SNAKEBITE
I. INTRODUCTION
Snakebite is one of the most neglected public health issues in the poor rural communities living
in
Cambodia.
The true burden of snakebite is not known
because of large-scale misreporting.
Cambodia is a heavily affected region due to widespread agriculture activities with home
environmental exposure
to hidden place of snakes, numerous venomous snake species and lack of functional
snakebite control programs.
Snake envenoming
is a
potential life threatening condition. It is characterized by systemic effects ranged from non-specific signs such as nausea, vomiting to coagulopathy, neurotoxicity, myotoxicity and renal
damage [1, 2].
In Cambodia, snakebites increase perceptibly during the rainy season particularly
in provinces along the Mekong and Tonle Sap floodplains [3]. Despite this perception, snakebite incidence,
disability, mortality are not currently
reported due to lack of accurate data within health referral offices as well as the Ministry of Health. A majority of snakebites injuries are
not treated in health facilities and
naturally the victims seek
traditional healers [3].
Seeing
the burden and complications of envenomed cases with a challenging
outcome of snakebites under conventional treatment by antibiotic application and surgical procedures (debridement, Fasciotomy), Kantha Bopha
Hospital has adapted
a protocol of treatment based on specific antivenom serums since
the beginning of year 2010. Over the year 2010, 46 snakebite cases which were
subjective to a retrospective study, were
treated in Kantha Bopha Hospital-
Phnom Penh.
II. DEFINITION
According to
the
International
Classification of Diseases code (E905
and E906) for bites and
stings,
a snakebite is definite
if a snake bit or spat and
was seen, probable if a snake was seen
nearby with fang marks or
clinical effects
suggestive of
snakebite without
fang marks and
possible if a snake was not
seen but definite fang
marks were found [4].
Ø Dry bites are bites not accompanied by any local effect because no venom is injected or
the snake is non-venomous
[5].
Ø Local envenoming is defined as only local effects such as pain, swelling, blisters or tissue necrosis
without systemic abnormalities because insufficient
venom is injected [1, 2].
Ø Systemic envenoming is defined as both local effects and at least one of coagulopathy,
neurotoxicity, myotoxicity and renal impairment or non-specific signs (nausea, vomiting,
abdominal pain, dizziness and
headache) [1,
2].
III.EPIDEMILOGY [6]
Venomous
snakes of Cambodia
Cambodia
shares many
aspects
of
its venomous snake fauna with neighbouring
Thailand,
Vietnam and Laos. There are approximately 86 different snake species including
17 species that are known to be venomous [6]. Among
17 venomous snakes, 6 species are responsible for the
majority of all severe illness and 5 species can cause potentially fatal illness. Cambodia’s
venomous snakes belong
to 2
main groups such as Elapidae and Viperidae that are easily
distinguished on the basis
of external morphology:
IV. PHYSIOPATHOLOGY [6]
Actions of snake venom
General effects of
snake venoms
Cytotoxins:
destroy cell tissue
by
increasing membrane permeability and cell membrane hydrolysis & proteolysis
Haemorrhagins: damage blood
vessel walls
Haemolysins:
damage blood
cell membranes
Procoagulant
toxins:
- disruption of normal haemostasis by causing abnormal activation of blood clotting factors
- factor depletion
( consumptive coagulopathy)
Platelet toxins:
destroy platelets, may either initiate aggregation or inhibit aggregation.
Neurotoxins:
α-neurotoxins
(postsynaptic- reversible)
block acetylcholine binding to
receptors in neuromuscular synaptic
β-Neurotoxins
(pre synaptic- irreversible) target nerve terminals
and destroy them from inside after
being internalized
by
endocytosis
Myotoxins:
Rhabdomyolysis
can lead to indirect
nephrotoxicity due to accumulation of cellular debris
in kidney nephrules
Nephrotoxins:
induce direct
nephrotoxicity by causing renal tubular necrosis
Cardiotoxins:
poisoning general myocardial
cell membranes causing irreversible cellular depolarization.
*** Commonly bites by the Viperidae result in hemotoxicity while bites by the Elapidae
cause neurotoxicity.
Understanding the
actions of venoms
of each type of snake can sometimes help identification of the species
responsible.
V. SYMPTOMATOLOGY
[1, 3]
1- Symptoms & signs
of Viper bite (Hematotoxic snake):
o Dry bite:
no local effects
o Local envenoming: starts progressively in
hours after bite: pain-edema-blisters-necrosis
o Systemic envenoming:
-Coagulopathy: Local
bleeding,
systemic bleeding (skin
ecchymosis –
gum bleeding,
GI
bleeding)
-Nephrotoxicity: Russel’s viper
can cause nephrotoxicity and neurotoxicity.
Severe rhabdomyolysis often
cause renal failure
2- Symptoms & signs
of Elapid bite (Neurotoxic snake):
o Dry bite:
no local effects
o Local envenoming: starts progressively in
hours after bite: pain-edema-blisters-necrosis
(for cobras),
numbness (for kraits)
o Systemic envenoming:
-Neurotoxicity: starting from
drowsiness to descending paralysis:
face-respiratory –trunk
& limb Blurring of vision,
pupillary abnormalities
(some patients may have long-term pupil
dilation after
krait envenoming), abnormalities
of taste & smell (may persist
for many months after
bite), urinary retention
-Cardiotoxicity: arrythmias:
VI. DIAGNOSIS [6]
6.1. Snakebite identification
Ø Identify the likely snake responsible for bite: Have the
victim or entourages
describe or point the snake species (on pictures
of snakes) that he or
they have seen on spot.
Ø Usually two fang marks are found.
Ø All
patients will be kept the patient under 24
h observations
Ø Determine the exact
time of the
bite
Ø Timing
of onset of toxinodromes after bite
o Coagulopathy: 1-2h.
o Neurotoxicity: 3-4h
o Cytotoxicity- Myotoxicity: hours
o Nephrotoxicity:
12-24h.
o Cardiotoxicity :
2-6h
6.2. Presumptive identification
6.3. Laboratory investigations
Ø 20-minute whole
blood clotting
test
(20’ WBCT)
If the 2 ml of freshly sampled venous blood in a small,
dry, glass vessel left undisturbed for
20 minutes is still unclotted and runs out, the patient has hypofibrinogenaemia
as
a result of venom-induced
consumption coagulopathy. In Cambodia, incoagulable blood is diagnostic of a viper bite and
rules out an elapid bite.
Ø Prothrombin Time (PT): Normal
range is 12-16 seconds.
Ø Partial Thromboplastin Time (PTT): Normal
range is 25-47 seconds.
Ø Fibrinogen
level: Normal
range is 1.5-4.5 g/L.
In DIC involving defibrination,
the
fibrinogen level will be critically below
these ranges, and
is often undetectable.
Ø Fibrin-degradation products (FDP):
defibrination,
the
FDP levels may be extremely high.
Ø Whole blood cell count
Ø CK, Kaliemia ,Urea-Creatinemia
Ø ECG,
X ray- Ultrasound- CT scan (If distant bleeding is suspected)
VII- FIRST AID TREATMENT
PROTOCOL
7.1. Recommended Method for Cambodia:
“Do it R.I.G.H.T”
Ø Reassure the patient: 80% of all Cambodian
snakes are non- venomous.
Only 60% of
bites by venomous species actually envenomate the patient
Ø Immobilize in the same way as a fractured
limb, use bandages
Ø Get
to Hospital immediately
Ø Tell the doctor
of symptoms
7.2. Discarded Method
Ø Tourniquets
Ø Cutting and Suction
Ø Electrical
Therapy and
Cryotherapy
7.3. Newer Method
Ø Immobilisation for viper bites
or unidentified snakebite
Ø Pressure Immobilisation
bandages (PIB) for Elapid bites
7.4. Snakebite Prevention
Ø Footwear
Ø Use a torch at night
Ø Walk
with a heavy step
Ø Pay close attention
to the leaves and
sticks collecting
Ø Avoid
sleeping on the ground
VIII. SNAKEBITE
TREATMENT PROTOCOL
8.1. Patient assessment on arrival
Ø Resuscitation of ABC (Airway,
Breathing, Circulation)
Ø Tetanus vaccination
(after
ASV
if clotting disorder)
Ø Antibiotics:
Ceftriaxone(100mg/kg/day)+ Metronidazole(30mg/kg/day)
if large wound
injuries
Ø Pain
killer: Tylenol (20mg/kg/dose)
Ø Handling Tourniquets: sudden
removal of the tourniquet
can lead to hypotension/
respiratory distress due to massive surge
of venom, but it is
safe to remove
it slowly or after ASV (anti-snake venom).
8.2. Antivenom treatment
8.2. 1. Choice of anti-snake venom (ASV)
8.2.2. ASV indication: Best results
when given
early! Never
delay! If either:
o Severe current local
envenoming (swelling>50% of the limb) or
o Systemic envenoming: coagulopathy,
neurotoxicity,
cardiotoxicity nephrotoxicity,
rhabdomyolysis
8.2.3. ASV dosage- no
ASV test doses
Children
should receive the same initial dose of
ASV
as adults, as snakes
inject
the same amount of venom into
children as adults.
8.2.4. Treatment
of ASV reactions
ASV reactions:
fever, chills, urticaria,
itching or
itchy throat. Monitor closely vital
signs
during infusion of ASV: watch
for
stridor, wheezing, dyspnea, syncope or arrythmias.
1- Discontinue ASV
2- H1 Antihistamine: Promethazin/ Chlorpheniramine maleate (0.2mg/kg IV) + Paracetamol PO
(20mg/kg/dose)
3- Hydrocortisone IV:
10mg/kg
4- Restart ASV
after recovery.
5- Adrenaline IM 0,01mg/kg is reserved for moderate to severe anaphylaxis.
8.2.5. Recovery phase
Reassessment, if an adequate dose
of appropriate ASV:
a) Systemic bleeding stops within 15-30 mn.
b) 20’WBCT (-) in 6 h.
c) Paralysis by Cobra improves
in 30’ or hours.
d) Paralysis by Krait improves
in considerable time
e) Active haemolysis & rhabdomyolysis cease within a few hours f)
Shock disappears after 30 mn.
g)
Rising platelet
rate
is not significantly accelerated
and blood CK was not decreased after ASV.
8.2.6. Repeat ASV
doses
o Persistent bleeding:
-Same
dose every 6h
until coagulation has been
restored (max dose: 30 vials)
-Vitamin K (10mg IV)/ others
haemostatic agents
-Use Fresh Frozen Plasma if available.
-Blood
products: only use if
severe uncontrollable
bleeding or adequate ASV has
been given
o Persistent neurotoxicity:
-Same
dose after 1-2h
(maximum dose:
20 vials)
-Neostigmine IM
(0,04mg/ kg) + Atropine IV (0,05mg/kg) half hourly x 8h
(Neostigmine is an
anticholesterase that
prolongs the life of acetycholine and
can therefore reverse the
respiratory failure and neurotoxic
symptoms.
8.2.7.
Others treatments
Ø Rhabdomyolysis:
-Mild (no complication):
Rehydration
-Severe:
Alkalinize urines
by IV
fluids
(30ml of 8, 4%NaHCO3/l of serum)
or hemodialysis
Ø Hyperkaliemia:
-Mild (no ECG changes): Diet,
stop medications responsible
-Severe:
Diuretic (Lasix:
1mg/kg/dose)
or (Glucose and Insulin,
Ca,
NaHCO3)
Ø Hypotension:
Beside a number of causes,
Russell’s viper is known to cause acute pituitary adrenal
insufficiency.
So Dopamine and Hydrocortisone are helpful.
Ø Renal
failure: Diuretic, Dialysis. ASV has
no efficacy
Ø Serum sickness:
Antihistaminic/ Prednisolone(1mg/kg/day) x 5days
Ø Wound care
-Prevent
rupture of bullae;
aspirate aseptically if large
-Clean skin daily gently with Betadine
or soap & water
-Elevate limbs
to reduce bleeding & swelling
Ø Surgical
intervention : when stable
after
ASV:
-Debridement: if tissue
necrosis
-Fasciotomy: if
compartment syndrome
-Skin
Grafting: if loss of tissues
-Amputation: if gangrene
Ø Rehabilitation &
Follow-up: kinesis,
next
tetanus toxoid dose.
REFERENCES
[1]- Isbister GK. Snake
bite: a
current approach to
management.
Aust Prescr [serial on the
Internet].
2006 [cited 2010 Jan 15]; 29:125-9.
Available from: http://www.australianprescriber.com/magazine/29/5/125/9.
[2]- Currie BJ. Snakebite in tropical Australia: a
prospective
study in the "Top End" of the
Northern
[3]- Warrel DA. Guideline for the clinical management of snake
bite in the
South East Asia region [homepage on the
Internet]. Geneva: World Health
Organization; [updated 1999; cited
2010 Jul 29]. Available
from: http://www.searo.who.int/LinkFiles/SDE_mgmt_snake-bite.pdf.
[4]- Tan HH. Epidemiology of snakebites from a general hospital in Singapore: a 5-year retrospective review
(2004-2008). Ann Acad Med
Singapore. 2010 Aug;39(8):640-7.
[5]- Alirol E, Sharma
SK, Bawaskar HS, Kuch U, Chappuis F. Snake bite in
South Asia: a
review. PLoS
Negl Trop
Dis. 2010 Jan 26;4(1):e603.
[6]- Williams DJ, Jensen SD, O’Shea M. Snake
bite
management in Cambodia: towards improved
prevention,
clinical treatment and rehabilitation [homepage on the Internet].
Geneva: World Health Organization; [updated 2009; cited
2010 Jun 23]. Available from: http://garudam.info/files/WHO2009- Cambodia.pdf.
No comments:
Post a Comment