APPENDIX A

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.

Figure A-1. Distribution of energy.

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 KT20 KT100 KT1 MT10 MT
NUCLEAR RADIATION (1,000 cGy)
BLAST (50% INCIDENCE OF TRANSLATION WITH SUBSEQUENT IMPACT WITH A NON-YIELDING SURFACE)
THERMAL (50% INCIDENCE OF 2ND-DEGREE BURNS TO 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
(APPROXIMATE %)
PEAK OVERPRESSURE
(ATMOSPHERES)
DISTANCE FROM
GROUND ZERO; METERS
12.3-2.9150
502.9-4.1123
1004.1+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 (KT)1% PROBABILITY OF SERIOUS INJURY 50% PROBABILITY OF SERIOUS INJURY99% PROBABILITY OF SERIOUS INJURY
10.280.220.17
100.730.570.44
200.980.760.58
501.41.10.84
1001.91.51.1
2002.51.91.5
5003.62.72.1
1,0004.83.62.7
    1INCIDENCE OF INJURY BASED ON SKIN AND TISSUE PERFORATION.
    2MISSILES 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 FRAGMENTS (gm)1%50%99%
IMPACT VELOCITY (METERS PER SECOND)
0.178136243
0.65391161
1.04682143
10.03860118

(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 INJURYVELOCITY (m/sec)
1%2.6
50%6.6
99%16.5
B. FATAL INJURIES
PROBABILITY OF FATALITYVELOCITY (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 (KT)VELOCITIES (m/sec)
2.66.617.0
RANGES (km)
10.380.270.19
101.00.750.53
201.30.990.71
501.91.41.0
1002.51.91.4
2003.22.51.9
5004.63.62.7
1,0005.94.83.6

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/cm2/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 WEAPON1 KT10 KT100 KT1 MT10 MT

RANGE (km) FOR PRODUCTION OF PARTIAL THICKNESS BURNS ON EXPOSED SKIN

0.782.14.89.114.5

DURATION OF THERMAL PULSE IN SECONDS

0.120.320.92.46.4

Cal/cm2/sec REQUIRED TO PRODUCE PARTIAL THICKNESS BURNS ON EXPOSED SKIN

4.04.55.36.37.0

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.

Figure A-2. Threshold distance for minimal chorioretinal burn and flash blindness versus yield (airburst) at night.

Table A-8. Characteristics of Nuclear Radiation

NAME AND SYMBOLWHAT IS IT SOURCE ENERGY AND SPEEDRANGE IN AIR RANGE IN TISSUESHIELDING REQUIREDBIOLOGICAL HAZARD
α
ALPHA PARTICLE
HELIUM NUCLEUS
DECAY OF URANIUM AND PLUTONIUM ENERGY VARIES: SPEED VARIES FROM 1/20 TO 1/10 SPEED OF LIGHT   ~ 5 cm CANNOT PENETRATE THE EPIDERMIS NONE NONE, UNLESS INGESTED OR INHALED IN SUFFICIENT QUANTITIES
β
BETA PARTICLE
HIGH-SPEED SPEED ELECTRON
DECAY OF FISSION PRODUCTS AND NEUTRON INDUCED ELEMENTS VARIES OF SKIN 5 METERS OR MODERATE SEVERAL LAYERS SKIN INJURY STOPPED BY A FEW cm OF Al CLOTHING SUPERFICIAL
γ
GAMMA RAY
ELECTRO-MAGNETIC ENERGY
DECAY OF FISSION PRODUCTS AND NEUTRON INDUCED ELEMENTS ENERGY VARIES: TRAVELS AT THE SPEED OF LIGHT UP TO 500 METERS, BUT IS ENERGY DEPENDENT VERY PENETRATING, BUT IS ENERGY DEPENDENT DENSE MATERIAL, SUCH AS CONCRETE, STEEL PLATE, EARTHWHOLE BODY INJURY, MANY CASUALTIES POSSIBLE
η
NEUTRON
UNCHARGED PARTICLE
FISSION AND FUSION REACTIONS VARIES LESS THAN GAMMA, BUT IS ENERGY DEPENDENT VERY PENETRATING, BUT IS ENERGY DEPENDENT HYDROGENOUS MATERIALS, SUCH AS WATER OR DAMP EARTHWHOLE BODY INJURY, MANY CASUALTIES POSSIBLE

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]

DOSE (RANGE)0-100 cGy (SUBCLINICAL RANGE)100-1000 cGy (SUBLETHAL RANGE)
100-200 cGy200-600 cGy600-1000 cGy
INITIAL PHASEINCIDENCE OF NAUSEA & VOMITINGNONE5-50%50-100%75-100%
TIME OF ONSET——APPROX 3-6 HRSAPPROX 2-4 HRSAPPROX 1-2 HRS
DURATION——LESS THAN 24 HRSLESS THAN 24 HRSLESS THAN 48 HRS
COMBAT EFFECTIVENESS100%100%CAN PERFORM ROUTINE TASKS. SUSTAINED COMBAT OR COMPARABLE ACTIVITIES HAMPERED FOR 6-20 HRS. CAN PERFORM ONLY SIMPLE ROUTINE TASKS. SIGNIFICANT INCAPACITATION IN UPPER PART OF RANGE. LASTS MORE THAN 24 HRS.
LATENT PHASEDURATION——MORE THAN 2 WEEKSAPPROX 7-15 DAYSNONE TO APPROX 7 DAYS
SECONDARY PHASESIGNS & SYMPTOMSNONEMODERATE LEUKOPENIASEVERE LEUKOPENIA; PURPURA, HEMORRHAGE; INFECTION; EPILATION ABOUT 300 cGy.
TIME OF ONSET POST EXPOSURE——2 WEEKS OR MORESEVERAL DAYS TO 2 WEEKS
CRITICAL PERIOD POST EXPOSURE——NONE4-6 WEEKS
ORGAN SYSTEM RESPONSIBLENONE HEMATOPOIETIC TISSUE
HOSPITAL-IZATIONPERCENTAGENONELESS THAN 5%90%100%
DURATION——45-60 DAYS60-90 DAYS90-120 DAYS
INCIDENCE OF DEATHNONENONE0-80%90-100%
AVERAGE TIME OF DEATH————3 WEEKS TO 2 MONTHS
THERAPYNONEREASSURANCE HEMATOLOGIC SURVEILLANCEBLOOD TRANSFUSION, ANTIBIOTICS

[Part 2]

DOSE (RANGE)OVER 1000 cGy (LETHAL RANGE)
1000-3000 cGyOVER 3000 cGy
INITIAL PHASEINCIDENCE OF NAUSEA & VOMITING100%
TIME OF ONSETLESS THAN 1 HR
DURATIONLESS THAN 48 HRSAPPROX 48 HRS
COMBAT EFFECTIVENESSPROGRESSIVE INCAPACITATION FOLLOWING AN EARLY CAPABILITY FOR INTERMITTENT HEROIC RESPONSE. PROGRESSIVE INCAPACITATION FOLLOWING AN EARLY CAPABILITY FOR INTERMITTENT HEROIC RESPONSE.
LATENT PHASEDURATIONNONE TO APPROX 2 DAYSNONE
SECONDARY PHASESIGNS & SYMPTOMSDIARRHEA; FEVER; DISTURBANCE OF ELECTROLYTE BALANCE.CONVULSIONS; TREMOR ATAXIA; LETHARGY.
TIME OF ONSET POST EXPOSURE2-3 DAYS
CRITICAL PERIOD POST EXPOSURE5-14 DAYS1-48 HRS
ORGAN SYSTEM RESPONSIBLEGASTROINTESTINAL TRACTCENTRAL NERVOUS SYSTEM
HOSPITAL-IZATIONPERCENTAGE100%100%
DURATION2 WEEKS2 DAYS
INCIDENCE OF DEATH90-100%
AVERAGE TIME OF DEATH1-2 WEEKS2 DAYS
THERAPYMAINTENANCE OF ELECTROLYTE BALANCESEDATIVES

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