five years of snake envenoming in far north queensland

Emergency Medicine (2003) 15, 500–510

Blackwell Publishing Ltd.ToxicologySnake envenoming in far north Queensland

Five years of snake envenoming in far north QueenslandRobyn Barrett and Mark LittleEmergency Department, Cairns Base Hospital, Cairns, Queensland, Australia

Abstract

Objective: To describe the epidemiology, clinical features, treatment and outcomes of patients withelapid snake envenoming in far north Queensland.

Methods: Review of patients admitted with snake envenoming to Cairns Base Hospital, Queensland,from 1 January 1996–31 December 2000.

Results: A total of 264 patients presented to the hospital with a diagnosis of snakebite. Of these,27 (10%) had clinical evidence of envenoming, including seven children. All envenomedpatients had been bitten on a limb. Two patients had correct initial first aid applied.Commercially available venom detection kits were used in 23 patients; 14 (61%) bitesite swabs were positive, but only four (23%) of 17 urine Venom Detection Kits werepositive. Antivenom was administered to 20 envenomed patients. The five brownsnake envenomed patients required a median of 9 ampoules of antivenom to treat theircoagulopathy. Sixteen patients were admitted to the ICU, with six requiring ventilation.Six patients were successfully managed in the ED observation ward. Three patientsenvenomed by a taipan, and one by a death adder were discharged with ongoingneurological symptoms. There was one death from brown snake envenoming.

Conclusions: The incidence of snakebite and envenoming in far north Queensland is higher thanreported from hospitals in capital cities and is a significant health issue.

Key words: antivenom, brown snake, envenoming, north Queensland, observation ward, snakebite, taipan.

Introduction

Snakebite is a rare condition in major city centres.In spite of this, many of the reports of snakebite inAustralia have been from major city hospitals1–5 orfrom antivenom usage reports.6–9 There is limiteddata from regional Australia, and other than indivi-dual case reports,10–14 there have not been any datapresented on the experience of snakebite in north

Queensland. Evidence from a recently publishedprospective study over 12 months from the RoyalDarwin Hospital (RDH) demonstrated that the rateof presentation of snakebite in tropical Australia wasfar greater than more southern capital cities.15 The70 suspected snakebite cases from RDH in one yearwere a greater case load than the 99 snakebite casesfrom the three major metropolitan teaching hospitalsin Perth over a 10 year period.1

Correspondence: Dr Mark Little, Department of Emergency Medicine, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia. Email: [email protected]

Robyn Barrett, MBBS, Emergency Registrar; Mark Little, MBBS, DTM & H, FACEM, MPH & TM, Staff Specialist and Clinical Toxicologist.

Snake envenoming in far north Queensland

501

As only approximately 5–10% of snakebite patientsare envenomed,7 the emergency physician experiencein the management of envenomed patients is limited,but essential, as this is a potentially lethal condition.Recommendations for management of snake envenomingare often based on anecdotal experience or opinion, so itis important to re-examine these recommendations inlight of new reports. For example, Isbister et al. recentlydemonstrated that the whole blood clotting testwas a valuable diagnostic test for the detection ofthe coagulopathic snake envenomed patient in ruralAustralia.15 Thus, the experience from centres intropical or regional Australia may help improve ourknowledge of snakebite. The aim of this study wasto review five years of snake envenoming presentingto Cairns Base Hospital (CBH) between 1996 and2000.

Methods

Cairns Base Hospital is a provincial 350 bed hospitalin far north Queensland (FNQ) which acts as a referralcentre for an area beginning 150 km south of Cairns,and extending north to include Cape York and theTorres Strait Islands. The population of Cairns is120 000, and the hospital provides a tertiary andreferral service for a total population of approximately225 000.

A retrospective review was performed on allsnakebite cases presenting to CBH for a five yearperiod between 1 January 1996 and 31 December 2000.All cases of snakebite presenting to CBH are routinelyadmitted to hospital, either to the observation wardin the ED, a medical ward, or the ICU. A search ofthe hospital admission database, the ED attendancedatabase, and the ICU admission register identifiedall snakebite cases. All case histories were reviewedby both authors. Definition of envenoming was basedon a similar definition used in previous studies.1,4

Systemic envenoming was present if there was:1. Clinical evidence of envenoming defined as the

presence of vomiting, abdominal pain, and at leastone of the following — neurotoxic effects includingptosis, clinical evidence of bleeding, convulsions, ordifficulty breathing or swallowing and/or:

2. Laboratory evidence of envenoming (coagulopathy,haemolysis, rhabdomyolysis or renal failure).If a patient had non-specific symptoms (headache,

vomiting and/or abdominal pain) they were consideredto be an envenomed patient if:

1. There was a witnessed snakebite, and2. A positive result using the venom detection kit

(VDK).A data extraction document was developed and

information regarding each patient’s presentationcollated. Details extracted included time and dateof bite, first aid measures used, time from bite topresentation at a medical facility, symptoms andsigns, laboratory investigation results, VDK results,amount and type of antivenom utilized, time elapsedbetween initial bite and antivenom (AV) administra-tion, disposition and outcome of the patient.

Results

Over the study period, 264 suspected snakebite caseswere admitted to CBH. Of these, 27 patients (10%) hadsigns and symptoms or laboratory features consistentwith our definition of envenoming. A summary ofthe patients and their demographics is in Fig. 1. Initialfirst aid was poor with only two patients receivingappropriate pressure immobilization bandaging (Fig. 1).

Those patients envenomed by a taipan alloriginated from areas north of Cairns, mainly from theCape York region, while all incidents of brown snakeenvenoming were from the Mareeba area, a townshipon the Atherton tablelands, west of Cairns. This isin contrast to patients envenomed by death adders,whose origins varied from Cairns, to the tablelandsand Cape York.

Clinical presentation

The clinical presentation and laboratory results ofpatients who were envenomed are listed in Table 1.Other than a 2.5-year-old boy, all envenomed patientssuspected they had been bitten by a snake. Only onepatient, a 37-year-old male, was asymptomatic, buthad incoagulable blood secondary to brown snakeenvenoming. Of the 10 patients who were hypotensiveon presentation, five were cases of taipan envenoming,four were brown snake envenomings and the lastwas a probable taipan envenoming that presented instatus epilepticus with haemodynamic instability.All patients became normotensive after AV.

There was one death. A 60-year-old woman diedfrom hypoxic brain damage following a pre hospitalcardiac arrest after brown snake envenoming. Threepatients envenomed by a taipan, and one envenomedby a death adder, were discharged from hospital with

R Barrett and M Little

502

Figure 1. Summary of snake envenoming presenting to Cairns Base Hospital from 1 January 1996–31 December 2000.


503

Tab

le 1

.M

ajor

feat

ures

of

27 p

atie

nts

wit

h en

veno

min

g tr

eate

d at

Cai

rns

Bas

e H

ospi

tal 1

996–

2000

Patie

nt/D

OP

His

tory

Sym

ptom

s/si

gns

Abn

orm

al in

vest

igat

ion

VD

KAV

am

ount

Dis

posi

tion

Com

men

tCo

agul

atio

nRh

abdo

myo

lysi

sRe

nal

Tai

pan

Defi

nite

03/9

7 13

yom

ale

Witn

esse

d bi

teA

bdom

inal

pai

n,N

&V,

pto

sis,

opht

halm

ople

gia,

hypo

tens

ion

Clot

ting

> 1

hPl

t 137

× 1

09/L

CK 1

000

U/L

Taip

an p

ositi

ve

(bite

site

)2

amp

MV

ICU

On

disc

harg

e di

plop

iapr

esen

t. Re

solv

ing

5 da

ys la

ter.

01/0

0 41

yo

mal

ePe

t Inl

and

Taip

an,

mul

tiple

bite

s

Gen

eral

ized

w

eakn

ess,

ptos

is,

hypo

tens

ion

PT 2

0 s,

APT

T 1

27 s

Pl

t 37

× 10

9 /L

CK 2

700

U/L

Myo

glob

inur

iaCr

eat

0.46

mm

ol/L

nega

tive

7 am

p M

V1

amp

PVIC

UVe

ntila

ted

12 d

ays

enve

nom

ings

and

AV.

01/0

0 30

yo

mal

eRe

mot

e Ca

pe Y

ork

com

mun

ity,

bite

mar

ks.

7 h

to P

IB

Alte

red

leve

l of

cons

ciou

snes

s, ag

itate

d, a

ctiv

ely

blee

ding

, pto

sis,

hypo

tens

ion

(on

pres

enta

tion)

Clot

ting

> 6

h,

Plt 9

2 ×

109 /L

(on

pres

enta

tion)

CK 7

000

U/L

Myo

glob

inur

ia

(on

pres

enta

tion)

Crea

t 0.

21 m

mol

/L

Taip

an p

ositi

ve

(urin

e)3

amp

PV4

amp

MV

ICU

AV a

t 8 h

pos

t bite

.Ve

ntila

ted

3 da

ys.

Pers

istin

g ey

e si

gns

day

7 po

st b

ite.

02/0

0 24

yo

mal

eRe

mot

e Ca

pe Y

ork

com

mun

ity.

Witn

esse

d bi

te.

Unc

onsc

ious

, st

ridor

, res

pira

tory

arre

st d

ue to

w

eakn

ess

(15

min

saf

ter b

ite),

activ

ely

blee

ding

, hy

pote

nsio

n

Coag

s (n

orm

al

post

-AV

), Pl

t 12

6 ×

109 /L

CK 1

580

U/L

Crea

t0.

17 m

mol

/Lne

gativ

e3

amp

PV2

amp

MV

ICU

Blee

ding

cea

sed

with

MV

and

FFP

. Ve

ntila

ted

5 da

ys.

Resi

dual

hyp

oxic

br

ain

inju

ry.

09/0

0 3y

o m

ale

Bite

mar

ksG

loba

l wea

knes

s,op

htha

lmop

legi

a,ac

tivel

y bl

eedi

ng,

dark

urin

e,

hypo

tens

ion

INR

> 1

0,aP

TT

> 6

00 s

CK 3

400

U/L

Myo

glob

inur

iaCr

eat

0.05

mm

ol/L

Taip

anpo

sitiv

e(b

itesi

te)

4 am

p M

VIC

UG

ood

resp

onse

to A

V.

Pro

babl

e12

/98

37yo

m

ale

Witn

esse

d bi

te

in v

icin

ity o

f CB

H

Stat

us e

pile

ptic

us

with

in 3

min

of

bite

, gen

eral

ized

w

eakn

ess,

card

iova

scul

ar

inst

abili

ty

Coag

s no

rmal

Plt 1

17 ×

109

/LCK

12

88 U

/L—

nega

tive

3 am

p PV

ICU

Intu

bate

d an

d AV

on

arriv

al.


504

04/0

0 27

yo

mal

eW

itnes

sed

bite

Ptos

is,

opht

halm

ople

gia

Clot

ting

> 8

0 m

in,

Coag

s no

rmal

(p

ost-A

V)

——

nega

tive

1 am

p PV

Obs

w

ard

Rapi

d re

spon

se to

1am

p AV

.

Dea

th a

dder

Defi

nite

03/9

3 19

yo

mal

eFe

lt st

rike,

bite

m

arks

, Cat

tle

stat

ion

Abd

omin

al p

ain,

N

&V,

loca

l pai

n,

regi

onal

ly

mph

aden

opat

hy

NA

DCK

218

U/L

—D

eath

add

er

posi

tive

(bite

site

)

No

AVO

bs

war

dSy

mpt

oms

reso

lved

over

12

h.

02/9

8 44

yo

mal

eFe

lt st

rike,

bite

m

arks

Gen

eral

ized

w

eakn

ess,

ptos

is, d

row

sy

All

NA

D—

—ne

gativ

e1

amp

MV

(Dea

th a

dder

)IC

URe

solu

tion

of

sym

ptom

s w

ith A

V.

07/9

8 3y

om

ale

Witn

esse

d m

ultip

le b

ites

Gen

eral

ized

w

eakn

ess

(pow

er 2

/5),

loca

l pai

n

All

NA

D—

—D

eath

add

er

posi

tive(

bite

site

)1

amp

MV

Paed

w

ard

Rapi

d re

solu

tion

of sy

mpt

oms w

ith A

V.

03/9

9 50

yo

mal

ePe

t sna

ke b

ite.

Dea

th a

dder

.6

h to

med

ical

ai

d. N

o PI

B.

Ptos

is,

dysa

rthr

ia,

dysp

noea

All

NA

D—

——

3 am

p M

V,1

amp

PVN

eost

igm

ine

atro

pine

ICU

Prev

ious

AV.

A

naph

ylac

tic re

actio

n to

PV.

Mar

ked

resp

onse

to

neos

tigm

ine

2.5

mg/

atro

pine

1.2

mg.

09/9

9 8y

o m

ale

Witn

esse

d bi

te

on fo

otBl

urre

d, d

oubl

e vi

sion

, sw

olle

n an

d pa

infu

l bite

site

All

else

NA

DCK

490

U/L

—D

eath

add

er

posi

tive

(bite

site

)

No

AVPa

ed

war

dSy

mpt

oms

reso

lved

ov

er 2

4 h.

10/0

0 10

yo

fem

ale

Witn

esse

d bi

teLo

cal p

ain,

N&

V,

abdo

min

al c

ram

ps,

fluct

uatin

g LO

C

PT 1

6 s,

aPT

T 3

6 s

CK 2

55 U

/L—

Dea

th a

dder

po

sitiv

e (b

itesi

te)

No

AVIC

USy

mpt

oms

reso

lved

.

Pro

babl

e08

/97

33yo

fem

ale

Rem

ote

Cape

Yor

k co

mm

unity

, fe

lt st

rike,

sa

w s

nake

.Bi

tem

arks

Hea

dach

e, N

&V,

D

iplo

pia

(sym

ptom

sw

orse

ned

with

re

mov

al o

f PI

B)

WBC

T n

orm

al—

—†B

row

n po

sitiv

e (u

rine)

1 am

p PV

ICU

Rap

id re

solu

tion

of

sym

ptom

s w

ith A

V.

Patie

nt/D

OP

His

tory

Sym

ptom

s/si

gns

Abn

orm

al in

vest

igat

ion

VD

KAV

am

ount

Dis

posi

tion

Com

men

tCo

agul

atio

nRh

abdo

myo

lysi

sRe

nal

Tab

le 1

Con

tinue

d


505

12/0

0 31

yo

mal

eRe

mot

e Ca

pe Y

ork

com

mun

ity.

Felt

som

ethi

ng,

saw

sna

ke.

Nys

tagm

us, p

tosi

s, op

htha

lmop

legi

aW

BCT

nor

mal

(pre

-AV

)A

ll N

AD

(p

ost-A

V)

——

†Bro

wn

posi

tive

(bite

site

)

2 am

p PV

Obs

war

dRe

solu

tion

of

sym

ptom

s with

AV

on

two

occa

sion

s. Pe

rsis

ting

dipl

opia

th

at re

solv

ed o

ver

5 da

ys.

Bla

ckP

roba

ble

11/0

0 75

yo

mal

eIn

long

gra

ss,

felt

strik

e, b

ite

mar

ks o

n le

g

Wou

nd p

ain,

m

yalg

ia,

abdo

min

al

disc

omfo

rt.

—CK

426

2 U

/L—

nega

tive

1 am

p PV

Obs

war

dCK

fell

to 2

550

U/L

with

in 6

h o

f AV

.

Bro

wn

Defi

nite

(all

resu

lts a

re in

itial

resu

lts)

12/9

7 37

yo

mal

eW

itnes

sed

bite

w

ith b

ite m

arks

Com

plet

ely

asym

ptom

atic

PT >

169

s,

aPT

T >

249

s,

Fib

< 0

.6 g

/L,

Plt 8

9 ×

109 /L

CK 2

64 U

/LM

yogl

obin

uria

Crea

t 0.

21 m

mol

/LBr

own

posi

tive

(bite

site

)3

amp

MV

ICU

Wor

seni

ng o

f W

BCT

at p

erip

hera

l hos

pita

l le

ad to

tran

sfer

.

02/9

8 60

yo

fem

ale

Witn

esse

d bi

te,

no P

IBPr

e ho

spita

l ca

rdio

resp

irato

ryar

rest

, act

ivel

y bl

eedi

ng

aPT

T >

249

s,

Fib

0.3

g/L,

Pl

t 60

× 10

9 /L

——

Brow

n po

sitiv

e(b

itesi

te)

3 am

p PV

7 am

p M

VIC

UD

ied

of h

ypox

ia b

rain

inju

ry.

03/9

8 38

yo

mal

eW

itnes

sed

bite

Colla

pse

10 m

in

afte

r bite

, con

fuse

d,

‘dus

ky’,

rapi

d A

F,

hypo

tens

ion,

ab

dom

inal

pai

n,

haem

atur

ia

Clot

ting

> 9

0 m

in,

Fib

< 0

.3 g

/L—

Crea

t nor

mal

Brow

n po

sitiv

e (b

itesi

te)

2 am

p PV

7 am

p M

VCC

UW

as o

n so

tolo

l for

tach

yarr

hyth

mia

s.

06/9

9 23

yo

mal

eW

itnes

sed

bite

w

ith b

ite m

ark

On

pres

enta

tion,

sw

eaty

, tac

hyca

rdia

(P

= 1

40),

hypo

tens

ion,

conf

used

, act

ivel

y bl

eedi

ng g

ums

PT >

150

s,

aPT

T >

250

s,

Fib

not d

etec

ted,

Plt 7

× 1

09/L

(p

ost-A

V)

——

Brow

n po

sitiv

e (u

rine)

4 am

p PV

8 am

p M

VIC

URe

peat

ed d

osin

g of

AV

to c

orre

ct

coag

ulop

athy

.

Patie

nt/D

OP

His

tory

Sym

ptom

s/si

gns

Abn

orm

al in

vest

igat

ion

VD

KAV

am

ount

Dis

posi

tion

Com

men

tCo

agul

atio

nRh

abdo

myo

lysi

sRe

nal

Tab

le 1

Con

tinue

d


506

11/0

0 59

yo

fem

ale

Felt

strik

e,

bite

mar

kN

ause

a,

hypo

tens

ion,

fluct

uatin

g co

nsci

ousn

ess,

grey

& p

ale

initi

ally

.

PT >

120

s,

aPT

T >

150

s,

D-d

imer

> 2

56,

Fib

< 0

.6 g

/L,

Plt 1

14 ×

109

/L

——

Brow

n po

sitiv

e(b

itesi

te)

1 am

p PV

8 am

p M

VIC

URe

peat

ed d

osin

g of

AV

to co

rrec

t co

agul

opat

hy.

Tig

er-s

nake

gro

upP

roba

ble

02/9

6 26

yo

fem

ale

Witn

esse

d bi

teH

eada

che,

N&

V,

loca

l pai

n.A

ll N

AD

——

Tig

er

posi

tive

(bite

site

)

No

AVO

bs w

ard

Sym

ptom

s re

solv

ed

over

12

h.

11/9

6 23

yo

mal

eW

itnes

sed

bite

foot

Loca

l pai

n an

d sw

ellin

g, N

&V,

te

nder

regi

onal

ly

mph

aden

opat

hy.

All

NA

D—

—T

iger

posi

tive

(bite

site

)

No

AVCC

USy

mpt

oms

reso

lved

ov

er 1

2 h.

03/9

9 2.

5yo

mal

ePl

ayin

g in

ga

rden

, bec

ame

unw

ell w

ith

abdo

min

al p

ain.

N

o hi

stor

y of

bite

.

Colla

pse,

ab

dom

inal

pa

in, N

&V.

PT 1

5 s,

aPT

T 5

1 s

CK 2

718

U/L

Myo

glob

inur

ia—

Tig

er

posi

tive‡

(urin

e)

2 am

p M

VIC

UIn

itial

ly a

dmitt

ed

unde

r sur

gery

—

note

d to

hav

e m

yogl

obin

uria

, po

sitiv

e V

DK

and

diag

nosi

s m

ade.

01/0

0 30

yo

mal

eW

itnes

sed

snak

ebite

, PI

B 30

min

saf

ter b

iteA

ther

ton

tabl

elan

ds.

Hea

dach

es,

mya

lgia

, ab

dom

inal

pa

in, G

IT u

pset

PT 5

0 s,

aPT

T 1

70 s

,Fi

b <

0.5

g/L

, Pl

t 98

× 10

9 /L

CK 1

62 U

/L,

Myo

glob

inur

ia—

Tig

erpo

sitiv

e‡(b

itesi

te)

6 am

p M

VIC

URe

turn

of

fibrin

ogen

w

ith 5

am

ps A

V.

Sea

snak

eD

efini

te07

/96

22yo

m

ale

Snak

e w

rapp

ed

arou

nd le

g an

dbi

t whi

lst

fishi

ng in

sea

.Re

mot

e A

borig

inal

co

mm

unity

Hea

dach

e, N

&V

NA

DCK

532

U/L

——

No

AVSe

asna

ke

(his

toric

ally

)

Obs

war

dSy

mpt

oms

reso

lved

ove

r 12

h

Patie

nt/D

OP

His

tory

Sym

ptom

s/si

gns

Abn

orm

al in

vest

igat

ion

VD

KAV

am

ount

Dis

posi

tion

Com

men

tCo

agul

atio

nRh

abdo

myo

lysi

sRe

nal

Tab

le 1

Con

tinue

d


507

05/9

7 28

yo

mal

eRe

mov

ing

snak

e fr

omtr

awle

r net

Gen

eral

ized

m

yalg

ia, N

&V

NA

DCK

374

5 U

/L,

(12

h po

st b

ite),

——

No

AVSe

asna

ke(h

isto

rical

ly)

War

dSy

mpt

oms

reso

lved

ov

er 3

6 h

†Thi

s ve

nom

det

ectio

n ki

t (V

DK

) was

con

side

red

a fa

lse

posi

tive,

as

it di

d no

t fit i

n w

ith th

e cl

inic

al p

ictu

re. ‡

The

tige

r sna

ke is

usu

ally

not

foun

d in

far n

orth

ern

regi

ons,

and

as

the

VD

K c

ross

reac

ts b

etw

een

tiger

sna

ke, r

ough

-sca

led

snak

es a

nd H

oplo

ceph

alus

spp

., th

e au

thor

s co

nsid

er th

e ‘ti

ger’

enve

nom

ings

pro

babl

y du

e to

roug

h-sc

aled

sna

kes

or

Hop

loce

phal

us s

pp. T

here

are

repo

rts

of H

ydro

ceph

alus

spe

cies

(e.g

. pal

e he

aded

sna

ke) c

ausi

ng e

nven

omin

g in

the

Ath

erto

n ta

blel

ands

as

happ

ened

for o

ne c

ase

in th

is s

erie

s.A

mp,

am

poul

e; aP

TT,

act

ivat

ed p

artia

l thr

ombo

plas

tin ti

me;

DO

P, d

ate

of p

rese

ntat

ion

(mon

th/y

ear);

AV,

ant

iven

om; C

K, C

reat

ine

kina

se; C

reat

, Cre

atin

ine;

Fib,

fibr

inog

en; M

V,

mon

oval

ent;

Plt,

plat

elet

s; PT

, pro

thro

mbi

n tim

e; PV

, pol

yval

ent;

N&

V, n

ause

a &

vom

iting

; NA

D, n

o ab

norm

ality

det

ecte

d; W

BCT,

who

le b

lood

clot

ting

test

. A sa

mpl

e of

bloo

d is

pla

ced

into

a g

lass

tube

, if

bloo

d ha

s no

t for

med

a c

lot w

ithin

20

min

then

con

side

red

to b

e an

indi

cato

r of

coag

ulop

athy

in th

e pr

esen

ce o

f a

snak

ebite

.15

Nor

mal

resu

lts ra

nge

for C

BH: C

reat

ine

kina

se: <

200

U/L

; Pla

tele

ts: 1

40–4

00 ×

109

/L; C

reat

inin

e: 0.

04–0

.12

mm

ol/L

.Co

agul

atio

n st

udie

s, IN

R: 0

.8–1

.2; P

roth

rom

bin

time,

12–

16 s

; Act

ivat

ed p

artia

l thr

ombo

plas

tin ti

me,

23–

37 s

; Fib

rinog

en 1

.5–4

.0 g

/L.

Patie

nt/D

OP

His

tory

Sym

ptom

s/si

gns

Abn

orm

al in

vest

igat

ion

VD

KAV

am

ount

Dis

posi

tion

Com

men

tCo

agul

atio

nRh

abdo

myo

lysi

sRe

nal

Tab

le 1

Con

tinue

d

ongoing neurological dysfunction. One of these patientshad significant neurological deficit due to inappropriatefirst aid, delayed presentation and hypoxic insult. Theremaining three had ongoing ptosis and ophthalmo-plegia, which was gradually resolving on discharge. Twopatients developed pneumonia during their admission.One was considered to be aspiration pneumonia, the othernosocomial. No patients had intracranial haemorrhage.

Snake identification

Venom detection kit was the most commonly usedmethod of snake identification in this study. Therewere a total of 23 bite site VDK performed and 14(61%) of these were positive. Of 17 urine VDK per-formed, only four (23%) were positive. Six patientshad negative results from both site and urine testing,despite clinical evidence of envenoming. There weretwo false positive VDK results, where the patient’sclinical condition and investigations did not correlatewith the VDK result.

In two cases, patients were bitten by their ‘pet’snake and in the two cases of sea snake envenomingthey were identified on historical grounds.

Management

1. AntivenomAntivenom was administered to 20 of the 27 patientswith evidence of envenoming (Table 1). Eight patientsreceived both monovalent and polyvalent AV.Polyvalent AV was used if no monovalent AV wasavailable. One patient received repeated doses ofneostigmine and atropine to augment death adderAV.12 Time taken for administration of AV (from thetime of envenoming) varied from 30 min (threepatients), to 2–6 h (14 patients), except in three patientswho did not receive AV until 12–14 h after the bite. Thedelay was often due to delayed presentation (usuallydue to distance) or a delay in diagnosis. Three patientsdeveloped anaphylactic reactions to AV, but two ofthese patients had received AV before.

All patients with brown snake envenoming developedsignificant consumptive coagulopathy with very low fibri-nogen (0–0.6 g/L) [normal range = 1.5–4.0 g/L]. Noneof these patients received fresh frozen plasma or othercoagulation factors, and the coagulopathy correctedwith large doses of AV. Patients received a mediandose of 9 ampoules of AV (3, 9, 9, 10, 12), and AVadministration was guided by clinical scenario (activebleeding) and/or 6-hourly blood examination.


508

Seven patients had evidence of envenoming, butdid not receive AV (Table 1). All seven patients wereadmitted for at least a 24 h period and had regularclinical examinations and laboratory testing. Allpatients’ symptoms resolved and they were dischargeduneventfully.

2. Intensive care unit admissionsMost ICU admitted patients had brief (24–36 h)stays, except five patients who required prolongedadmissions. Of these five patients, three had evidenceof taipan envenoming and required ventilatorysupport for four, five and 14 days, respectively. Thefourth patient had brown snake envenoming, hadpresented to a rural hospital in cardiac arrest, andrequired 10 days of ventilatory support. The fifthpatient with laryngeal spasm associated with deathadder envenoming and AV administration, requiredthree days of ventilatory support. No patient requiredhaemofiltration or dialysis.

3. Observation ward admissionsIt is the policy of the CBH Emergency Departmentthat non-envenomed adults are admitted to the obser-vation ward for ongoing investigations and repeatedexamination. Six envenomed patients were admittedto the short stay/observation ward located in theED (Table 1). Three patients had received AV, wereasymptomatic with stable clinical signs and invest-igations, and were managed safely in the observationward.

Discussion

Envenoming from snakes found in FNQ continues tobe problematic for the population as well as the healthservices in the area. Patients with snake envenominguse considerable resources in their managementincluding AV, ICU admissions and use of retrievalservices.

The incidence of snakebite and envenoming inFNQ demonstrated in this study is higher than thatreported from other (capital city) centres, and confirmsan earlier observation made by Flecker.13 In hispublished report there were 95 admissions to tropicalcoastal Queensland hospitals due to snakebite in1938. This was significantly higher than the threesnakebites in tropical inland Queensland and 48subtropical coastal Queensland reported for the sameyear. In a review of 10 years’ snakebites at Fremantle

Hospital (Western Australia), a similar sized hospitalto CBH, 76 patients were admitted with snakebite,with only 13 envenomings.2 Similarly, in a 10 years’review of snakebites presenting to three adult EDsin Perth (approximately eight times the population ofFNQ) 99 patients were bitten with 53 instances ofenvenoming.1 Mead and colleagues described their10 years’ experience of snakebite in children present-ing to the tertiary paediatric hospital EmergencyDepartment in Perth.4 During this time 156 childrenpresented with snakebite, with only 14 children beingenvenomed. A study from the Royal Children’sHospital in Brisbane over 10 years of 218 childrenbitten by snakes revealed that only 14 cases requiredantivenom.3 Further south, in a 12-year period, only11 patients envenomed by snakes were admitted toRoyal North Shore Hospital in Sydney.5

There are a limited number of taipan envenomingsreported in Australia, and most of these are fromnorth Queensland. Most experience of envenoming bythis snake comes from Papua New Guinea.16 Oneearly Australian article reported three cases, withtwo deaths13 and another reported three deathsfrom presumed taipan bite in the Cairns region.14

Southern and colleagues reported five cases of taipanenvenoming with survival from the Townsvilleregion.17 Our study presented five definite and twoprobable taipan envenomings. They all presentedwith rapid onset of neurological symptoms, profoundcoagulopathy and early hypotension in five cases.All survived, although three patients had ongoingneurological problems.

There have only been a handful of reports ofenvenoming by the inland taipan (Oxyuranusmicrolepidotus). As in our patient, they have onlyoccurred in herpetologists. In a survey conducted on28 Queensland herpetologists (14 being from the CapeYork Peninsular Society in Cairns) four reported thatthey had been bitten by an inland taipan although noclinical information was provided.18 In an earlier casea herpetologist took 4 weeks to recover after a bite,due to the misidentification of the snake resultingin brown snake antivenom being administered.19 In amore recent case early treatment of a bite in SouthAustralia resulted in rapid resolution of symptoms.20

In our case the 40-year-old male herpetologist, whohad been previously envenomed by a number ofhis other captured snakes, was bitten on the hand.He applied a tourniquet promptly, but suffered aconvulsion on arrival at the peripheral hospital.He initially declined antivenom until his condition


509

deteriorated and he required ventilation. He wasventilated for 12 days and his course was com-plicated by acute respiratory distress syndrome, haem-olysis, renal failure, thrombocytopenia and mildrhabdomyolysis.

Of particular concern was the inadequate first aidthat was applied to many of our patients. The pressurebandage and immobilization technique has beenaccepted as appropriate first aid since Sutherlandsuggested it in 1979.21 Earlier reports have suggestedthat up to 60% of victims were utilizing this method,but more recent accounts indicate a significantdecrease in the incidence of appropriate first aid.8,15

In this small series of envenomed patients, as shownin Table 1, only two had effective pressureimmobilization applied, whilst another four appliedpressure bandages only. A total of 12 patients did notreceive any first aid at all prior to the first medicalfacility they attended.

Although it has been standard care for envenomedpatients to be admitted to ICU, our study suggests thatadequately treated stable patients, without respiratoryor cardiovascular compromise, can be safely managedwith close observation in an ED observation ward.Further prospective studies would need to confirmthis observation.

Of the five patients who had brown snakeenvenoming, four patients received 9 ampoules ormore of AV which is more than twice the currentlyrecommended dose by CSL21 and supports in vitroevidence that increased doses of AV are requiredto treat brown snake envenoming complicated bycoagulopathy with fibrinogen depletion.22

This was a retrospective case series of patientspresenting to one hospital. We chose to concentrate onthe envenomed patients only, and this may have biasedsome of the findings in the study. In addition, patientswere not followed up after discharge to ensure that nofurther complications had developed.

Conclusions

The incidence of snakebite and envenoming in FNQappears higher than reports from Australian capitalcities and remains a significant health problem infar north Queensland. All were admitted, mainly toICU, however, a few envenomed patients with nocomplications were managed safely in the EDobservation ward. Six patients required ventilation,and there was one death due to cardiac arrest after

envenoming from a brown snake. Our antivenom usagesuggested that larger quantities of antivenom arerequired than currently recommended21 when treatingbrown snake envenoming with defibrination.

Accepted 11 June 2003

References

1. Jelinek G, Hamilton T, Hirsch RL. Admissions for suspectedsnake bite to Perth Adult Teaching hospitals 1979–88. Med.J. Aust. 1991; 155: 761–4.

2. Jelinek G, Breheny FX. Ten years of snake bites at FremantleHospital. Med. J. Aust. 1990; 153: 658–61.

3. Jamieson R, Pearn J. An epidemiological study of snake bitesin childhood. Med. J. Aust. 1989; 150: 698–701.

4. Mead HJ, Jelinek GA. Suspected snakebite in children: a studyof 156 patients over 10 years. Med. J. Aust. 1996; 164: 467–70.

5. Fisher MM, Bowey CJ. Urban envenoming. Med. J. Aust. 1989;150: 695–8.

6. Sutherland S. Deaths from snake bite in Australia, 1981–91.Med. J. Aust. 1992; 157: 740–5.

7. Sutherland S, Leonard R. Snakebite deaths in Australia 1992–94 and a management update. Med. J. Aust. 1995; 163: 616–18.

8. Sutherland S. Antivenom use in Australia. Med. J. Aust. 1992;157: 734–9.

9. White J. Envenoming and Antivenom use in Australia. Toxicon.1998; 36: 1483–92.

10. Southern DA, Callanan VI, Gordon GS. Severe envenoming bythe Taipan (Oxyuranus Scutellatus) Med. J. Aust. 1996; 165:662–4.

11. Furtado MA, Lester IA. Myoglobinuria following snakebite.Med. J. Aust. 1968; 1: 674–6.

12. Little M, Pereira P. Successful treatment of death adderneurotoxicity using anticholinesterases. Emerg. Med. 2000;12: 241–5.

13. Flecker H. Snake bite in practice. Med. J. Aust. 1940; 2: 8–13.

14. Flecker H. More fatal cases of bites of the taipan (Oxyuranusscutellanus). Med. J. Aust. 1944; 2: 383–4.

15. Isbister GK, Currie BJ. Suspected snakebite: One yearprospective study of emergency department presentations.Emerg. Med. 2003; 15: 160–169.

16. Trevett AJ, Lalloo DG, Nwokolo NC et al. The efficacy ofantivenom in the treatment by the Papuan taipan (Oxyuranusscutellatus canni). Trans. Royal Soc. Trop. Med. 1995; 89:322–5.

17. Southern DA, Callanan VI, Gordon GS. Severe envenoming bythe taipan (Oxyuranus scutellatus). Med. J. Aust. 1996; 165:662–4.

18. Pearn JH, Covacevich J, Charles N, Richardson P. Snakebite inherpetologists. Med. J. Aust. 1994; 161: 706–708.

19. Sutherland S. Australian Animal Toxins: The creatures, theirtoxins and care of the poisoned patient. Melbourne, Australia:Oxford University Press, 2001.


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20. Mirtschin PJ, Crowe GR, Thomas MW. Envenomation by theinland taipan, Oxyuranus microlepidotus. Med. J. Aust. 1984;141: 850–1.

21. Sutherland S, Coulter A, Harris R. Rationalisation offirst aid measures for elapid snake bite. Lancet 1979; 1:183–5.

22. White J. CSL Antivenom Handbook. Melbourne, Australia:CSL Ltd, 2001.

23. Sprivulus P, Jelinek GA, Marshall L. Efficacy and potencyof antivenoms in neutralising the procoagulant effects ofAustralian snake venoms in dog and human plasma. Anaesth.Int. Care 1996; 24: 379–81.

five years of snake envenoming in far north queensland

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