Bioterrorism

MICROBIAL BIOTERRORISM

Microbial bioterrorism refers to the use of microbial pathogens as weapons of

terror that target civilian populations. A primary goal of bioterrorism is not

necessarily to produce mass casualties but to destroy the morale of a society

through creating fear and uncertainty. The events of September 11, 2001, followed

by the anthrax attacks through the U.S. Postal Service illustrate the vulnerability

of the American public to terrorist attacks, including those that use

microbes. The key to combating bioterrorist attacks is a highly functioning

system of public health surveillance and education that rapidly identifies and

effectively contains the attack.

Agents of microbial bioterrorism may be used in their natural form or may

be deliberately modified to maximize their deleterious effect. Modifications that

increase the deleterious effect of a biologic agent include genetic alteration of

microbes to produce antimicrobial resistance, creation of fine-particle aerosols,

chemical treatment to stabilize and prolong infectivity, and alteration of the host

range through changes in surface protein receptors. Certain of these approaches

fall under the category of weaponization, a term that describes the processing

of microbes or toxins in a manner that enhances their deleterious effect after

release. The key features that characterize an effective biologic weapon are

summarized in Table 31-1.

The U.S. Centers for Disease Control and Prevention (CDC) has classified

microbial agents that could potentially be used in bioterrorism attacks into three

categories: A, B, and C (Table 31-2). Category A agents are the highest-priority

pathogens. They pose the greatest risk to national security because they (1) can

be easily disseminated or transmitted from person to person, (2) are associated

withh ighcase fatality rates, (3) have potential to cause significant public panic

and social disruption, and (4) require special action and public health preparedness.

Table 31-1

Key Features of Biologic Agents Used as Bioweapons

1. Highmorbidity and mortality

2. Potential for person-to-person spread

3. Low infective dose and highly infectious by aerosol

4. Lack of rapid diagnostic capability

5. Lack of universally available effective vaccine

6. Potential to cause anxiety

7. Availability of pathogen and feasibility of production

8. Environmental stability

9. Database of prior researchand development

10. Potential to be “weaponized”

Category A Agents

ANTHRAX (BACILLUS ANTHRACIS) Anthrax as a Bioweapon

Anthrax in many ways is the prototypic bioweapon. Although it is only rarely

spread by person-to-person contact, it has many of the other features of an ideal biologic weapon listed in Table 31-1. The potential impact of anthrax as a

bioweapon is illustrated by the apparent accidental release in 1979 of anthrax

spores from a Soviet bioweapons facility in Sverdlosk, Russia. As a result of

this atmospheric release of anthrax spores, at least 77 cases of anthrax (of which

66 were fatal) occurred in individuals within an area 4 km downwind of the

facility. Deaths were noted in livestock up to 50 km from the facility. The

interval between probable exposure and onset of symptoms ranged from 2 to

43 days, with the majority of cases occurring within 2 weeks. In September of

2001 the American public was exposed to anthrax spores delivered through the

U.S. Postal Service. There were 22 confirmed cases: 11 cases of inhaled anthrax

(5 died) and 11 cases of cutaneous anthrax (no deaths). Cases occurred in individuals who opened contaminated letters as well as in postal workers involved

in processing the mail.

Microbiology and Clinical Features (See also Chap. 205, HPIM-16)

• Anthrax is caused by infections with B. anthracis, a gram-positive, nonmotile,

spore-forming rod that is found in soil and predominantly causes disease

in cattle, goats, and sheep.

Spores can remain viable for decades in the environment and be difficult to

destroy withstandard decontamination procedures. These properties make anthrax

an ideal bioweapon.

• Naturally occurring human infection generally results from exposure to infected

animals or contaminated animal products.

There are three major clinical forms of anthrax:

1. Gastrointestinal anthrax is rare and is unlikely to result from a bioterrorism

event.

2. Cutaneous anthrax follows introduction of spores through an opening in

the skin. The lesion begins as a papule followed by the development of a

black eschar. Prior to the availability of antibiotics, about 20% of cutaneous

anthrax cases were fatal.

3. Inhalation anthrax is the form most likely to result in serious illness and

death in a bioterrorism attack. It occurs following inhalation of spores that

become deposited in the alveolar spaces. The spores are phagocytosed by

alveolar macrophages and are transported to regional lymph nodes where

they germinate. Following germination, rapid bacterial growth and toxin

production occur. Subsequent hematologic dissemination leads to cardiovascular

collapse and death. The earliest symptoms are typically those of

a viral-like prodrome withfever, malaise, and abdominal/chest symptoms

that rapidly progress to a septic shock picture. Widening of the mediastinum

and pleural effusions are typical findings on chest radiography. Once considered

100% fatal, experience from the Sverdlosk and U.S. Postal outbreaks

indicate that with prompt initiation of appropriate antibiotic therapy,

survival may be _50%.

TREATMENT (See Table 31-3)

Anthrax can be successfully treated if the disease is promptly recognized and

appropriate antibiotic therapy is initiated.

• Penicillin, ciprofloxacin, and doxycycline are currently licensed for the

treatment of anthrax.

• Clindamycin and rifampin have in vitro activity against the organism and

may be used as part of the treatment regimen.

• Patients with inhalation anthrax are not contagious and do not require

special isolation procedures.

Vaccination and Prevention

• Currently there is a single vaccine licensed for use; produced from a cellfree

culture supernatant of an attenuated strain of B. anthracis (Stern strain).

• Since the efficacy of this vaccine in the postexposure setting has not been

established, current recommendation for postexposure prophylaxis is 60 days

of antibiotics (see Table 31-1)

PLAGUE (YERSINIA PESTIS) (See also Chap. 99) Plague as a

Bioweapon Although plague lacks the environmental stability of anthrax, the

highly contagious nature of the infection and the high mortality rate make it a

potentially important agent of bioterrorism. As a bioweapon, plague would

likely be delivered via an aerosol leading to primary pneumonic plague. In such

an attack, person-to-person transmission of plague via respiratory aerosol could

lead to large numbers of secondary cases.

TREATMENT See Table 31-3 and Chap. 99, p. 482.

SMALLPOX (VARIOLA MAJOR AND V. MINOR) (See also Chap. 167,

HPIM-16) Smallpox as a Bioweapon Smallpox as a disease was globally

eradicated by 1980 through a worldwide vaccination program. However, with

the cessation of smallpox immunization programs in the United States in 1972

(and worldwide in 1980), close to half the U.S. population is fully susceptible

to smallpox today. Given the infectious nature and the 10–30% mortality of

smallpox in unimmunized individuals, the deliberate release of virus could have

devastating effects on the population. In the absence of effective containment

measures, an initial infection of 50–100 persons in a first generation of cases

could expand by a factor of 10 to 20 witheachsucceeding generation. These

considerations make smallpox a formidable bioweapon.

Microbiology and Clinical Features The disease smallpox is caused by

one of two closely related double-strand DNA viruses, V. major and V. minor.

Both viruses are members of the Orthopoxvirus genus of the Poxviridae family.

Infection with V. minor is generally less severe, withlow mortality rates; thus,

V. major is the only one considered as a potential bioweapon. Infection with V.

major typically occurs following contact withan infected person from the time

that a maculopapular rash appears through scabbing of the pustular lesions.

Infection is thought to occur from inhalation of virus-containing saliva droplets

from oropharyngeal lesions. Contaminated clothing or linen can also spread

infection. About 12–14 days following initial exposure the patient develops

high fever, malaise, vomiting, headache, back pain, and a maculopapular rash

that begins on the face and extremities and spreads to the trunk. The skin lesions

evolve into vesicles that eventually become pustular with scabs. The oral mucosa

also develops macular lesions that progress to ulcers. Smallpox is associated

witha 10–30% mortality. Historically, about 5–10% of naturally occurring

cases manifest as highly virulent atypical forms, classified as hemorrhagic and

malignant. These are difficult to recognize due to their atypical manifestations.

Both forms have similar onset of a severe prostrating illness characterized by

high fever, severe headache, and abdominal and back pain. In the hemorrhagic

form, cutaneous erythema develops followed by petechiae and hemorrhage into

the skin and mucous membranes. In the malignant form, confluent skin lesions

develop but never progress to the pustular stage. Both of these forms are often

fatal, withdeath occurring in 5–6 days.

TREATMENT

Treatment is supportive. There is no licensed specific antiviral therapy for

smallpox. While certain antiviral agents, such as cidofovir, have in vitro activity

against V. major, these agents have not been tested clinically. Smallpox

is highly infectious to close contacts; patients who are suspected cases should

be handled with strict isolation procedures.

Vaccination and Prevention Smallpox is a preventable disease following

immunization with vaccinia. Past and current experience indicates that the

smallpox vaccine is associated witha very low incidence of severe complications

(see Table 205-5, p. 1285, HPIM-16). The current dilemma facing our

society regarding assessment of the risk/benefit of smallpox vaccination is that, while the risks of vaccination are known, the risk of someone deliberately and

effectively releasing smallpox into the general population is unknown.

TULAREMIA (FRANCISELLA TULARENSIS) (See also Chap. 99)

Tularemia as a Bioweapon Tularemia has been studied as a biologic agent

since the mid-twentieth century. Reportedly, both the United States and the

former Soviet Union had active programs investigating this organism as a possible

bioweapon. It has been suggested that the Soviet program extended into

the era of molecular biology and that some strains of F. tularensis may have

been genetically engineered to be resistant to commonly used antibiotics. F.

tularensis is extremely infectious and can cause significant morbidity and mortality.

These facts make it reasonable to consider this organism as a possible

bioweapon that could be disseminated by either aerosol or contamination of

food or drinking water.

Microbiology and Clinical Features See Chap. 99, p. 481.

TREATMENT See Table 31-3 and Chap. 99, p. 481.

VIRAL HEMORRHAGIC FEVERS (See also Chap. 112.) Hemorrhagic

Fever Viruses as Bioweapons Several of the hemorrhagic fever viruses

have been reported to have been weaponized by the former Soviet Union and

the United States. Nonhuman primate studies indicate that infection can be

established with very few virions and that infectious aerosol preparations can

be produced.

Microbiology and Clinical Features See Chap. 112, p. 554.

TREATMENT See Table 31-3 and Chap. 112, p. 555.

BOTULINUM TOXIN (CLOSTRIDIUM BOTULINUM) (See also

Chap. 100) Botulinum Toxin as a Bioweapon In a bioterrorism attack, botulinum

toxin would likely be dispersed as an aerosol or used to contaminate

food. Contamination of the water supply is possible, but the toxin would likely

be degraded by chlorine used to purify drinking water. The toxin can also be

inactivated by heating food to_85_ C for_5 min. The United States, the former

Soviet Union, and Iraq have all acknowledged studying botulinum toxin as a

potential bioweapon. Unique among the Category A agents for not being a live

organism, botulinum toxin is one of the most potent and lethal toxins known to

man. It has been estimated that 1 g of toxin is sufficient to kill 1 million people

if adequately dispersed.

Microbiology and Clinical Features See Chap. 100, p. 487.

TREATMENT See Table 31-3 and Chap. 100, p. 487.

Category B and C Agents (See Table 31-2)

Category B agents are the next highest priority and include agents that are

moderately easy to disseminate, produce moderate morbidity and low mortality,

and require enhanced diagnostic capacity.

Category C agents are the third highest priority agents in the biodefense

agenda. These agents include emerging pathogens, such as SARS (severe acute

respiratory syndrome) coronavirus, to which the general population lacks immunity.

Category C agents could be engineered for mass dissemination in the future. It is important to note that these categories are empirical, and, depending

on future circumstances, the priority ratings for a given microbial agent may

change.

Prevention and Preparedness

As indicated above, a diverse array of agents have the potential to be used

against a civilian population in a bioterrorism attack. The medical profession

must maintain a high index of suspicion that unusual clinical presentations or

clustering of rare diseases may not be a chance occurrence, but rather the first

sign of a bioterrorism attack. Possible early indicators of a bioterrorism attack

could include:

• The occurrence of rare diseases in healthy populations

• The occurrence of unexpectedly large numbers of a rare infection

• The appearance in an urban population of an infectious disease that is usually

confined to rural settings

Given the importance of rapid diagnosis and early treatment for many of

these diseases, it is important that the medical care team report any suspected

cases of bioterrorism immediately to local and state health authorities and/or

the CDC (888-246-2675).

CHEMICAL BIOTERRORISM

The use of chemical warfare agents (CWAs) as weapons of terror against civilian

populations is a potential threat that must be addressed by public health

officials and the medical profession. The use of both nerve agents and sulfur

mustard by Iraq against Iranian military and Kurdishcivilians and the sarin

attacks in 1994–1995 in Japan underscore this threat.

A detailed description of the various CWAs can be found in Chap. 206,

HPIM-16, and on the CDC website at www.bt.cdc.gov/agent/agentlistchem.asp.

In this section only vesicants and nerve agents will be discussed as these are

considered the most likely agents to be used in a terrorist attack.

Vesicants (Sulfur Mustard, Nitrogen Mustard, Lewisite)

Sulfur mustard is the prototype for this group of CWAs and was first used on

the battlefields of Europe in World War I. This agent constitutes both a vapor

and liquid threat to exposed epithelial surfaces. The organs most commonly

affected are the skin, eyes, and airways. Exposure to large quantities of sulfur

mustard can result in bone marrow toxicity. Sulfur mustard dissolves slowly in

aqueous media suchas sweat or tears, but once dissolved it forms reactive

compounds that react with cellular proteins, membranes, and importantly DNA.

Much of the biologic damage from this agent appears to result from DNA alkylation and cross-linking in rapidly dividing cells in the corneal epithelium,

skin, bronchial mucosal epithelium, GI epithelium, and bone marrow. Sulfur

mustard reacts with tissue within minutes of entering the body.

Clinical Features The topical effects of sulfur mustard occur in the skin,

airways, and eyes. Absorption of the agent may produce effects in the bone

marrow and GI tract (direct injury to the GI tract may occur if sulfur mustard

is ingested in contaminated food or water).

• Skin: erythema is the mildest and earliest manifestation; involved areas of

skin then develop vesicles that coalesce to form bullae; high-dose exposure may

lead to coagulation necrosis within bullae.

• Airways: initial and, withmild exposures, the only airway manifestations

are burning of the nares, epistaxis, sinus pain, and pharyngeal pain. With ex posure to higher concentrations, damage to the trachea and lower airways may

occur, producing laryngitis, cough, and dyspnea. With large exposures, necrosis

of the airway mucosa occurs leading to pseudomembrane formation and airway

obstruction. Secondary infection may occur due to bacterial invasion of denuded

respiratory mucosa.

• Eyes: the eyes are the most sensitive organ to injury by sulfur mustard.

Exposure to low concentrations may produce only erythema and irritation. Exposure

to higher concentrations produces progressively more severe conjunctivitis,

photophobia, blepharospasm pain, and corneal damage.

• GI tract manifestations include nausea and vomiting, lasting up to 24 h.

• Bone marrow suppression withpeaks at 7–14 days following exposure may

result in sepsis due to leukopenia.

TREATMENT

Immediate decontamination is essential to minimize damage. Immediately

remove clothing and gently washskin withsoap and water. Eyes should be

flushed with copious amounts of water or saline. Subsequent medical care is

supportive. Cutaneous vesicles should be left intact. Larger bullae should be

debrided and treated withtopical antibiotic preparations. Intensive care similar

to that given to severe burn patients is required for pts with severe exposure.

Oxygen may be required for mild/moderate respiratory exposure. Intubation

and mechanical ventilation may be necessary for laryngeal spasm

and severe lower airway damage. Pseudomembranes should be removed by

suctioning; bronchodilators are of benefit for bronchospasm. The use of granulocyte colony-stimulating factor and/or stem cell transplantation may be effective for severe bone marrow suppression.

Nerve Agents

The organophosphorus nerve agents are the deadliest of the CWAs and work

by inhibiting synaptic acetylcholinesterase, creating an acute cholinergic crisis.

The “classic” organophosphorus nerve agents are tabun, sarin, soman, cyclosarin,

and VX. All agents are liquid at standard temperature and pressure. With

the exception of VX, all these agents are highly volatile, and the spilling of

even a small amount of liquid agent represents a serious vapor hazard.

Mechanism

Inhibition of acetylcholinesterase accounts for the major lifethreatening

effects of these agents. At the cholinergic synapse, the enzyme acetylcholinesterase

functions as a “turn off” switch to regulate cholinergic synaptic

transmission. Inhibition of this enzyme allows released acetylcholine to accumulate, resulting in end-organ overstimulation and leading to what is clinically

referred to as cholinergic crisis.

Clinical Features The clinical manifestations of nerve agent exposure are

identical for vapor and liquid exposure routes. Initial manifestations include

miosis, blurred vision, headache, and copious oropharyngeal secretions. Once

the agent enters the bloodstream (usually via inhalation of vapors) manifestations

of cholinergic overload include nausea, vomiting, abdominal cramping,

muscle twitching, difficulty breathing, cardiovascular instability, loss of consciousness, seizures, and central apnea. The onset of symptoms following vapor

exposure is rapid (seconds to minutes). Liquid exposure to nerve agents results

in differences in speed of onset and order of symptoms. Contact of a nerve agent

withintact skin produces localized sweating followed by localized muscle fasciculations.

Once in the muscle, the agent enters the circulation and causes the

symptoms described above.

TREATMENT

Since nerve agents have a short circulating half-life, improvement should be

rapid if exposure is terminated and supportive care and appropriate antidotes

are given. Thus, the treatment of acute nerve agent poisoning involves decontamination,

respiratory support, antidotes.

1. Decontamination: Procedures are the same as those described above for

sulfur mustard.

2. Respiratory support: Deathfrom nerve agent exposure is usually due to

respiratory failure. Ventilation will be complicated by increased airway

resistance and secretions. Atropine should be given before mechanical

ventilation is instituted.

3. Antidotal therapy (see Table 31-4):

a. Atropine: Generally the preferred anticholinergic agent of choice for

treating acute nerve agent poisoning. Atropine rapidly reverses cholinergic

overload at muscarinic synapses but has little effect at nicotinic

synapses. Thus, atropine can rapidly treat the life-threatening

respiratory effects of nerve agents but will probably not help neuromuscular

effects. The field loading dose is 2–6 mg IM, with repeat

doses given every 5–10 min until breathing and secretions improve.

In the mildly affected pt with miosis and no systemic symptoms,

atropine or homoatropine eye drops may suffice.

b. Oxime therapy: Oximes are nucleophiles that help restore normal

enzyme function by reactivating the cholinesterase whose active site

has been occupied and bound by the nerve agent. The oxime available

in the United States is 2-pralidoxime chloride (2-PAM Cl).

Treatment with2-PAM may cause blood pressure elevation.

c. Anticonvulsant: Seizures caused by nerve agents do not respond to

the usual anticonvulsants such as phenytoin, phenobarbital, carbamazepine,

valproate, and lamotrigine. The only class of drugs known

to have efficacy in treating nerve agent–induced seizures are the

benzodiazepines. Diazepam is the only benzodiazepine approved by

the U.S. Food and Drug Administration for the treatment of seizures

(although other benzodiazepines have been shown to work well in

animal models of nerve agent–induced seizures).

RADIATION BIOTERRORISM

Nuclear or radiation-related devices represent a third category of weapon that

could be used in a terrorism attack. There are two major types of attacks that

could occur. The first is the use of radiologic dispersal devices that cause the

dispersal of radioactive material without detonation of a nuclear explosion. Such

devices could use conventional explosives to disperse radionuclides. The second,

and less probable, scenario would be the use of actual nuclear weapons by

terrorists against a civilian target.

Types of Radiation

Alpha radiation consists of heavy, positively charged particles containing two

protons and two neutrons. Due to their large size, alpha particles have limited

penetrating power. Cloth and human skin can usually prevent alpha particles

from penetrating into the body. If alpha particles are internalized, they can cause

significant cellular damage.

Beta radiation consists of electrons and can travel only short distances in

tissue. Plastic layers and clothing can stop most beta particles. Higher energy

beta particles can cause injury to the basal stratum of skin similar to a thermal

burn.

Gamma radiation and x-rays are forms of electromagnetic radiation discharged

from the atomic nucleus. Sometimes referred to as penetrating radiation,

bothgamma and x-rays easily penetrate matter and are the principle type

of radiation to cause whole-body exposure (see below).

Neutron particles are heavy and uncharged; often emitted during a nuclear

detonation. Their ability to penetrate tissues is variable, depending upon their

energy. They are less likely to be generated in various scenarios of radiation

bioterrorism.

The commonly used units of radiation are the rad and the gray. The rad is

the energy deposited within living matter and is equal to 100 ergs/g of tissue.

The rad has been replaced by the SI unit of the gray (Gy). 100 rad _ 1 Gy.

Types of Exposure

Whole-body exposure represents deposition of radiation energy over the entire

body. Alpha and beta particles have limited penetration power and do not cause

significant whole-body exposure unless they are internalized in large amounts.

Whole-body exposure from gamma rays, x-rays, or high-energy neutron particles

can penetrate the body, causing damage to multiple tissues and organs.

External contamination results from fallout of radioactive particles landing

on the body surface, clothing, and hair. This is the dominant form of contamination

likely to occur in a terrorist strike that utilizes a dispersal device. The

most likely contaminants would emit alpha and beta radiation. Alpha particles

do not penetrate the skin and thus would produce minimal systemic damage.

Beta emitters can cause significant cutaneous burns. Gamma emitters cannot

only cause cutaneous burns but can also cause significant internal damage.

Internal contamination will occur when radioactive material is inhaled, ingested,

or is able to enter the body via a disruption in the skin. The respiratory

tract is the main portal of entrance for internal contamination, and the lung is

the organ at greatest risk. Radioactive material entering the GI tract will be

absorbed according to its chemical structure and solubility. Penetration through

the skin usually occurs when wounds or burns have disrupted the cutaneous

barrier. Absorbed radioactive materials will travel throughout the body. Liver,

kidney, adipose tissue, and bone tend to bind and retain radioactive material

more than do other tissues.

Localized exposure results from close contact between highly radioactive

material and a part of the body, resulting in discrete damage to the skin and

deeper structures.

Acute Radiation Sickness

Radiation interactions withatoms can result in ionization and free radical formation

that damages tissue by disrupting chemical bonds and molecular structures

in the cell, including DNA. Radiation can lead to cell death; cells that

recover may have DNA mutations that pose a higher risk for malignant transformation.

Cell sensitivity to radiation damage increases as replication rate increases.

Bone marrow and mucosal surfaces in the GI tract have high mitotic

activity and thus are significantly more prone to radiation damage than slowly

dividing tissues suchas bone and muscle. Acute radiation sickness (ARS) can

develop following exposure of all or most of the human body to ionizing radiation.

The clinical manifestation of ARS reflect the dose and type of radiation

as well as the parts of the body that are exposed.

Clinical Features ARS produces signs and symptoms related to damage

of three major organ systems: GI tract, bone marrow, and neurovascular. The type and dose of radiation and the part of the body exposed will determine the

dominant clinical picture.

• There are four major stages of ARS:

1. Prodrome occurs between hours to 4 days after exposure and lasts from

hours to days. Manifestations include: nausea, vomiting, anorexia, and

diarrhea.

2. The latent stage follows the prodrome and is associated with minimal

or no symptoms. It most commonly lasts up to 2 weeks but can last as

long as 6 weeks.

3. Illness follows the latent stage.

4. Death or recovery is the final stage of ARS.

• The higher the radiation dose, the shorter and more severe the stage.

• At low radiation doses (0.7 to 4 Gy), bone marrow suppression occurs and

constitutes the main illness. The pt may develop bleeding or infection secondary

to thrombocytopenia and leukopenia. The bone marrow will generally recover

in most pts. Care is supportive (transfusion, antibiotics, colony-stimulating factors).

• With exposure to 6–8 Gy, the clinical picture is more complicated; the bone

marrow may not recover and deathwill ensue. Damage to the GI mucosa producing

diarrhea, hemorrhage, sepsis, fluid and electrolyte imbalance may occur

and complicate the clinical picture.

• Whole-body exposure to _10 Gy is usually fatal. In addition to severe bone

marrow and GI tract damage, a neurovascular syndrome characterized by vascular

collapse, seizures, and deathmay occur (especially at doses _20 Gy).

TREATMENT

Treatment of ARS is largely supportive (Fig. 31-1).

1. Persons contaminated either externally or internally should be decontaminated

as soon as possible. Contaminated clothes should be removed;

showering or washing the entire skin and hair is very important. A radiation

detector should be used to check for residual contamination. Decontamination

of medical personnel should occur following emergency

treatment and decontamination of the pt.

2. Treatment for the hematopoietic system includes appropriate therapy for

neutropenia and infection, transfusion of blood products as needed, and

hematopoietic growth factors. The value of bone marrow transplantation

in this situation is unknown.

3. Partial or total parenteral nutrition is appropriate supportive therapy for

pts withsignificant injury to the GI mucosa.

4. Treatment of internal radionuclide contamination is aimed at reducing

absorption and enhancing elimination of the ingested material (Table

207-2, HPIM-16).

a. Clearance of the GI tract may be achieved by gastric lavage, emetics,

or purgatives, laxatives, ion exchange resins, and aluminum-containing

antacids.

b. Administration of blocking agents is aimed at preventing the entrance

of radioactive materials into tissues (e.g., potassium iodide,

which blocks the uptake of radioactive iodine by the thyroid).

c. Diluting agents decrease the absorption of the radionuclide (e.g.,

water in the treatment of tritium contamination).

d. Mobilizing agents are most effective when given immediately; however,

they may still be effective for up to 2 weeks following exposure.

Examples include antithyroid drugs, glucocorticoids, ammo nium chloride, diuretics, expectorants, and inhalants. All of these

should induce the release of radionuclides from tissues.

e. Chelating agents bind many radioactive materials, after which the

complexes are excreted from the body.