxins produce effects similar
to those caused by chemical agents; however, the victims
will not respond to the first-aid measures that work against
chemical agents. Unlike live agents, mycotoxins (T2) can
penetrate intact skin; other toxins cannot. Because the effects
on the body are direct, the symptoms of an attack may appear
very rapidly. The potency of most toxins is such that very
small doses will cause injuries and/or death. Thus, their use
by an enemy may be an alternative to chemical agents because
it allows the use of fewer resources to cover the same or a
larger area. Slight exposure at the edges of an attack area
may produce severe symptoms or death from exposure to toxins
because of their extreme toxicity. Lethal or injury downwind
hazard zones for toxins may be far greater than those of CW
agents.

A-9. Behavior of Biological Weapons

Biological agents can be disseminated in a spectrum of physical states. They may be living microorganisms or spore forms of the organism. See Table A-11 for stability of various biological agents. They may be spread by--

· Arthropods.

· Contact with infected animals.

· Contamination of food and water.

· Aerosol, liquid, or solid dispersion.

The only requirement is that they must be stable enough to survive transport and dissemination. The toxicity of biological agents is not the same for everyone; each individual does not react exactly the same way to the same amount of an agent. Some are more resistive than others because of race, sex, age, or other factors. The dose is the quantity of a biological agent received by the subject. The penetration of agents by various routes need not be accompanied by irritation or damage to the absorbent surface. There are often unique signs and identifying symptoms depending on entry route (inhalation, ingestion, or dermal).

_a._ Biological agents dispersed by spray often enter the body through the respiratory tract (inhalation injury). The agent may be absorbed by any part of the respiratory tract from the mucosa of the nose and mouth to the alveoli of the lungs.

_b._ Liquid droplets and (less commonly) solids may be absorbed from the surface of the skin, digestive tract, and mucous membranes. Agents penetrating the skin may form temporary reservoirs under the skin.

_c._ Contaminated food and water can produce casualties when ingested.

_Table A-11. Types and Characteristics of Some Biological Agents_

=========================================================================
ENTRANCE
TYPE OF AGENT STABILITY INCUBATION TIME AEROSOL NONAEROSOL
-------------------------------------------------------------------------
ANTHRAX HIGH HOURS TO 7 DAYS INHALATION SKIN, MOUTH
-------------------------------------------------------------------------
BOTULINUM TOXIN HIGH 24 TO 36 HOURS INHALATION MOUTH, WOUND
-------------------------------------------------------------------------
BRUCELLOSIS HIGH IN 1 TO 4 WEEKS INHALATION MOUTH, SKIN,
WET ENV- EYES
IRONMENT
-------------------------------------------------------------------------
CHOLERA MODERATE HOURS TO 5 DAYS MOUTH
-------------------------------------------------------------------------
PLAGUE(PNEUMONIC) LOW 2 TO 4 DAYS INHALATION
-------------------------------------------------------------------------
PLAGUE (BUBONIC) MODERATE 2 TO 10 DAYS BITE OF VECTOR
-------------------------------------------------------------------------
RICIN HIGH <36 HOURS INHALATION MOUTH
-------------------------------------------------------------------------
SMALLPOX HIGH 7 TO 17 DAYS INHALATION LESION CONTACT
-------------------------------------------------------------------------
STAPHYLOCOCCAL HIGH 1 TO 6 HOURS INHALATION MOUTH
ENTEROTOXIN B
-------------------------------------------------------------------------
TRICHOTHECENE HIGH MINUTES TO HOURS INHALATION MOUTH, SKIN
MYCOTOXIN
-------------------------------------------------------------------------
TULAREMIA LOW 2 TO 10 DAYS INHALATION MOUTH, SKIN,
BITE OF VECTOR
-------------------------------------------------------------------------
VENEZUELAN EQUINE MODERATE 1 TO 6 DAYS INHALATION BITE OF VECTORS
ENCEPHALITIS
-------------------------------------------------------------------------
VIRAL HEMORRHAGIC LOW DAYS TO MONTHS INHALATION BITE OF VECTORS
FEVERS
=========================================================================

A-10. Management of Biological Warfare Patients

_a._ _Management._ Management of patients suffering from the effects of BW agents may include the need for isolation. Barrier nursing for patients suspected of suffering from exposure to BW agents will reduce the possibility of spreading the disease to health care providers and other patients. Specimens must be collected and submitted to the designated supporting laboratory for identification. For details on hospital infection control aspects of managing BW casualties, see FM 8-284.

_b._ _Mass Casualty._ A BW agent attack can produce a mass casualty situation at all levels of HSS. A major problem with a BW mass casualty situation is that HSS personnel are more susceptible to becoming a casualty to BW agents. Also, the ill patient may be the first indicator that a BW agent has been dispersed.

_c._ _Decontamination._ Decontamination is an individual and unit responsibility. However, some individuals may arrive at the MTF that have not been decontaminated or that become contaminated en route to the MTF. These individuals must be decontaminated at the MTF before they are admitted to prevent contamination of the MTF and exposure of medical personnel to the biological agent. See Appendix G for details on patient decontamination.

_d._ _Treatment._ Specific treatment is dependent upon the BW agent used. Patients are treated for symptomatic presentation unless the BW agent identity is known. Field Manuals 8-9 and 8-284 provide detailed information on medical management and treatment.

A-11. Effects of Chemical Weapons

_a._ A chemical agent is a chemical that is used to kill, seriously injure, or incapacitate man because of its physiological effects. They can be disseminated by artillery, aircraft, rocket, or by nonconventional means used by terrorists. When first employed in combat during World War I, the chemical weapon (chlorine) was so effective that the attacking Germans were not prepared to exploit the success.

_b._ Chemical agents are very effective weapons against poorly trained and equipped forces; however, they are less effective against well-trained forces.

A-12. Behavior of Chemical Weapons

Chemical agents can be disseminated as a gas, vapor, or aerosol under ambient conditions. They have a range of odors varying from none to highly pungent characteristics. Their stability is dependent upon the environmental conditions in the area of employment. See Table A-11 for persistency of various chemical agents.

_a._ The toxicity of a chemical agent is not the same for everyone; each individual does not react exactly the same way to the same amount of an agent. Some are more resistant than others because of physiological factors. The dose is the quantity of a chemical received by the individual for percutaneous or oral doses and as a time-weighted concentration, milligrams-minute (m3), for inhalation. It is usually expressed as milligrams of agent per kilogram of subject body weight (mg/kg). The LD50 is the dose that kills 50 percent of the exposed population. The incapacitation dose 50 (ID50) is the incapacitation dose for 50 percent of the exposed subjects. The penetration of agents by various routes need not be accompanied by irritation or delayed superficial damage to the absorbent surface, but there are often unique signs and symptoms identifiable by the route of entry.

(1) Gaseous, vapor, and aerosol chemical agents often enter the
body through the respiratory tract (inhalation injury). The
agent may be absorbed by any part of the respiratory tract from
the mucosa of the nose and mouth to the alveoli of the lungs.
Aerosol particles larger than 5 μ tend to be retained in the
upper respiratory tract; particles in the 1 to 5 μ range are
retained in the deep volume of the lungs; while those below
1 μ tend to be breathed in and out again; although a few are
retained in the deep volume of the lungs.

(2) Vapors and droplets of liquids can be absorbed from the
surface of the skin and mucous membranes. Toxic compounds that
are harmful to the skin can produce their effects in liquid or
solid state. Agents penetrating the skin may form temporary
reservoirs under the skin; the vapors of some volatile liquids
can penetrate the skin and cause intoxication. Additionally,
wounds and abrasions may present areas that are more permeable
than intact skin.

_b._ Chemical agents may be divided into two main categories (persistent and nonpersistent) that describe how long they are capable of producing casualties. Table A-12 lists the common chemical agents, their effects and time of effectiveness. Table A-13 lists the types and characteristics of common chemical agents.

(1) Persistent agents continue to present a hazard for
considerable periods (days) after delivery by remaining as a
contact hazard, or by slowly vaporizing to produce a hazard by
inhalation.

(2) Nonpersistent agents disperse rapidly after release and
present an immediate, short duration (hours) hazard. They are
released as airborne particles, aerosols, and gases.

_Table A-12. Common Chemical Warfare Agents_

=========================================================================
COMMON NAME EFFECT TIME TO EFFECT
-------------------------------------------------------------------------
TABUN (GA) INHALATION: SECONDS TO MINUTES
SARIN (GB) LETHAL NERVE AGENTS TOPICAL: MINUTES
SOMAN (GD) INGESTION: MINUTES TO HOURS
V-AGENTS
-------------------------------------------------------------------------
HYDROGEN CYANIDE LETHAL BLOOD AGENT MINUTES
-------------------------------------------------------------------------
MUSTARD BLISTER AGENTS 1 TO 12 MINUTES
LEWISITE MINUTES
-------------------------------------------------------------------------
LSD AND BZ INCAPACITATING AGENTS 15 TO 60 MINUTES
-------------------------------------------------------------------------
PHOSGENE LUNG-DAMAGING (CHOKING) MINUTES
CHLORINE SECONDS TO MINUTES
=========================================================================

_Table A-13. Types and Characteristics of Chemical Agents_

[Part 1]
================================================================
TYPE OF PERSISTENCE RATE OF
AGENT SYMBOL SUMMER WINTER ACTION
----------------------------------------------------------------
GA, GB, GD 10 MIN-24 HR 2 HR-3 DAYS VERY QUICK
=NERVE= -------------------------------------------------------
VX 2 DAYS-1 WK 2 DAYS-WEEKS QUICK
----------------------------------------------------------------
=CHOKING= CG, DP 1-10 MIN 10 MIN-1 HR IMMEDIATE
----------------------------------------------------------------
HD, HN 3 DAYS-1 WK WEEKS SLOW
------------------------------------------------------
=BLISTER= L, HL 1-3 DAYS WEEKS QUICK
------------------------------------------------------
CX DAYS DAYS VERY QUICK
----------------------------------------------------------------
=BLOOD= AC, CK 1-10 MIN 10 MIN-1 HR VERY QUICK

================================================================

[Part 2]
================================================================
TYPE OF ENTRANCE
AGENT SYMBOL VAPOR/AEROSOL LIQUID
----------------------------------------------------------------
GA, GB, GD EYES, LUNGS EYES, SKIN, MOUTH
=NERVE= -------------------------------------------------------
VX EYES, LUNGS EYES, SKIN, MOUTH
----------------------------------------------------------------
=CHOKING= CG, DP LUNGS EYES
----------------------------------------------------------------
HD, HN EYES, SKIN, LUNGS EYES, SKIN
------------------------------------------------------
=BLISTER= L, HL EYES, SKIN, LUNGS EYES, SKIN, MOUTH
------------------------------------------------------
CX EYES, LUNGS, SKIN EYES, SKIN, MOUTH
----------------------------------------------------------------
=BLOOD= AC, CK EYES, LUNGS EYES, MOUTH,
INJURED SKIN
================================================================

A-13. Characteristics of Chemical Agents

The effectiveness of a chemical agent is a measure of how much agent is required to produce the desired effect. Thus, an agent that is toxic at a lower dose than another similar agent is more effective. Besides dose required for a given effect, persistency may be used to measure effectiveness. Persistency depends on the agent's physical characteristics, the amount of agent delivered, its physical state, weapons system used, the terrain, and weather in the target area. The desired effects will determine the physical, chemical, and toxicological properties of the chemical agent employed.

_a._ Nerve agents are primarily organophosphorus esters similar to insecticides. Those of military importance are combined under this term. Although some have been given names, they are usually known by their code letters: GA; GB; GD; and VX. They are all liquids, varying in volatility that is in a range between gasoline and heavy lubricating oil. Their freezing points are -40 degrees Celsius or lower.

(1) Liquid nerve agents are pale yellow to colorless and are
almost odorless. They are moderately soluble in water and
highly soluble in lipids (oil). They are rapidly destroyed by
strong alkalies and chlorinating compounds. Normal clothing
is readily penetrated by liquid or vapor agents. Butyl rubber
and synthetic material are more resistant than natural fibers.
Agents can penetrate into nonabsorbent material such as web
belts and can continue to present a hazard by desorption
(off-gassing) of the vapor. Although local sweating and
twitching may occur, usually there is no local irritant change
after cutaneous exposure. Toxicity depends upon the route of
entry and physical characteristics.

(2) Nerve agents strongly inhibit the cholinesterase enzymes.
When acetylcholine is released by the nerve junction, it
is hydrolyzed by the enzyme. Acetylcholine is the chemical
mediator for transmission of the nerve impulses in numerous
synapses of the central nervous system (CNS) and the autonomic
nervous system and at the endings of the cholinergic nerves
(for example: affecting the smooth muscles of the iris,
ciliary, bronchial tree, and gastrointestinal tract). The
inhibition of cholinesterase by nerve agents is almost
irreversible, so the effects are prolonged. Until the
cholinesterase level is restored to normal, there is an
increased susceptibility to nerve agent exposure. During this
time, the effects of repeated exposure are cumulative and the
patient may feel "subpar" (for example: tired, fatigue easily,
poor appetite, impaired concentration) until recovery is
complete.

(3) Nerve agent poisoning is easily identified by the
characteristic signs and symptoms as follows:

(_a_) =MILD= symptoms (self-aid). Casualties with MILD symptoms may
experience most or all of the following:

· Unexplained runny nose.

· Unexplained sudden headache.

· Sudden drooling.

· Difficulty in seeing (dimness of vision) (miosis).

· Tightness in the chest or difficulty in breathing.

· Localized sweating and muscular twitching in the contaminated
area.

· Stomach cramps.

· Nausea.

(_b_) Casualties with =MODERATE= symptoms (buddy aid) will
experience an increase in the severity of most or all of the MILD
symptoms. Especially prominent will be an increase in fatigue,
weakness, and muscle fasciculations. The progress of symptoms from
MILD to MODERATE indicates either inadequate atropine treatment or
continuing exposure to agent.

(_c_) =SEVERE= symptoms (buddy aid). Casualties with SEVERE
symptoms may experience most or all of the MILD symptoms, plus most
or all of the following:

· Strange or confused behavior.

· Wheezing, dyspnea (severe difficulty in breathing), and
coughing.

· Severely pinpointed pupils.

· Red eyes with tearing.

· Vomiting.

· Severe muscular twitching and general weakness.

· Involuntary urination and defecation.

· Convulsions.

· Unconsciousness.

· Respiratory failure.

_b._ There are three major families of blister agents (vesicants); HD and HN, L, and CX. Most vesicants (except CX) are relatively persistent. Mustards can modify the structure of nucleic acids, cellular membranes, and proteins by combining with certain functional groups (particularly the sulfhydryl-containing enzymes) for which they have an affinity.

(1) The cutaneous syndrome is divided into four phases: latent,
erythema, vesication, and necrosis. Vesicants can penetrate the
skin by contact with either liquid or vapor. The latent period
is characteristic of the agent. For mustards it is usually
several hours, for L it is short, and for CX it is negligible.
The latent period is also affected by the dose, temperature,
and humidity. The symptoms of the erythema phase are red,
painful itching followed by painful necrosis that heals slowly.

(2) In the eyes, vesicants produce intense pain and
photophobia. Blistering of the eyelids and mucous membranes can
result in temporary blindness. Even after recovery, scars on
the cornea can reduce visual acuity.

(3) In the respiratory tract, these agents attack the mucous
membranes irritating them. They can paralyze vocal chords and
can lead to chemical pneumonitis, or possibly death.

(4) Although blister agents can affect other organs and produce
deleterious effects, the skin, eyes, and respiratory tract are
the principle organs effected.

_c._ Chemical agents that attack lung tissue (choking agents) and cause pulmonary edema are classed as lung damaging agents. Choking agents consist of CG and DP, CL, and PS. Phosgene is typical of the lung-damaging agents; it is used as the example here.

(1) Phosgene is a colorless gas that has an odor resembling new
mown hay. Although effects are primarily confined to the lungs,
phosgene may also cause mild irritation of the eyes and upper
respiratory tract. Phosgene causes a shift in the membrane
potential of the alveoli allowing the passage of fluid into
the alveoli, resulting in massive pulmonary edema and severely
impairing the exchange of oxygen (O_{2}) and carbon dioxide
(CO_{2}) between the capillary blood and the alveolar air.

(2) Initially hypoxemia occurs and is followed shortly by
hyperventilation when the frothy edema fluid fills the
bronchioli and CO_{2} expiration stops.

(3) Signs and symptoms during and immediately following
exposure are coughing, tightness of chest, nausea, occasionally
vomiting, headache, and lacrimation (tearing).

_d._ Blood agents consist of AC and CK; both are readily absorbed by the mucous membranes and the intact skin. The odor of AC resembles bitter almonds, but many people cannot detect it. Detecting the odor of CK is difficult because of its irritating and lacrimatory effects. It is also poorly absorbed by the metallic salt-impregnated charcoal filters in the protective mask. These agents inhibit certain enzymes (particularly cytochrome oxidase) that are important for oxidation-reduction in the cells; therefore, cell respiration is inhibited and oxygen carried by the hemoglobin is not consumed causing the venous blood to remain bright red. Initial symptoms are characterized by violent convulsions, increased deep respiratory movements, followed by cessation of respiration within one minute, slowing of heart rate to death. High concentrations exert their effects rapidly; however, if the patient is still alive after the cloud has passed, he will probably recover spontaneously.

_e._ Incapacitating agents are chemicals that produce a temporary disabling condition that persists for hours to days after exposure to the agent has ceased (unlike that produced by riot control agents). While not required, medical treatment produces a more rapid recovery. Characteristics of these agents are that they--

· Are highly potent and logistically feasible.

· Produce their effects mainly by altering or disrupting the
higher regulatory activity of the CNS.

· Produce effects that last for hours or days rather than
momentary or fleeting.

· Do not seriously endanger life, except in exceedingly high
doses.

· Produce no permanent injury.

The two types likely to be encountered are CNS depressants and CNS stimulants.

(1) Central nervous system depressants are compounds that have
a predominant effect of depressing or blocking the activity
of the CNS; often by interfering with the transmission of
information across synapses. An example of this type of agent
is BZ. The action of acetylcholine, both peripherally and
centrally, appears to be blocked by BZ. Low doses disrupt
higher integrative functions of memory, problem solving,
attention, and comprehension. High doses produce toxic delirium
that destroys the ability to perform any military task. Within
the CNS, BZ seems to produce its effects in the same way as
atropine. Small doses cause sleepiness and decreased alertness
with elevated heart rate, dry skin and eyelids, drowsiness,
increased pupil size, and elevated skin temperatures.
Progressive intoxication is marked by an inability to respond
effectively to the environment (4 to 12 hours), followed by
increasing activity and random/unpredictable behavior (12 to 96
hours). Because the patient cannot sweat, heat stress becomes a
problem.

(2) Central nervous system stimulants are agents that cause
excessive nervous activity, often by boosting or facilitating
transmission of impulses across synapses. The effect is
to "flood" the cortex and other higher regulatory centers
with too much information, making concentration difficult
and causing indecisiveness and an inability to act. These
include LSD, psilocybin, and mescaline. Intoxication shows
sympathetic stimulation (rapid heart rate, sweaty palms,
pupillar enlargement, and cold extremities) and mental
excitation (nervousness, trembling, anxiety, and inability to
relax or sleep); feelings of tension, exhilaration, heightened
awareness, paranoid ideas, and profound states of terror may
also occur.

A-14. Management of Chemical Agent Patients

_a._ _Management._ Movement of chemical agent casualties can spread the contamination to clean areas. All casualties are decontaminated as far forward as the situation permits. All patients must be decontaminated before they are admitted into a clean MTF. The admission of one contaminated patient into an MTF will contaminate the facility; thereby reducing its treatment capabilities.

_b._ _Mass Casualty._ A mass casualty situation is presented when chemical agents are employed. Additional HSS personnel and equipment must be provided in a short period of time if the level of care is to be maintained. Treatment at far forward MTFs is limited to life- or limb-saving care. Patients that can survive evacuation to the next level of care are not treated at the forward facility. This provides time for treating those patients that cannot survive the evacuation time.

_c._ _Decontamination._ Decontamination is an individual and unit responsibility. However, some individuals may arrive at the MTF that have not been decontaminated or that become contaminated en route to the MTF. These individuals must be decontaminated at the MTF before they are admitted to prevent contamination of the MTF and exposure of medical personnel to the chemical. See Appendix G for detailed information on patient decontamination procedures.

_d._ _Treatment._ Field Manuals 8-9 and 8-285 provide treatment procedures for chemical agent patients.

A-15. Management of Toxic Industrial Material Patients

_a._ _Management._ Movement of TIM casualties can spread the contamination to clean areas. All casualties are decontaminated as close to the incident site as possible. All patients must be decontaminated before they are admitted into a clean MTF. The admission of one contaminated patient into an MTF may contaminate the facility; thereby reducing its treatment capabilities.

_b._ _Mass Casualty._ A mass casualty situation is presented when the number of casualties exceeds the capabilities of medical personnel at the location to provide needed care at the incident site. Treatment at the incident site is limited to life- or limb-saving care. Patients that can survive are evacuated to the nearest MTF with a patient decontamination capability.

_c._ _Decontamination._ Decontamination is an individual and first responder responsibility. However, some individuals that self evacuated or were evacuated due to the mass casualty situation arrive at the MTF that have not been decontaminated. These individuals must be decontaminated at the MTF before they are admitted to prevent contamination of the MTF and exposure of unprotected medical personnel and other patients to the TIM. See FM 8-500 for detailed information on decontamination procedures for TIM contaminated casualties.

_d._ _Treatment._ Field Manual 8-500 provides treatment procedures for some TIM casualties. Treatment for many TIM casualties is agent specific and receiving MTFs must be prepared for these events.

EXAMPLE: Treatment for a casualty exposed to toxic levels of an inorganic phosphate pesticide would be treated in the same manner as a nerve agent casualty except the amount of antidote for the pesticide poisoned casualty will be many times greater than for the nerve agent casualty.

APPENDIX B

SAMPLE/SPECIMEN COLLECTION AND MANAGEMENT

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