SNAKE BITS

Introduced by
D. Abdallah Abd El Rahman Ali Mohammedia

CLASSIFICATION
EPIDEMIOLOGY
MORFOLOGY OF
SNAKE
VENOM
SYMPTOMS OFB
ENVINOMATION
MANEGMENT

SNEKE belong to the fallowing family

viperidae
elapidae
hydrophiidae
atractaspididae(most of them are non
venomous)
colupridae (most of them are nonvenomous)

Epidemiology

Bites rate are highest in temperate and tropical

Regions where population subsist by manual
agriculture

Snake anatomy

Snake venom apparatus consist of bilateral venom

gland situated below and behind the eye and
connected by duct to hallow anterior maxillary
teeth
In viprid teeth are long mobile fang retracted
against the roof of the mouth
In elapid and sea snake the fang are smaller and
fixed in erect position

Fact about snake

significant

envenomation occur in 50% of all

venomous snakebites
Differentiation venomous from non venomous
can be difficult
Color pattern is notoriously misleading in
identifying venomous snake bite

Venoms

Are complex mixture of enzyme ,low molecular

weight polypeptide, metal ion
haemorrhagins promote vascular bleeding and
cause both local and systolic bleeding
proteolytic enzymes cause local tissue necrosis
myocardial depressant factors reduce cardiac
output
neurotoxin pre or post synapticaly to inhibit
peripheral nerve impulses
Most snake venom have multisystem effect on
their victims

Clinical manifestation

most viper and some elapid has necrotizing

venoms and present with the fallowing :
1.
local manifestation
o progressive local swelling
o pain
o ecchymosis
o hemorrhagic bullae and serum filed
vesicle(over hours or days)
2. Systemic manifestation
o Change in taste
o Mouth numbness
o Muscle fasciculation
o Tachycardia or bradycardia
o Hypotension
o Pulmonary edema
o Hemorrhage from any anatomical site
o Renal dysfunction

most elapid have nurotoxic venom that cause

neurological dysfunction in the form of fallowing:
onset vary from minute to hours

early finding include cranial nerve

weakness (ptosis ) and altered mental status
o

sever envenomation result in paralysis

include muscle of respiration which lead to
death from respiratory failure and aspiration
o

sea snake envenomation usually cause the

fallowing : onset delayed for hours

local pain
oMyalgias
oRhabdomyolysis
oneurotoxicity
o

management

important point to remember

1. don't attempt to kill the snake after you
have bitten
2. Dont handle with even killed snake
3. Dont consult traditional healers
4. Avoid incising wound , applying suction to
the bite as they are ineffective
5. Avoid tourniquet use as it can lead to
amputation and loss of function
6. Pressure immobilization should be use only
if the offending snake is reliably identified
and known to be primarily neurotoxic

management

1.
2.

3.
4.

5.

6.

7.
8.

Stabilize airway ,breathing and circulation

Institute monitoring (cardiac and pulse
oximeter)
Establish two large bore IV line
If the pt hypotensive so pollus NS (2040ML/KG) if hypotension persist then
considered 5% albumin (10-20 ml/kg)iv
Take rapid history and perfume rapid
examination and put the affected limb at
the level of the heart
Measure circumferences of bitten extremity
every 15 minute until swelling stabilized
Identify offending reptile if possible
Take blood for (CBC,PT ,INR,PTT,FIBRINOGEN
LEVEL,BG,RFT)AND do UG (20 minute whole
blood clotting test can be don) repeated 6
hourly after antivenom administration

management

Determine the severity of envenomation

.
Non: fang mark only
.
Mild: local finding only(pain
,ecchemosis,nonprogressive swelling)
.
Moderet:prgressive swelling systemic sign or
symptoms
.
Sever: respiratory distress ,neurological
dysfunction and/ or cardiovascular
instability)
9. Administer antivenom as indicated
.
Non or mild: non
.
Moderate :4-6 vials
.
Sever:6vials
Mix reconstituted vials in 250ml NS give it iv
over 1 hour( be in close attendance)
Here you can give prophylactic anti histamine
9.

management
10.

11.

12.

13.
14.

If acute reaction to antivenome occur then:

Stop infusion

Standard dose epinephrine im

,antihistamine iv and glucocorticoid

When reaction controlled restart

antivenome with further dilution
Then monitor clinical status over 1 h

Improved :hospital admission

Progress or not improved :repeat the

dose.
Pain management: paracetamole or narcotic
(avoid aspirin and NSAIDs)
Tetanus immunization as need
Prophylactic antibiotic is no necessary unless
prehospital care include incision or mouth
suction

management
15.

16.

17.

18.

19.
20.

Blood product and coagulation factor rarely

needed if required should be given after
anti venom administration
Admit to hospital (if no evidence of
envenoimation monitor for 8 h before
discharge)
Monitor for evidence of intra compartment
pressure
Wound care (dry dressing )and aseptic
debridement of necrotic tissue if
coagulation restored
Begin physical therapy
Warn the pt at discharge about possibility of
recurrent caagulopathy and symptoms and
sign of delayed serum sickness

management
21.

If any evidence of neurological deficit it

harder to reverse with antivenom

Give atropine 0.6 mg iv

Fallow by edrophonium 10 mg iv or
neostigmine 1.5-2 mg im

If improved at 5 minute continue

neostigmine 0.5 mg every 30 min as
needed with atropine infusion 0.6 mg
over 8 h

Monitor for aspiration risk and secure

air way with endotracheal intubation
as needed

management
22.

Renal failure in mostly is reversible(acute

tubular necrosis ) and should be evaluated
by nephrologists and refer the pt for
peritoneal dialysis or haemodialysis as
needed , rarely bilateral cortical necrosis
may need renal transplantation

antivenom
.

.
.

.
.

Is an IgG molecule isolated from serum of

hoarse or sheep when it developed due to
injection of venom to the animal blood
May be mono specific or poly specific
It bind up circulatory venom before they
attach to target tissue
You should no the species covered by
antivenom
It must be specific to for offending snake
If antivenom does not contain antibody to that
snake venom component it will be of no value
and may lead to unnecessary complication
The efficacy of antivenom in prevention of
tissue damage by necrotizing venom is limited