Preparedness for Acts of Nuclear, Biological, and Chemical ...samples.jbpub.com/9781449637774/onlinechapters/21_Preparedness for... · 1A Biologic Weapons. The CDC has classified

Preparedness for Acts of Nuclear, Biological, and Chemical TerrorismRussell E. Berger, MDMichele Burns Ewald, MD, FAAP

chapter 21

Introduction

Background

Major Biological Agents: Class 1A Biologic Agents Inhalational Anthrax Botulism Plague Smallpox Tularemia Viral Hemorrhagic Fevers

Chemical Agents Cyanide Nerve Agents (Sarin Gas)Vesicants

Nuclear AgentsRadiation Exposure

Conclusions

Chapter Outline

1 Distinguish signs and symptoms of common childhood illnesses from those caused by biological agents.

2 Formulate a treatment plan for children exposed to chemical agents.

3 Discuss short-term and long-term effects of radiation exposure in children.

Objectives

Copyright © 2012 by the American Academy of Pediatrics and the American College of Emergency Physicians

21-3

IntroductionOn September 11, 2001, our world changed forever. The attacks on the World Trade Center complex and the Pentagon killed thousands of innocent men, women, and children. In the immediate wake of those tragedies, attention turned to protecting our citizens against new threats. Emerging threats in-clude attacks that use chemical, biologic, and nuclear weapons designed to create mass casualties and hysteria. Emergency physicians are

on the frontlines of treating and triaging critically ill and injured children and therefore must be prepared to act if faced with any of these threats. This chapter addresses the major manifestations, pathogenesis, and natural history of the agents most likely to be encountered in a terrorist attack. Special attention is paid to the Centers for Disease Control and Prevention (CDC) class 1A biologic weapons, common chemical and nerve agents, and finally nuclear threats.

CASE

SCE

NARI

O 1 You are working the medical control telephone at Children’s Hospital and receive a

call from paramedics, who are bringing in schoolchildren exposed to a downtown gas attack. The hazardous materials team has yet to identify the agent but tells you that many people are dead on the scene. Those who are not dead are in extremis secondary to respiratory distress. Seizures are noted in some patients. Others have a strange reddish hue. Emergency medical services (EMS) officials report that the first patient they are bringing to you is hypotensive.

1. What agent is most likely to cause this presentation?2. What type of decontamination or treatment is needed?


21-4 Preparedness for Acts of Nuclear, Biological, and Chemical Terrorism

BackgroundDespite the increased attention to and recogni-tion of the complications of attack, most health care professionals feel ill prepared and poorly trained to deal with the unique challenges of disaster-stricken children. In a survey of 1,396 pediatricians, 86% believed that their medical training had not adequately prepared them to deal with the aftermath of the 9/11 attacks.1

In addition to training gaps among practi-tioners, in many places, the infrastructure for crisis management has not been established. In a survey of 3,670 school superintendents, only 42.8% had ever met with local EMS officials to discuss emergency planning at their schools.2

Although most hospitals have mass casualty protocols, only 64% include pediatric patients in their disaster drills.3 Most potential antidotes for exposures have not been tested in children, and there is a lack of weight-appropriate anti-dotes and treatment for exposures.4

Major Biological Agents: Class 1A Biologic WeaponsThe CDC has classified six biological agents as those posing the greatest threat in an attack: anthrax, botulism, plague, smallpox, tularemia, and viral hemorrhagic fevers.

The natural diseases caused by these agents have characteristic incubation times and natural histories. For frontline health care professionals, it is essential to be able to rapidly distinguish these entities (see Table 21-1).

Inhalational Anthrax

Clinical FeaturesInhalational anthrax is caused by the gram-pos-itive, rod-shaped, spore-forming bacteria Bacil-lus anthracis.5 Spores enter the body through inhalation and are taken up by macrophages in the lung. Macrophages transport the spores to lymph nodes, where the spores germinate into bacteria and escape into the bloodstream.5

Anthrax spores are resistant to drying, heat, UV radiation, and gamma radiation. Reports indicate that anthrax spores can remain biologi-cally active for a period of up to 200 years. Large

stores of weaponized anthrax are still believed to exist despite efforts to destroy stockpiles.6

Anthrax has a long and well-documented history of causing disease in patients. Early re-ports of disease date back thousands of years. Despite this long history, the number of pedi-atric patients documented in the literature is incredibly small. Thus, little is known about the natural history of this disease in children.

Most experts believe that anthrax infections are markedly underreported. Respiratory infec-tions are a leading cause of death in the developing world; thus, childhood death due to anthrax can be attributed to other, more common, pathogens. In addition, confirmatory pathology reports are rarely available to make postmortem diagnoses.7

Signs and SymptomsIn the few cases that are documented in the literature, some patterns have emerged. First, and this is true for the adult patients as well, children affected by fulminant anthrax have a mortality rate approaching 100%.8 Second, there are strong parallels between the prodro-mal phase of anthrax and influenza. With the 2009 outbreak of the H1N1 virus, we as physi-cians must remain vigilant for underlying and

Y O U R F I R S T C L U E

Signs and Symptoms of Inhalational Anthrax

• Nonfebrileillnessassociatedwithrapidonset of severe respiratory distress and shock.

T H E C L A S S I C S

Radiographic Findings of Inhalational Anthrax

• Pleuraleffusions

• Infiltrates

• Mediastinalwidening(Figure 21.1)


Major Biological Agents: Class 1A Biologic Weapons 21-5

TAB

LE 2

1-1

Cri

tica

l Bio

log

ical

Ag

ents

of T

erro

rism

Dis

ease

Ori

gin

Cli

nic

al F

ind

ings

aIn

cub

atio

n

Peri

od, d

Dia

gnos

tic

Sam

ple

sD

iagn

osti

c A

ssay

Isol

atio

n

Prec

auti

onsb

Init

ial

Trea

tmen

tPr

oph

ylax

is

An

thra

xB

acill

us

anth

raci

sIn

hal

atio

n: f

ebri

le

pro

dro

me

wit

h

rap

id p

rogr

essi

on

to m

edia

stin

al

lym

ph

aden

itis

, m

edia

stin

itis

(c

hes

t ra

dio

grap

h:

wit

h o

r w

ith

out

infi

ltra

tes,

wid

ened

m

edia

stin

um

, ple

ura

l ef

fusi

ons)

; sep

sis;

sh

ock;

men

ingi

tis

1–5

Blo

od

CSF

Pleu

ral fl

uid

Cu

ltu

re

Gra

m s

tain

ELIS

A

PCR

Stan

dar

dC

ipro

flox

acin

, 15

mg/

kg

(max

imu

m,

500

mg)

IV

ev

ery

12 h

, or

dox

ycyc

lin

e,

2.2

mg/

kg

(max

imu

m,

100

mg)

IV

ev

ery

12 h

c

Cip

rofl

oxac

in,

15 m

g/kg

(m

axim

um

, 500

m

g) o

rall

y ev

ery

12 h

3 6

0d,d

or

dox

ycyc

lin

e,

2.2

mg/

kg

(max

imu

m, 1

00

mg)

ora

lly

ever

y 12

hc 3

60d

d

Plag

ue

Yers

inia

pe

stis

Febr

ile

pro

dro

me

wit

h r

apid

p

rogr

essi

on

to f

ulm

inan

t p

neu

mon

ia w

ith

bl

ood

y sp

utu

m,

sep

sis,

DIC

2–4

Blo

od

Spu

tum

Lym

ph

nod

eas

pir

ate

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ltu

re

Gra

m o

rW

righ

tG

iem

sa s

tain

ELIS

A, I

FA

Ag-

ELIS

A

Pneu

mon

ic:

dro

ple

t u

nti

l p

atie

nt

trea

ted

fo

r 3

day

s

Gen

tam

icin

, 2.

5 m

g/kg

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ev

ery

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or

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lin

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kg I

V

(max

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m,

100

mg)

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ev

ery

12h

, or

ci

pro

flox

acin

, 15

mg/

kg

(max

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m,

500

mg)

IV

ev

ery

12 h

, or

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ram

ph

en-

icol

, 15

mg/

kg

(max

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m, 1

g)

eve

ry 6

h

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lin

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mg/

kg

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m, 1

00

mg)

ora

lly

ever

y 12

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10

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r ci

pro

flox

acin

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kg

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m,

500

mg)

ora

lly

ever

y 12

h ×

10

d, o

r ch

lora

-m

ph

enic

ol,

15 m

g/kg

(m

axim

um

, 1 g

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ally

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ry

6 h

× 7

d

Smal

lpox

Var

iola

vir

us

Febr

ile

pro

dro

me

Syn

chro

nou

s ve

sico

pu

stu

lar

eru

pti

on,

pre

dom

inan

t on

fac

e an

d e

xtre

mit

ies

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aryn

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s

wab

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mat

eria

l

ELIS

A, P

CR

Vir

us

is

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ion

Air

born

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ple

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tact

Sup

por

tive

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acci

nat

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w

ith

in 4

d

(con

sid

er

Vac

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a im

mu

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n, 0

.6

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kg, I

M

wit

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of

exp

osu

re

for

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ine

com

pli

cati

ons,

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mu

no-

com

pro

mis

ed

per

son

s) (con

tin

ues

)



TAB

LE 2

1-1

Cri

tica

l Bio

log

ical

Ag

ents

of T

erro

rism

, con

tin

ued

Dis

ease

Ori

gin

Cli

nic

al F

ind

ings

aIn

cub

atio

n

Peri

od, d

Dia

gnos

tic

Sam

ple

sD

iagn

osti

c A

ssay

Isol

a-

tion

Pre

- ca

uti

onsb

Init

ial T

reat

men

tPr

oph

ylax

is

Tula

rem

iaFr

anci

sella

tu

lare

nsis

Pneu

mon

ic: a

bru

pt-

onse

t fe

ver,

fu

lmin

ant

pn

eum

onia

(c

hes

t ra

dio

grap

h:

pro

min

ent

hil

ar

aden

opat

hy)

Typ

hoi

dal

: fev

er,

mal

aise

, abd

omin

al

pai

n

2–10

B

lood

Spu

tum

Seru

m

Tis

sue

Cu

ltu

ref

sero

logy

: ag

glu

tin

atio

n

EM

Stan

dar

dG

enta

mic

in, 2

.5 m

g/kg

IM

or

IV e

very

8h

,e or

dox

ycyc

lin

e, 2

.2 m

g/kg

(max

imu

m, 1

00

mg)

IV

eve

ry 1

2 h

, or

cip

rofl

oxac

in, 1

5 m

g/kg

(max

imu

m, 5

00

mg)

IV

eve

ry 1

2 h

, or

cip

rofl

oxac

in, 1

5 m

g/kg

(max

imu

m, 5

00

mg)

UV

eve

ry 1

2 h

, or

chlo

ram

ph

enic

ol, 1

5 m

g/kg

(max

imu

m,

1 g)

IV

eve

ry 6

h

Dox

ycyc

lin

e,

2.2

mg/

kg

(max

imu

m, 1

00

mg)

ora

lly

ever

y 12

h ×

14

d, o

r ci

pro

flox

acin

, 15

mg/

kg

(max

imu

m, 5

00

mg)

ora

lly

ever

y 12

h ×

14

d

Bot

uli

smC

lost

ridi

um

bo

tulin

um

to

xin

Afe

bril

e

Des

cen

din

g fl

acci

d

par

alys

is

Cra

nia

l ner

ve p

alsi

es

Sen

sati

on a

nd

m

enta

tion

inta

ct

1–5

Nas

al s

wab

Mou

se

bioa

ssay

Ag-

ELIS

A

Stan

dar

dC

DC

hep

tava

len

t an

tito

xin

(ser

otyp

es

A-G

), 1

vial

(20

mL)

IV

Non

e

Vir

al

hem

or-

rhag

ic

feve

rs

Filo

viri

dae

(E

bola

, M

arbu

rg)

Febr

ile

pro

dro

me;

ra

pid

pro

gres

sion

to

sh

ock,

pu

rpu

ra,

blee

din

g d

iath

esis

4–21

Se

rum

Blo

od

Vir

al is

olat

ion

Ag-

ELIS

A

RT-

PCR

Sero

logy

:

Ab-

ELIS

A

Con

tact

, d

rop

let;

co

nsi

der

ai

rbor

ne

if m

assi

ve

hem

or-

rhag

e

Sup

por

tive

car

eN

one

Hen

reti

g FM

, Cie

slak

TJ,

Eitz

en Jr

EE.

Bio

logi

cal a

nd

ch

emic

al t

erro

rism

. Jou

rnal

of

Ped

iatr

ics.

200

2; 1

41(3

):311

–326

. Ad

apte

d w

ith

per

mis

sion

.

Abb

revi

atio

ns:

Ab,

an

tibo

dy;

Ag,

an

tige

n; C

DC

, Cen

ters

for

Dis

ease

Con

trol

an

d P

reve

nti

on; C

SF, c

ereb

rosp

inal

flu

id; D

IC, d

isse

min

ated

intr

avas

cula

r co

agu

lati

on; E

LISA

, en

zym

e-li

nke

d im

mu

nos

orbe

nt

assa

y; E

M,

elec

tron

mic

rosc

opy;

IFA

, im

mu

nofl

uor

esce

nt

assa

y; I

M, i

ntr

amu

scu

larl

y; I

V, in

trav

enou

sly;

PC

R, p

olym

eras

e ch

ain

rea

ctio

n; R

T, r

ever

se t

ran

scri

pta

se.

a Syn

dro

me

exp

ecte

d a

fter

aer

osol

exp

osu

re.

b Bri

ef d

efin

itio

n o

f is

olat

ion

pre

cau

tion

s: S

tan

dar

d—

han

dw

ash

ing;

glo

ves,

mas

ks, e

ye p

rote

ctio

n, f

ace

shie

lds,

an

d n

onst

eril

e, fl

uid

-res

ista

nt

gow

ns

for

bloo

d, b

ody

flu

id e

xpos

ure

; ap

pro

pri

ate

han

dli

ng

of p

atie

nt

care

eq

uip

men

t, li

nen

s, e

tc; a

void

ance

of

nee

dle

-sti

ck, s

har

ps

inju

ry. A

irbo

rne—

stan

dar

d, p

lus

pri

vate

, neg

ativ

e-p

ress

ure

roo

m w

ith

ext

ern

al e

xhau

st o

r H

EPA

filt

ered

rec

ircu

late

d a

ir; s

pec

ial “

fitt

ed”

and

“se

alin

g” r

esp

irat

or

mas

ks (e

g, N

95).

Dro

ple

t—st

and

ard

, plu

s p

riva

te r

oom

, “ro

uti

ne”

mas

k w

ith

in91

cm

(3 f

t) o

f p

atie

nt.

Con

tact

—st

and

ard

, plu

s p

riva

te r

oom

; glo

ves

at a

ll t

imes

; han

d-w

ash

ing

afte

r gl

ove

rem

oval

; gow

ns

at a

ll t

imes

, re

mov

ed p

rior

to

leav

ing

pat

ien

t’s r

oom

. Ad

apte

d f

rom

: Am

eric

an A

cad

emy

of P

edia

tric

s. I

nfe

ctio

n c

ontr

ol f

or h

osp

ital

ized

ch

ild

ren

. In

: Pic

keri

ng

LK, e

d. 2

000

Red

book

: Rep

ort

of t

he C

omm

itte

e on

Inf

ecti

ous

Dis

ease

s. 2

5th

ed

. Elk

Gro

ve V

illa

ge, I

L: A

mer

ican

Aca

dem

y of

Ped

iatr

ics;

200

0:12

7–13

7.c T

he

CD

C r

ecom

men

ded

on

e or

tw

o ad

dit

ion

al a

nti

biot

ics

for

inh

alat

ion

al a

nth

rax

in t

he

fall

200

1 ou

tbre

ak: r

ifam

pin

, van

com

ycin

, pen

icil

lin

or

amp

icil

lin

, cli

nd

amyc

in, i

mip

enem

, or

clar

ith

rom

ycin

. Rec

omm

end

atio

ns

in f

utu

re o

utb

reak

s m

igh

t ev

olve

rap

idly

, an

d f

req

uen

t co

nsu

ltat

ion

wit

h lo

cal h

ealt

h d

epar

tmen

ts a

nd

th

e C

DC

(ww

w.b

t.cd

c.go

v) is

en

cou

rage

d.

d A

mox

icil

lin

, 80

mg/

kg p

er d

ay d

ivid

ed e

very

8 h

ours

, can

be

subs

titu

ted

if s

trai

n p

rove

s su

scep

tibl

e.e S

trep

tom

ycin

, 15

mg/

kg I

M e

very

12

hou

rs, c

an b

e su

bsti

tute

d if

ava

ilab

le.

f Lab

orat

ory

mu

st b

e n

otifi

ed t

hat

tu

lare

mia

is s

usp

ecte

d.



insidious attacks that can be superimposed over a background of natural disease.

In the pediatric anthrax literature, some patterns of disease have been identified. In the prodromal phase of anthrax, dizziness, visual changes, and syncope are key symptoms to help distinguish between an acute viral syndrome and anthrax.7 Pediatric patients presenting with sore throat or rhinorrhea are much more likely to have a common viral illness than anthrax.7

Diagnostic Studies and ManagementAntibiotic treatment for inhalation anthrax is ef-fective in preventing mortality when begun with-in the first day or two. However, index cases are notoriously difficult to recognize. Early detection could prevent excess morbidity and mortality.

Botulism

Clinical FeaturesBotulism is one of the most potent toxins. A single gram of aerosolized toxin could kill at least 1.5 million people. Botulism is caused by a gram-positive, rod-shaped, spore-forming, ob-ligate anaerobe. Its spores are hearty, resistant to

gastric acidity, and survive temperatures higher than 100°C (>212°F).9 Botulism causes irrevers-ible damage to the neuromuscular junction.

Signs and SymptomsPatients with botulism are afebrile and experi-ence a descending symmetric paralysis. Patients have no fevers or chills, have normal blood pres-sure and heart rate, but can experience blurring of their vision.9 Symptoms begin after a latency of approximately 24 hours.10 Despite their paral-ysis, these patients have preserved sensation and mental status. Botulism is not contagious.9,10

Diagnostic Studies and ManagementThe diagnosis of botulism is made via enzyme-linked immunosorbent assay (ELISA) testing. A new equine-derived heptavalent (toxin types A-G) botulinum antitoxin (called HBAT) is available for the treatment of noninfantile bot-ulism from the CDC. Although it can help in-terrupt disease progression, it does not reverse damage to already paralyzed muscles.11 Death

Figure 21.1 Chest radiograph demonstrating mediastinal widening and pleural effusion associated with inhalational anthrax.


Signs and Symptoms of Botulism

• Afebrile

• Symmetric,descendingflaccidparalysis(poor tone in infants)

• Cranialnervepalsiesandbulbarfindings(decreased suck in infants)

• Normalmentalstatusassociatedwithother profound neurologic findings

W H AT E L S E

Differential Diagnosis of Botulism

• Polio:asymmetricparalysis

• Guillain-Barrésyndrome:symmetric,ascending paralysis

• Myastheniagravis:ophthalmoplegia,positive Tensilon test result

• Transversemyelitis:ascendingparalysis



from botulism is primarily secondary to respirato-ry failure. Thus, prompt intubation and support-ive care are necessary.10 Serum, feces, or gastric aspirates can be obtained to confirm the diagnosis. Differential diagnosis includes myasthenia gravis, tick paralysis, Guillain-Barré syndrome, polio, stroke, and heavy metal intoxication.9

Plague

Clinical FeaturesPlague is caused by Yersinia pestis, a gram-neg-ative, nonmotile, pleomorphic, nonsporulat-ing bacterium.12 Plague has a storied history of killing as many as 75 million people during the black death of the late 1300s, fully one-third of the population of Europe. Because of this devas-tation, plague has been identified as a potential bioweapon.13

During World War II, a secret branch of the Japanese Army dropped plague-infected fleas over populated areas of China.13 Since then, both the US government and the former Soviet govern-ment have worked to create aerosols of this agent.

Airborne exposure via aerosol would pro-duce the most devastating effects on a popula-tion. If 50 kg of Y. pestis was aerosolized in a city of 5 million people, 150,000 cases of plague would result, and approximately 36,000 people would die.13 Once a population was infected, pneumon-ic plague could spread from person to person.14 Untreated pneumonic plague carries a mortality rate of 100%, whereas treated pneumonic plague is fatal approximately 50% of the time.12

Signs and SymptomsThe disease begins with rapid onset of severe flulike illness, including fever, headache, myal-gias, and exhaustion and weakness after a 1- to 6-day incubation period. The disease rapidly turns into hemorrhagic pneumonia character-ized by hemoptysis and respiratory failure.13

Diagnostic Studies and ManagementLaboratory work can reveal leukocytosis with toxic granulations, liver function test (LFT) de-rangements, coagulopathy, and other signs of multiorgan failure. Yersinia is difficult to isolate; growth can take up to 48 hours.14

Streptomycin is the drug of choice based on nonrandomized studies performed in the 1940s

and 1950s. Doxycycline is indicated for post-exposure prophylaxis when these individuals encounter patients with untreated pneumonic plague. This therapy should continue for a mini-mum of 7 days. Although a vaccine has been developed for Y. pestis, it was discontinued in 1999 and is no longer available, though it does exist in the military sector.13

Smallpox

Clinical FeaturesSmallpox (Variola virus) is a deadly viral infec-tion that has been considered eradicated world-wide. However, it is feared that there remain large stockpiles of weaponized smallpox that have not yet been destroyed. If these stockpiles truly remain, they could produce a devastating outbreak if they fell into the wrong hands.15


Signs and Symptoms of Smallpox

• Distinguishingsmallpoxfromchickenpoxinfections

• Featuresofsmallpox

• Vesicularlesionsinsimilarstageofdevelopment

• Beginonfaceandextremitiesthenspreadto trunk and abdomen

• Hightemperature

• Exhaustionandweakness

T H E C L A S S I C S

Diagnostic Findings of Plague

• Chestradiographrevealspatchyorconsolidated pneumonia.

• Pneumonicplaguesareassociatedwithsignificant hemoptysis and progression to respiratory failure.

• Mortalityisalmostuniversalinpatientspresenting with advanced pneumonic plague.




Findings of Tularemia

• LFTresultsaretheonlycommonlaboratory test abnormalities.

• Nodularinfiltratesandapleuraleffusionon chest radiograph are suggestive of the diagnosis.

Figure 21.2 Smallpox lesions in a child.

Signs and SymptomsSmallpox is highly contagious and rapidly fatal, with a mortality rate of approximately 30%. It begins with a febrile prodrome, and then the characteristic exanthem of the infection emerg-es. In contrast to Varicella infection, smallpox lesions, which are small fluid-filled vesicles, all appear at the same stage of development. These lesions tend to concentrate on the face and cen-trifugally migrate from the head out15,16 (Figure 21.2). The lesions tend to concentrate on ventral surfaces and spare the axillae, palms, soles, and antecubital areas.15

Diagnostic Studies and ManagementThe diagnosis of smallpox requires a 1- to 4-day febrile prodrome followed by the classic smallpox lesions, all at the same stage of development.15

An outbreak of smallpox requires airborne, droplet, and contact precautions to be strictly maintained. Unvaccinated caregivers are at sig-nificant risk of contracting the disease. How-ever, exposed individuals, vaccinated within 3 to 4 days of exposure, can be protected from contracting the disease or can have a less ful-minant course.15,16

Vaccination for smallpox is with a live but attenuated virus. Thus, immunocompromised patients should not be vaccinated. In addition, vaccination is category D for pregnant women, and thus benefits must be carefully weighed against fetal risk. Treatment is otherwise sup-portive care.15,16

Tularemia

Clinical FeaturesTularemia is caused by Francisella tularensis, a gram-negative, intracellular, nonmotile, coc-cobacillus.17,18 It is a hardy organism that can remain alive for weeks to years. Mortality linked to tularemia infection ranges from 2% to 4% after exposure. A 50-kg aerosol dispersal in a population of 5 million would kill approxi-mately 19,000 people and lead to approximately 250,000 hospitalizations.19

Tularemia is not contagious but is highly infectious.18 As few as 10 organisms can pre-cipitate fulminant disease.

Signs and SymptomsThe most common signs and symptoms of tu-laremia are fever, lymphadenopathy, pharyngi-tis, nausea, and vomiting.17 Given these signs, a high index of suspicion for this disease must be maintained.

Diagnostic Studies and ManagementBasic blood work is frequently normal, although 50% of patients with tularemia will have LFT re-sult abnormalities.17,18 Complete blood cell counts might not demonstrate leukocytosis or left shift. Chest radiograph might reveal only peribronchial infiltrates. The presence of nodular infiltrates and a pleural effusion is suggestive of the diagnosis, al-though nonspecific.17 Tularemia, thus, represents a significant diagnostic challenge.

Streptomycin combined with gentamicin are the preferred treatments once the diagnosis has been made. Doxycycline and ciprofloxacin might be acceptable alternative treatments. In other countries, tularemia vaccines have been developed, but these are not commercially avail-able in the United States.17,18



Viral Hemorrhagic Fevers

Clinical FeaturesViral hemorrhagic fevers due to Ebola and Mar-burg fever are highly lethal and contagious. These viruses are nonsegmented, negative-sense, single-stranded RNA viruses that belong to the Filovirus class.20 Their high infectivity and lethality make them potential bioweapons.

To date, all natural cases of these infections have begun in sub-Saharan Africa. A laboratory incident in Germany exposed German scientists to a swift but deadly outbreak in the 1970s. The natural reservoir for Marburg virus was recently discovered in the African fruit bat. The animal host for the Ebola virus has not yet been identified.20

Signs and SymptomsBoth Marburg and Ebola begin with a viral pro-drome and rapidly lead to a fatal multisystem organ failure, with a case fatality rate of 20% to 25%.21 These viruses turn on a potent cy-tokine storm, releasing tumor necrosis factor αinterleukin 1, interleukin 6, nitric oxide, and macrophage chemotactic protein. The result is a disseminated vascular leak syndrome, produc-ing hypotension and ultimately death.20

Diagnosis and ManagementELISA testing and polymerase chain reaction can be used to confirm the diagnosis. For patients exposed to Ebola, they can have a dark red, discolored soft palate and conjunctival injection along with hypotension and mucous membrane hemorrhage.20,21 It is believed that that these viruses can spread in the blood, vomit, urine, feces, and even sweat.19 Thus, use of protec-tive gowns, gloves, and masks must be used by

health care professionals. In addition, affected patients must be strictly isolated. Equipment must be sterilized before use. No effective treat-ment has been identified for these diseases.

Chemical AgentsThe infamous Tokyo subway sarin attack of 1995 brought the terrifying prospect of gas attacks again into the forefront of international atten-tion. This attack led to thoughtful consideration of other chemical agents that could be used as ter-rorist tools; mustard gas, cyanide, and vesicants were identified. Chemical agents would cause relatively rapid onset of clinical effects ranging from minutes to hours (see Table 21-2).

Cyanide

Clinical FeaturesCyanide uncouples aerobic respiration by disrupt-ing cytochrome oxidase and blocking the final step in oxidative phosphorylation.22 Cyanide lev-els higher than 0.5 mg/dL are considered toxic.23

Signs and SymptomsClinical manifestations of cyanide poisoning are nonspecific and reflect deprivation of oxygen to the heart and to the brain.24 Early manifes-tations include headaches, anxiety, dyspnea, tachycardia, and hypertension. Later manifesta-tions include coma, seizures, hypotension, and ventricular arrhythmias.23

The physical findings include cherry red discoloration of the skin and notably reddened retinal veins, reflecting the cell’s inability to ex-tract oxygen from the blood. Exposed patients might have a bitter almond odor on their breath.24


Signs and Symptoms of Cyanide Exposure

• Rapidlyproducesrespiratoryarrest

• Produceslaboratorytestresultsthatsuggestprofoundandrefractorymetabolicacidosis


Signs and Symptoms of Viral Hemorrhagic Fever

• Conjunctivalinjection

• Discolorationofthesoftpalate

• Hypotension

• Multiorganfailure


Chemical Agents 21-11

TAB

LE 2

1-2

Prim

ary

Ch

emic

al A

gen

ts o

f Ter

rori

sm

Age

nt

Tox

ic E

ffec

tsC

lin

ical

Fin

din

gsO

nse

tD

econ

tam

inat

ion

aM

anag

emen

t

Ner

ve a

gen

ts:

tabu

n, s

arin

, so

man

, VX

An

tich

olin

este

rase

: m

usc

arin

ic,

nic

otin

ic a

nd

CN

S ef

fect

s

Vap

or: m

iosi

s,

rhin

orrh

ea, d

ysp

nea

Liq

uid

: Dia

ph

ores

is,

vom

itin

g

Bot

h: c

oma,

par

alys

is,

seiz

ure

s, a

pn

ea

Seco

nd

s: v

apor

Min

ute

s-h

ours

: li

qu

id

Vap

or: f

resh

air

, rem

ove

clot

hes

, w

ash

hai

r

Liq

uid

: rem

ove

clot

hes

, cop

iou

s w

ash

ing

skin

, hai

r w

ith

soa

p a

nd

w

ater

, ocu

lar

irri

gati

on

AB

Cs

Atr

opin

e: 0

.05

mg/

kg I

Vb

or I

Mc

(min

imu

m, 0

.1 m

g; m

axim

um

, 5

mg)

, rep

eat

ever

y 2–

5 m

in

prn

for

mar

ked

sec

reti

ons,

br

onch

osp

asm

Pral

idox

ime:

25

mg/

kg I

V o

r IM

d (m

axim

um

, 1 g

IV

; 2 g

IM

), ca

n r

epea

t w

ith

in 3

0–60

min

p

rn, t

hen

aga

in e

very

1 h

for

1

or 2

dos

es p

rn f

or p

ersi

sten

t w

eakn

ess,

hig

h a

trop

ine

req

uir

emen

t

Dia

zep

am: 0

.3 m

g/kg

(m

axim

um

, 10

mg)

IV

; Lo

raze

pam

: 0.1

mg/

kg I

V o

r IM

(m

axim

um

, 4 m

g); M

idaz

olam

: 0.

2 m

g/kg

(max

imu

m, 1

0 m

g)

IM p

rn f

or s

eizu

res

or s

ever

e ex

pos

ure

Ves

ican

t:

mu

star

dA

lkyl

atio

nSk

in: e

ryth

ema,

ve

sicl

es

Eye:

infl

amm

atio

n

Res

pir

ator

y tr

act:

in

flam

mat

ion

Hou

rs

Skin

: soa

p a

nd

wat

er

Eyes

: wat

er (o

nly

eff

ecti

ve if

don

e w

ith

in m

inu

tes

of e

xpos

ure

)

Sym

pto

mat

ic c

are

(con

tin

ues

)



TAB

LE 2

1-2

Prim

ary

Ch

emic

al A

gen

ts o

f Ter

rori

sm, c

onti

nue

d

Age

nt

Tox

ic E

ffec

tsC

lin

ical

Fin

din

gsO

nse

tD

econ

tam

inat

ion

aM

anag

emen

t

Cya

nid

eC

ytoc

hro

me

oxid

ase

inh

ibit

ion

: ce

llu

lar

anox

ia,

lact

ic a

cid

osis

Tach

ypn

ea, c

oma,

se

izu

res,

ap

nea

Seco

nd

sFr

esh

air

Skin

: soa

p a

nd

wat

er

AB

Cs,

100

% o

xyge

n

Sod

ium

bic

arbo

nat

e p

rn f

or

met

abol

ic a

cid

osis

Sod

ium

nit

rite

(3%

)

Esti

mat

ed

Dos

e (m

L/k

g)

Hgb

(g/d

L)

0.

27

10

0.

33

12

0.

39

14

(max

10/

mL)

Sod

ium

th

iosu

lfat

e (2

5%):

1.65

m

L/kg

(max

imu

m, 5

0 m

L)

Hyd

roxo

coba

lam

in (7

0 m

g/kg

u

p t

o 5

g (a

du

lt d

ose)

Hen

reti

g FM

, Cie

slak

TJ,

Eitz

en Jr

EE.

Bio

logi

cal a

nd

ch

emic

al t

erro

rism

. Jou

rnal

of

Pedi

atri

cs. 2

002;

141

(3):3

11–3

26. R

epri

nte

d w

ith

per

mis

sion

.

Abb

revi

atio

ns:

AB

Cs,

air

way

, bre

ath

ing,

an

d c

ircu

lato

ry s

up

por

t; C

NS,

cen

tral

ner

vou

s sy

stem

; Hgb

, hem

oglo

bin

; IM

, in

tram

usc

ula

rly;

IV,

intr

aven

ousl

y; p

rn, a

s n

eed

ed.

a Dec

onta

min

atio

n, e

spec

iall

y fo

r p

atie

nts

wit

h s

ign

ifica

nt

ner

ve a

gen

t or

ves

ican

t ex

pos

ure

, sh

ould

be

per

form

ed b

y h

ealt

h c

are

pro

fess

ion

als

garb

ed in

ad

equ

ate

per

son

al p

rote

ctiv

e eq

uip

men

t. F

or e

mer

gen

cy

dep

artm

ent

staf

f, t

his

con

sist

s of

non

enca

psu

late

d, c

hem

ical

ly r

esis

tan

t bo

dy

suit

, boo

ts, a

nd

glo

ves

wit

h a

fu

ll-f

ace

air

pu

rifi

er m

ask/

hoo

d.

b In

trao

sseo

us

rou

te is

like

ly e

qu

ival

ent

to t

he

IV r

oute

.c A

trop

ine

mig

ht

hav

e so

me

ben

efit

via

end

otra

chea

l tu

be o

r in

hal

atio

n, a

s m

igh

t ae

roso

lize

d ip

ratr

opiu

m.

dPr

alid

oxim

e is

rec

onst

itu

ted

to

50 m

g/m

L (1

g in

20

mL

of w

ater

) for

IV

ad

min

istr

atio

n, a

nd

th

e to

tal d

ose

infu

sed

for

30

min

, or

can

be

give

n b

y co

nti

nu

ous

infu

sion

(loa

din

g d

ose

of 2

5 m

g/kg

for

30

min

, th

en 1

0 m

g/kg

per

hou

r). F

or I

M u

se, i

t m

igh

t be

dil

ute

d t

o a

con

cen

trat

ion

of

300

mg/

mL

(1 g

ad

ded

to

3 m

L of

wat

er—

by a

nal

ogy

to t

he

US

Arm

y’s

Mar

k 1

auto

inje

ctor

con

cen

trat

ion

) to

effe

ct a

rea

son

able

vol

um

e fo

r in

ject

ion

. Ea

ch M

ark

1 ki

t h

old

s tw

o au

toin

ject

ors,

on

e ea

ch o

f at

rop

ine,

2 m

g (0

.7 m

L), a

nd

pra

lid

oxim

e, 6

00 m

g (2

mL)

; alt

hou

gh n

ot a

pp

rove

d f

or p

edia

tric

use

, th

ey m

igh

t be

con

sid

ered

as

init

ial t

reat

men

t in

dir

e (e

spec

iall

y ou

t-of

-hos

pit

al) c

ircu

mst

ance

s fo

r ch

ild

ren

wit

h s

ever

e, li

fe-t

hre

aten

ing

ner

ve a

gen

t to

xic

effe

cts

wh

o la

ck I

V a

cces

s an

d f

or w

hom

mor

e p

reci

se I

M d

osin

g w

ould

be

logi

stic

ally

imp

ossi

ble.

Su

gges

ted

dos

ing

guid

elin

es a

re o

ffer

ed; n

ote

pot

enti

al e

xces

s of

init

ial a

trop

ine

and

pra

lid

oxim

e d

ose

for

age

and

wei

ght,

alt

hou

gh w

ith

in g

ener

al g

uid

elin

es f

or r

ecom

men

ded

tot

al d

uri

ng

the

firs

t 60

to

90 m

inu

tes

of t

her

apy

of

seve

re e

xpos

ure

s:

Ap

pro

xim

ate

Age

, yA

pp

rox

imat

e W

eigh

t, k

gN

o. o

f A

uto

inje

ctor

s (E

ach

Typ

e)

Atr

opin

e D

ose

Ran

ge,

mg/

kg

Pral

idox

ime

dos

e ra

nge

(m

g/k

g)

3–7

13–2

5 1

0.08

–0.1

324

-46

8–14

6–

50

20.

08–0

.13

24-4

6

>14

>

51

3≤0

.11

35 o

r le

ss


Chemical Agents 21-13

Nerve Agents (Sarin Gas)

Clinical FeaturesNerve agents are organophosphate analogues that lead to overstimulation of cholinergic receptors. The organophosphorus compounds have been known since the early 1800s and are synthesized by combining alcohols with phosphoric acid.27

Signs and SymptomsAt low exposure levels, pupils constrict and vi-sion is interrupted for several days.27,28 For higher doses, acetylcholinesterase activity is inhibited.27

Acetylcholinesterase is the enzyme responsi-ble for breakdown of acetylcholine in the synapse. As this enzyme’s activity is compromised, toxic levels of acetylcholine build at the synapse, result-ing in cholinergic toxicity. Salivation, lacrimation, urinary incontinence, defecation, and vomiting result. Severe nerve agent exposure produces se-vere bronchorrhea, resulting in respiratory com-promise, hypoxia, coma, and ultimately death.29

Long-term effects of sarin exposure among survivors include neurobehavioral syndromes, personality changes, new-onset headaches, and memory deficits.29

Diagnostic Studies and ManagementThe early and ultimate goal of treatment for nerve agent exposure is to restore cholinester-ase activity. After sarin exposure, the half-life for “aging” (irreversible cholinesterase inhibition) is approximately 5 hours. Once aging occurs, acetylcholinesterase is not able to metabolize acetylcholine again.30,31

Treatment first involves decontamination of patients. For most agents, soap and water will suf-fice, but for liquid formulations of nerve agents, methodical cleaning with thorough scrubbing must be undertaken. The patient should be taken to a well-ventilated area. Clothing that is removed should be double-bagged to protect patients and caretakers from exposure. Physicians must be wary of direct contact with patients because they can still be subject to exhaled poison.31

Patients exposed to cholinergic toxins should receive appropriate supportive care. If they expe-rience isolated eye symptoms (miosis, conjunc-tival injection, or ocular pain), atropine is not indicated and will not work.31 These patients can be treated with tropicamide ophthalmic drops.30

The differential diagnosis for cyanide poi-soning includes drug intoxication, hypogly-cemia, electrolyte disturbances, and postictal state. A hallmark of cyanide poisoning is the presence of a profound and refractory metabolic acidosis and increased anion gap.22

Children might be particularly vulnerable to the effects of cyanide, although there have not been many studies documenting this. Children’s vulnerability seems to reflect their higher re-spiratory rate, their lower body mass, and their immature metabolic mechanisms.24

Long-term effects of cyanide exposure in-clude parkinsonism, dysarthria, ataxia, and overall intellectual decline.

Diagnostic Studies and ManagementManagement of cyanide poisoning begins with removal of the patient from the source, car-diopulmonary resuscitation, and provision of 100% oxygen via nonrebreather mask or en-dotracheal tube. One treatment option is the use of the cyanide antidote kit, which contains amyl nitrite, sodium nitrite, and sodium thiosul-fate.24,25 Amyl nitrite ampules are crushed and the contents inhaled. This is followed by the use of intravenous (IV) sodium nitrite to induce methemoglobinemia.24 Methemoglobinemia is desirable in this clinical context because cyanide has a higher affinity for methemoglobin than it does for cytochrome oxidase. Once cyanide combines with methemoglobin, sodium thio-sulfate is added. The sodium thiosulfate acts as a sulfur atom donor, forming thiocyanate, a compound readily excreted in the urine.22,24,26

The induction of methemoglobinemia can be risky. High concentrations of methemoglo-bin reduce the oxygen-carrying capacity of the blood and can be dangerous and even fatal.22,24 A new agent, hydroxycobalamin (Cyanokit), is gaining favor as the antidote of choice for acute cyanide intoxication. Hydroxycobalamin directly combines with cyanide to form cyano-cobalamin (vitamin B

12), which is excreted in

the urine. The compound produces a reddish discoloration of the skin, mucous membranes, and urine and can induce self-limited hyperten-sion.25 The current adult treatment is 5 g of IV hydroxycobalamin.24,25 A pediatric dose of 70 mg/kg has been used in France.24



If patients have signs of systemic cholinergic toxic effects, they should receive initial therapy with atropine right away. They should immedi-ately receive 2 or 4 mg of atropine with retreat-ment every 5 to 10 minutes with persistent signs of respiratory distress.31 If the patient requires rapid sequence intubation, succinylcholine should be avoided because it is metabolized by plasma cholinesterases.30

Patients will benefit from atropine, which will serve to block the activity of synaptic ace-tylcholine and, in particular, benefit from early administration of pralidoxime. Pralidoxime restores acetylcholinesterase activity if rapidly administered before “aging.”

Sarin has been demonstrated to inhibit the release of central nervous system g-aminobu-tyric acid supplies, resulting in a lowered sei-zure threshold. Benzodiazepines, particularly valium, have been shown to prevent seizures from developing and therefore should be ad-ministered with atropine and pralidoxime.31

As patients recover from their exposures, erythrocyte acetylcholinesterase activity can be measured as an index of poisoning.30

Vesicant

Clinical FeaturesMustard is a vesicant sought by terrorist orga-nizations. Mustard gas was invented in 1886 by Meyer and was first used in 1917 in Belgium. There it killed 5,000 soldiers immediately and created 10,000 additional casualties.32

Mustard is an oily liquid that smells faintly like garlic and is capable of penetrating cloth-ing.33 The gas is highly lipophilic and concen-trates in the skin, eyes, gastrointestinal tract, and respiratory tract.34 Mustard gas alkylates DNA, inhibits mitosis, decreases tissue respiration, and ultimately leads to cell death.32

Signs and SymptomsThe mortality rate after exposure is approxi-mately 3%.33 When death occurs, it is usually secondary to overwhelming infection. The most susceptible areas for gas exposures are the warm and moist areas of the groin and axillae.33 In these areas, deep and painful burns can develop.

Long-term effects include the development of tracheobronchial stenosis, bronchiectasis,

and, most notably, chronic bronchitis.34 Bron-chiolitis obliterans has also been documented.35 Chronic respiratory disease ultimately leads to right heart strain and cor pulmonale.32

Patients exposed to mustard will also experi-ence desquamation of their skin after the develop-ment of flaccid blisters that are prone to infection. These patients will require careful wound care, debridement, burn treatment, and antibiotics.36

Diagnosis and TreatmentTherapy for vesicant gas exposure consists of rapid decontamination and supportive care. The patients, although frequently able to survive the initial attack, will represent a significant and continued source of disease and strain on the affected population.

Nuclear Agents

Radiation Exposure

Clinical FeaturesRadiation exposure is one of the most feared and potentially devastating of all terrorist ac-tions. Any radiation release, unintentional or deliberate, would produce significant panic and psychological stress among those affected, even with a minimal, non–life-threatening exposure.

Signs and SymptomsRadiation exposure damages tissue directly through imparting high-energy particles and indirectly via the generation of oxygen free radi-cals. If enough tissue is disturbed, organ failure results. The tissues most at risk include rapidly dividing cells. Thus, the intestinal mucosa and the bone marrow are at particular risk.37

Damage to progenitor cells in the bone mar-row sets the stage for hematopoietic malignant tumors, beginning as early as 2 years after ex-posure.38 Solid organ malignant tumors tend to lag behind and on average begin 10 years after initial exposures.38 In the wake of the Chernobyl meltdown, childhood thyroid cancer peaked 4 years after the initial exposure.38

Children are a particularly vulnerable group because of their greater minute ventilation (in-haled gases) and because they are closer to the ground (radioactive fallout).38 Infants rely on


Conclusions 21-15

their mother’s milk for nutrition. Radioactive io-dine concentrates in maternal mammary glands, making this an unsafe source of nutrition.38

Pediatric gonads experience a dose-de-pendent reduction in fertility after radiation exposure.39 The eyes, too, are a particularly vulnerable site. Doses as little as 0.2 Gy can cause cataracts.39 Fetal radiation exposure produces growth retardation, congenital malformations, carcinogenesis, and fetal death.39

Whole-body exposure to penetrating ra-diation or internal absorption will result in acute radiation syndrome. The symptoms vary with individual radiation sensitivity, type of ra-diation, and dose absorbed.39 Within 6 to 12 hours of a significant exposure, the syndrome typically begins with a prodromal phase. This is manifested by rapid onset of nausea, vomiting, diarrhea, headache, and, in more severe cases, fever.37,39 In fact, the time to emesis decreases with increasing radiation dose.37 The gastroin-testinal manifestations last 24 to 48 hours and are followed by a latent phase, during which the patient is relatively asymptomatic. The latent phase typically lasts up to 2 weeks, although it can be absent in very severe exposures.37,39 The overt or critical illness phase follows and is dose dependent. At doses exceeding 2 Gy, the bone marrow is injured, with the resulting hemato-poietic syndrome. Many patients will have lym-phopenia within 48 hours of exposure, which can predict the occurrence of this syndrome.37–39 These patients usually have maximal neutro-penia and thrombocytopenia at 3 to 4 weeks, when infection and hemorrhage are the primary challenges to medical care.37,39

Without treatment, the midlevel lethal ra-diation is 3.5 Gy (the dose that will kill 50% of the population within 30 days).37 Casualties whose radiation exposure range from 2 to 6 Gy are most amenable to treatment. Nearly every-one who receives more than 6 Gy is unlikely to survive.37

Nuclear power plant incidents and atomic or nuclear weapon detonation result in high-level radiation exposure with multiple types of radioactive isotopes and particles that persist in the environment. The more likely terror-ism scenario is a single isotope (eg, cesium)

dispersed either manually or in the water system or detonated with a conventional explosive to disperse the radioactive material (known as a “dirty bomb”). The degree and amount of radio-activity are much smaller and can be limited to a specific isotope that can have a specific antidote or protection measure.

Diagnosis and TreatmentEarly treatment means removing patients from the source of radiation and, in particular, re-moving all of their clothing and shoes. Removal of outer clothing reduces contamination by ap-proximately 90%.37,38 Decontamination includes assessment of contamination with a radiation detector, washing the skin and hair with warm water and soap, and gentle brushing to dislodge particles on the skin, followed by repeat radia-tion assessment.37,38,40 For patients who have in-ternal contamination with radioactive materials, biologic fluids, including saliva, blood, urine, and stool, must be handled carefully.38

Initial management includes assessment of the ABCs. Patients with exposures should un-dergo blood work, including a complete blood cell count with differential every 4 to 6 hours to check for decreasing lymphocyte and neu-trophil counts.37 Potassium iodide should be rapidly administered after a radiation disaster but not after a “dirty bomb”38 (see Table 21-3). Potassium iodide floods the thyroid with iodine, blocking the uptake of inhaled or ingested ra-dionuclides. Potassium iodide is generally well tolerated but should be avoided in patients with dermatitis herpetiformis and hypocomplement-emic vasculitis. Adverse effects include rash and gastric upset.38 Recommendations for repeated dosing depend on environmental evaluation by federal or state authorities.38

Treatment for internal contamination with other potential radioactive elements is listed in Table 21-4, but expert consultation is advised be-fore treatment because experience in pediatric patients is limited.

ConclusionsThe world we live in has changed forever, and we need to be prepared to react. Children are



of fear and contagion. We must work to build robust response capabilities into our pharma-ceutical companies and pressure international leaders to destroy stores of nuclear, chemical, and biological weapons. These combined steps will translate into our own safety and the safety of generations to come.

both vulnerable and innocent and should be

protected from the violence of war and terror. As

health care professionals, we have an obligation

to help protect the public health.

When faced with disaster, we must work as

coordinated teams to help prevent the spread

TABLE 21-3 Threshold Thyroid Radioactive Exposures and Recommended Doses of Potassium Iodide for Different Risk Groups

Patient Age Predicted Thyroid Exposure, Gy (rad)

Potassium Iodide Dose, mg

No. of 130-mg Tablets

No. of 65-mg Tablets

>40 ya >5 (500) 130 1 2

>18–40 y >0.1 (10) 130 1 2

Pregnant or lactating

≥0.05 (5) 130 1 2

>12–18 yb ≥0.05 (5) 65 ½ 1

>3–12 ≥0.05 (5) 65 ½ 1

>1 mo to 3 yc ≥0.05 (5) 32 ¼ ½

Birth to 1 moc,d ≥0.05 (5) 16 / ¼

Adapted from: American Academy of Pediatrics Committee on Environmental Health. Policy Statement: Radiation Disasters and Children. Pediatrics. 2003;111:1455–1466.aOlder patients are more likely to experience adverse effects from potassium iodide, including iodine-induced thyrotoxicosis, goiter, and hypothyroidism in iodide-deficient areas.bAdolescents approaching 70 kg or more in weight should be given the full adult dose (130 mg).cInfants and young children can be given potassium iodide as a fresh saturated solution diluted in milk, formula, syrup (raspberry disguises the taste best), or flat cola soda.dNeonates should have their thyrotropin and free thyroxine monitored with free thyroxine (levothyroxine) replacement therapy as needed. Adverse effects can also include gastrointestinal distress, rash, and sialadenitis.

81


Conclusions 21-17

TABLE 21-4 Radioactive Elements and Treatment Modalities

Radioactive Element Absorption Therapeutic Approach

Treatment

Americium 241 Wounds, GI or non-GI Chelation Ca-DTPA then Zn-DTPA if in first 24–48 h

Cesium 134,137 Inhalation, GI, wound Reduction of GI absorption

Prussian blue

Cobalt 60 Inhalation, <5% GI Reduction of GI absorption chelation if severe

Gastric lavage, purgatives; severe cases use penicillamine

Iodine 125, 131,132,134,135

Primarily thyroid Blockage mobilization Potassium iodide; alternatives are propylthiouracil or methimazole

Phosphorus 32 All sites Lavage, aluminum hydroxide, oral phosphates

Plutonium 239,238 Inhalation, GI or non-GI wounds variable

Reduction of GI absorption chelation

Ca-DTPA within 24 h followed by Zn-DTPA

Radium 226 GI Reduction of GI absorption

Mobilization

10% Magnesium sulfate lavage followed by saline and magnesium purgatives, ammonium chloride can increase stool elimination

Strontium 89,90 Inhalation, GI Reduction of GI absorption blockage, displacement, mobilization

Aluminum phosphate orally stable strontium can competitively inhibit metabolism; increase urinary excretion by acidification with ammonium chloride and large doses of calcium

Tritium (hydrogen 3) Inhalation, GI Dilution Hydration with caution to avoid iatrogenic water intoxication

Uranium 238,235, 239 Inhalation Mobilization Sodium bicarbonate and tubular diuretics to decrease renal toxic effects

Abbreviations: Ca-DTPA, pentetate calcium trisodium; GI, gastrointestinal; Zn-DTPA, pentetate zinc trisodium.

Adapted from: Koenig KL, Goans RE, Hatchett RJ, et al. Medical treatment of radiologic casualties. Ann Emerg Med. 2005;45:643–65237 and Allen JY, Endom EE. Management of radiation injury in children. In: Wiley JF, ed. UpToDate. Waltham, MA: UpToDate; 2010.



Check Your Knowledge1. An afebrile patient with mediastinal

widening and pleural effusions is most likely to have:A. tularemia.B. anthrax.C. botulism.D. pneumococcal pneumonia.E. viral hemorrhagic fever.

2. Which of the following is FALSE regarding botulism?A. Patients experience an ascending

paralysisB. A single gram of aerosolized toxin

could kill 1.5 million peopleC. There can be a latency of up to 24

hours before patients are symptomaticD. Botulism can resist gastric acidityE. Death is secondary to respiratory

failure3. Which of the following is FALSE

regarding smallpox?A. Lesions begin on the torso and spread

out from thereB. Strict precautions must be maintained

when ministering to smallpox patients C. Mortality rate is approximately 30%D. Postexposure vaccination can

reduce severity of disease in affected individuals

E. It is widely believed that stores of weaponized smallpox still exist

4. The following are long-term effects of sarin exposure EXCEPT:A. personality change.B. new-onset headaches.C. memory deficits.D. neurobehavioral syndromes.E. hypersalivation.

5. The following are anatomical sites that are particularly vulnerable to radiation exposure EXCEPT:A. the heart.B. the small intestine.C. the bone marrow.D. the eyes.E. the gonads.

6. All of the following are early manifestations of cyanide exposure EXCEPT:A. headaches.B. anxiety.C. dyspnea.D. bradycardia.E. hypertension.

References1. Hu YY, Adams RE, Boscarino JA, et al. Training needs of

pediatricians facing the environmental health and bioterrorism consequences of September 11th. Mt Sinai J Med. 2006;73:1156–1164.

2. Graham J, Shirm S, Liggin R, Aitken ME, et al. Mass casualty events at schools: a national preparedness survey. Pediatrics. 2006;117:e8–e15.

3. Thompson T, Lyle K, Mullins SH, et al. A state survey of emergency department preparedness for the care of children in a mass casualty event. Am J Disaster Med. 2009;4:227–232.

4. Markenson D, Reynolds S. The pediatrician and disaster preparedness. Pediatrics. 2006;117:e340–e362.

5. Lewerin, et al. Anthrax outbreak in a Swedish beef cattle herd-first case in 27 years: case report. Acta Veterinaria Scandinavica. 2010;52:7.

6. Swartz MN. Recognition and management of anthrax—an update. N Engl J Med. 2001;345:1621–1626.

7. Bravata DM, Wang E, Holty JE, et al. Pediatric Anthrax: Implications For Bioterrorism Preparedness: Evidence Report/Technology Assessment, Agency for Health Care Research and Quality. Washington, DC: US Dept of Health and Human Services; 2006:141.

8. Wilson, KH. Clinical manifestations and diagnosis of anthrax. In: Sexton DJ, ed. UpToDate. Waltham, MA: UpToDate; 2009.

9. Pegram PS, Stone SM. Botulism. In: Bartlett JG, ed. UpToDate. Waltham, MA: UpToDate; 2009.

10. Patt HA, Feigin RD. Diagnosis and management of suspected cases of bioterrorism: a pediatric perspective. Pediatrics. 2002;109:685–692.

11. Zhang JC, Sun L, Nie QH. Botulism, where are we now? Clin Toxicol. 2010;48:867-879.

12. Wayangankar S, Jackson R, Bronze MS, et al. Plague. Emedicine. October 2009.

13. Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and public health management. JAMA. 2000;283:2281–2290.

14. Margolis DA, Burns J, Reed Sl, et al. Case report: septicemic plague in a community hospital in California. Am J Trop Med Hyg. 2008;78:868–871.

15. Hogan CJ, Harchelroad F. Smallpox. Emedicine. 2009.16. Friedman HM, Isaacs SN. Smallpox. In: Hirsch MS, ed.

UpToDate. Waltham, MA: UpToDate; 2010.17. Everett ED. Clinical manifestations, diagnosis, and treatment

of tularemia. In: Calderwood SB, Edwards MS, eds. UpToDate. Waltham, MA: UpToDate; 2010.

18. Bossi P, Tegnell A, Baka A, et al. Bichat guidelines for the clinical management of tularemia and bioterrorism related tularemia. Eurosurveillance. 2004;9:e9–e10.

19. Obrien KK, Higdon ML, Halverson JJ. Recognition and management of bioterrorism infections. Am Fam Physician. 2003;67:1927–1934.

20. Bray M. Diagnosis and treatment of Ebola and Marburg hemorrhagic fever. In: Hirsch MS, ed. UpToDate. Waltham, MA: UpToDate; 2010.

C H A P T E R R E V I E W


Chapter Review 21-19

21. Centers for Disease Control and Prevention. http://www.emergency.cdc.gov/agent/vhf/. Accessed June 15, 2011.

22. Riordan M, Rylance G, Berry K. Poisoning in children 5: rare and dangerous poisons. Arch Dis Child. 2002;87:407–410.

23. Mokhlesi B, Leikin JB, Murray P, et al. Adult toxicology in critical care: part II: specific poisonings. Chest. 2003;123:897–922.

24. Geller RJ, Barthold C, Saiers JA, Hall AH. Pediatric cyanide poisoning: causes, manifestations, management, and unmet needs. Pediatrics. 2006;118:2146–2158.

25. Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxycobalamin for the empiric treatment of cyanide poisoning? Ann Emerg Med. 2007;49:806–813.

26. Martin CO, Adams HP Jr. Neurological aspects of biological and chemical terrorism: a review for neurologists. Arch Neurol. 2003;60:21–25.

27. Khurana D, Prabhakar S. Organophosphorus intoxication. Arc Neurol. 2000;57:600–602.

28. Kato T, Hamanaka T. Ocular signs and symptoms caused by exposure to sarin gas. Am J Emerg Med. 2000;18:113–114.

29. Newmark J. Therapy for nerve agent poisoning. Arch Neurol. 2004;61:649–652.

30. Lee EC. Clinical manifestations of sarin nerve gas exposure. JAMA. 2003;290:659–662.

31. Leikin JB, Thomas RG, Walter FG, Klein R, Meislin HW. A review of nerve agent exposure for the critical care physician. Crit Care Med. 2002;30:2346–2354.

32. Freitag L, Firusian N, Stamatis G, Greschuchna D. The role of bronchoscopy in pulmonary complications due to mustard gas inhalation. Chest. 199;100:1436–1441.

33. Evison D, Hinsley D, Rice P. Chemical Weapons. BMJ. 2002;324:332–335.

34. Emad A, Rezaian GR. The diversity of the effects of sulfur mustard gas inhalation on respiratory system 10 years after a single heavy exposure: analysis of 197 cases. Chest. 1997;112:734–738.

35. Thomason JW, Rice TW, Milstone AP. Bronchiolitis obliterans in a survivor of a chemical weapons attack. JAMA. 2003;290:598–599.

36. Momeni AZ, Enshaeih S, Meghdadi M, Amindjavaheri M. Skin manifestations of mustard gas: a clinical study of 535 patients exposed to mustard gas. Arch Dermatol. 1992;128:775–780.

37. Koenig KL, Goans RE, Hatchett RJ, et al. Medical treatment of radiological casualties: current concepts. Ann Emerg Med. 2005;45:643–652.

38. American Academy of Pediatrics Committee on Environmental Health. Radiation disasters and children. Pediatrics. 2003;111(6 pt 1):1455–1466.

39. Allen JY, Endom EE. Clinical features of radiation injury in children. In: Wiley JF, ed. UpToDate. Waltham, MA: UpToDate; 2010.

40. Allen JY, Endom EE. Management of radiation injury in children. In: Wiley JF, ed. UpToDate. Waltham, MA: UpToDate; 2010.

CASE

SUM

MAR

Y 1 YouareworkingthemedicalcontroltelephoneatChildren’sHospitalandreceivea

callfromparamedics,whoarebringinginschoolchildrenexposedtoadowntowngasattack.Thehazardousmaterialsteamhasyettoidentifytheagentbuttellsyouthatmanypeoplearedeadonthescene.Thosewhoarenotdeadareinextremissecondarytorespiratorydistress.Seizuresarenotedinsomepatients.Othershaveastrangereddishhue.Theemergencymedicalservicesofficialsreportthatthefirstpatienttheyarebringingtoyouishypotensive.

1. What agent is most likely to cause this presentation?2. What type of decontamination or treatment is needed?

Basedonknockoutpresentationandreddenedappearanceofpatientsandseizureactivityandhypotension,cyanidepoisoningisthemostlikelyexplanationforthepatient’ssymptoms.Patientsshouldbeundressed,cardiopulmonaryresuscitationbegunasneeded,100%oxygenbynonrebreathermaskprovided,intubationperformedifneeded,andemergentadministrationofhydroxycobalaminundertaken.

Photo Credits

Opener © Asianet-Pakistan/Alamy Images; 21-1 Courtesy CDC/Dr. P.S. Brachman; 21-2 Courtesy CDC/Dr. John Noble, Jr

Unless otherwise indicated, all photographs and illustrations are under copyright of Jones & Bartlett Learning, courtesy of Maryland Institute for Emergency Medical Services Systems, or the American Academy of Pediatrics.

Some images in this book feature models. These models do not necessarily endorse, represent, orparticipate in the activities represented in the images.

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