Snakes

POISONS
IRRITANTS
INORGANIC
NON-
METALLIC
METALLIC
ORGANIC
ANIMAL VEGETABLE
MECHANICAL

snake
Poisonous Non- Poisonous
1. Elapids (Neurotoxic venom
2. Viper (Vasculotoxic Venom)
3. Sea Snakes (Myotoxic Venom)

Snakes
Poisonous
Elapids
(Neurotoxic
venom)
Viper
(Vasculotoxic
Venom)
Sea Snakes
(Myotoxic
Venom)
Non- poisonous

There are more than 2,700 species of snakes in the
world
of which about four fifths are non-venomous,
are distributed throughout the temperate and tropical
zones of the world
(except in New Zealand, Ireland, and some isolated
oceanic islands) and are found in greatest profusion in
the tropics.
About two thirds of all snake species belong to the
family Colubridae; most of these are non-venomous.

Snakes constitute the suborder Serpentes (or Ophidia).
In most snakes limbs are entirely lacking, but a few have
traces of hind limbs.
The skin, which is covered with horny scales, is shed, usually
several times a year.
The extremely long, narrow body is associated with
distinctive internal features.
The number of vertebrae is much larger than in most
vertebrates, paired internal organs are arranged linearly
rather than side by side, and only one lung is developed,
except in members of the boa family, which have two lungs.

The jaws of snakes are loosely jointed and extremely
flexible.
The pointed, backward-curved teeth are fused to the
supporting bones of the head.
There are no ears or movable eyelids.
They do not hear airborne sound waves, but can perceive
low-frequency vibrations (100–700 Hz) transmitted from
the ground to the bones of the skull.

 Flexible jaw bones mouth can open as wide as the
breadth of the prey

Some snakes can smell with their noses but ALL snakes smell with
their tongues.
When a snake sticks out its tongue it smells its surroundings.
The moist tongue collects scents and smell animals from the air
it.
When the tongue goes back into the mouth the forks touch a
special sensory spot called the Jacobson's organ on the roof of the
mouth and tells the snake what it smells.
Snakes have a small notch in their lips that they can stick their
tongues through so they don’t need to open their mouths.

In all except a few species [sea snakes], scales are an
essential aid to locomotion.
A snake is helpless on glass where scales can effect no
‘grip’ on the surface.
Snakes have four ways of moving around.

Concertina method:
this is when snakes bunch themselves up
and then throw themselves forward.

 Serpentine method:
 This motion is what most people think of when
they think of snakes.
 Snakes will push off of any bump or other surface,
rocks, trees, etc., to get going.
 They move in a wavy motion.
 They wouldn’t be able to move over slick surfaces
like glass at all.

 Side winding:
 This method is similar to an inchworm’s
movement.
 The snake will lift the middle of its body up
and then push it down forcing its head to
move forward.


 Rectilinear Method:
 This is a slow, creeping, straight
movement.
 The snake uses some of the wide scales
on its belly to grip the ground while
pushing forward with the others.

Small snakes feed on insects and larger ones on proportionately
larger animals.
Their teeth are designed for catching and holding prey, but not
for chewing.
The construction of the jaws, the ribs, and the expandable skin
enable them to swallow very large prey whole.
Some snakes capture animals by pinning them to the ground;
some—the constrictors—crush them by wrapping their bodies
around them and squeezing;
still others—the venomous snakes—inject poison into their
victims.

Most snakes are ovi-parous
meaning they lay eggs,
that after a period of incubation hatch into young that
are small replicas of the adult animals.
While other species are ovo-vivi-parous
meaning the eggs are retained within the body of the
female until they hatch,
so that live snakes are born.

 Differentiate between:
 Elapedea and vipredea snake bites.
 Venomous and non-venomous snakes.
 Mention the main toxic constituents in snake
venom and its action.
 Queen Cleopatra was unable to ask for help
despite she was conscious till her death. (give
reason).

How to rapidly differentiate between
venomous and non-venomous snakes
By examining the
eyes
*It is rounded in non-
venomous snakes
*and slit like in
venomous ones

DIFFERENCES OF POISONOUS & NONPOISONOUS SNAKES
Poisonous Non-Poisonous
1. Body scales
(By turning Belly
upward)
They are large &
cover the entire
breadth of belly
Small or moderately large &
don’t cover the entire
breadth of the belly
2. Head Scales Usually small but some
poisonous snakes have
large head scales.
Usually large
3. Fangs Long & canalized like
hypodermic needle
Short & solid
4. Tail Compressed Not markedly compressed
5. Habits Generally Nocturnal Nothing in particular
6. Bite Two fang marks with
or without small marks
of other teeth.
A number of small teeth
marks in a row. [ usually
leave a U-shaped
impression of the bite]

Snake venom is highly modified saliva that is produced by special glands of
certain species of snakes.
The gland which secretes the zootoxin is a modification of the parotid salivary
gland of other vertebrates, and is usually situated on each side of the head below
and behind the eye, invested in a muscular sheath.
It is provided with large alveoli in which the venom is stored before being
conveyed by a duct to the base of the channeled or tubular fang through which it
is ejected.
Snake venom is a combination of many different proteins and enzymes.
Many of these proteins are harmless to humans, but some are toxins.
Note that snake venoms are generally not dangerous when ingested, and are
therefore not technically poisons.

CHARACTERISTICS OF SNAKE VENOM
IN FRESH STATE
Clear
Transparent
Amber tinted fluid
DRIED UP VENOM
Dries into a yellow granular mass
Retains its activity for many years
Contains toxalbumins

There are approximately 20 types of toxic enzymes found in
snake poisons throughout the world known to man.
Although no venomous snake has all of these toxins, most
snakes employ between six to twelve of these enzymes in
their venom.
Each of these enzymes has its own special function. Some
aid in the digestive process, while others specialize in
paralyzing the prey.

Chemical composition of snake
venom
 Fibrinolysins

 Proteolysins

 Neurotoxins
 Cholinesterase
(predominant in elapid
venom)
 Haemolysins
(predominant in viper
venom)
 Thromboplastins
 Agglutinins
 Cardiotoxins
 Coagulase
 Hyaluronidase
 lecithinase

Scientists have identified the following chemicals from snake venom and the specific purpose of each as
follows:
cholinesterase
attacks the nervous system, relaxing muscles to the point where the victim has very little control.
amino acid oxidase
plays a part in digestion and the triggering of other enzymes
(is responsible for venom's characteristic light yellowish coloring.)
hyaluronidase
causes other enzymes to be absorbed more rapidly by the victim.
proteinase
plays a large part in the digestive process, breaking down tissues at an accelerated rate.
(causes extensive tissue damage in human victims)
adenosine triphosphatase
believed to be one of the central agents resulting in the shock of the victim and immobilizing smaller
prey.
(present in most snakes.)
phosphodiesterase
accounts for the negative cardiac reactions in victims, most notably a rapid drop in blood pressure.

Hemotoxic venom
acts on the heart and cardiovascular system.
Neurotoxic venom
acts on the nervous system and brain.
Cytotoxic venom
has a localized action at the site of the bite.
myotoxic venom
The most important symptoms are rhabdomyolysis (rapid breakdown of
skeletal muscle tissue) and paralysis.
Many snakes incorporate both neurotoxic and hemotoxic venom in their
bites so when telling them apart one goes by which type is more
predominant.

3 Visible fang marks
Blister formation , necrosis of
tissue
Sloughing off skin , tissue necrosis

The Elapidae, or elapids, are a family of venomous snakes found in
tropical and subtropical regions around the world, including the
Indian Ocean and the Pacific.
They are characterized by possessing a set of hollow, fixed, short
and grooved fangs through which they inject venom, and come in a
wide range of sizes, from only 18 cm up to
6 m in length.
Currently, 61 genera that include 235 species are recognized.
These include
Cobra
King cobra
Common krait
Banded krait
Coral.`

COBRA
This snake is black in color, 1.5 – 2.0 m in length.
Head expands as a hood bearing spectacle marks.
KING COBRA
Young is jet black while adult is yellow/green/brown black.
Grows to a length of 2.5 – 4.5 m.
It has a hood but no spectacle marks.
COMMON KRAIT
Grows to a length of 1- 1.5 m.
Glistening black color with a row of hexagonal scales on back.
BANDED KRAIT.
Bigger and stouter than common krait up to a length of 2 m.
Has alternate black and yellow bands across its back.

Almost all have long and slender bodies with smooth scales, a head that is
covered with large shields and not always distinct from the neck, and eyes
with round pupils.
All elapids have a pair of fangs that are used to inject venom from glands
located towards the rear of the upper jaws.
The fangs are the first two teeth on each maxillary bone, which are enlarged
and hollow, and usually only one is in place on each side at any time.
The fangs are usually below the front edge of the eye and are angled
backwards,
due to this construction, most elapids must actually bite in order to
envenomate.
This is the reason that elapids cannot bite through clothing or inject a
complete dose.
This action is therefore not as quick as with the vipers, that can envenomate
with only a quick, stabbing motion.

A few species are capable of spraying their venom from
forward facing holes at the tips of their fangs as a means
of defense.
The spray is aimed at the eyes of an aggressor and is so
painful that the snake has the chance to escape.
If the eyes are washed out immediately with lots of water
(or any bland liquid) no permanent damage will follow
but neglected cases can result in blindness.
Elapids use their venom both to immobilize their prey
and in self-defense.

Pain is minor
Clinically there is unimpressive local reaction
There is more severe systemic manifestations
With little symptomatology at the actual site of
envenomation
Even after an asymptomatic period of up to 12 hours.

The effect of the venom of elapid snakes is mainly on the
nervous system.
Respiratory paralysis being quickly produced by
bringing the venom into contact with the central
nervous mechanism which controls respiration.
The pain and local swelling which follow a bite are not
usually severe.

THE SEVERITY AND CLINICAL MANIFESTATION OF ENVENOMATION
DEPEND UPON NUMBER OF FACTORS INCLUDING
NUMBER OF STRIKES
DEPTH OF ENVENOMATION
SIZE OF THE SNAKE
POTENCY OF VENOM
AMOUNT OF VENOM INJECTED
SIZE OF VICTIM
UNDERLYING HEALTH OF VICTIM
LOCATION OF THE BITE

THEREFORE THE MOST EFFECTIVE BITE WOULD BE OF A
LARGE SNAKE INJECTING A COMPLETE DOSE OF POTENT
VENOM IN
CHILD
OR
SMALL ADULTS
OR
ADULTS WITH UNDERLYING MEDICAL CONDITIONS LIKE
DIABETES MELLITUS
CARDIOVASCULAR DISEASE.

Injection of elapid venom
Acetylcholine receptor are blocked by cobra venom.
A similar effect can be achieved by
high doses of
curare
or
nicotine

FANG MARKS
Usually 2 or may be 1 if bite is sideways.
Distance between the fang marks may give an idea of size of a snake.
LOCAL SYMPTOMS
These are mild in reaction as slight burning at the bite site.
MISCELLANEOUS
Parasthesias,
Nausea, Salivation, Vomiting,
Euphoria, Weakness,
Giddiness, Dizziness, Diplopia, Dyspnea,
Diaphoresis ,muscle tenderness Fasciculations
And confusion

MUSCULAR WEAKNESS
Specially in legs manifested by staggering gait.
SPREADING PARALYSIS
Leading to difficulty in speaking
Dysphagia
Ptosis
Paralysis of extraoccular muscles
Breathing becomes slow and labored
Till this time the conscious level is maintained
But the patient is unable to speak
AFTER A COUPLE OF HOURS RESPIRATION CEASES WITH OR
WITHOUT CONVULSIONS AND HEART STOPS LEADING TO DEATH.

PATIENT CAN DEVELOP TOTAL BODY PARALYSIS THAT MAY LAST 3-5 DAYS
THIS PARALYSIS MAY TAKE WEEKS TO RESOLVE COMPLETELY
WITH RESPIRATORY SUPPORT HOWEVER THE PARALYSIS IS COMPLETELY
REVERSIBLE
PULMONARY ASPIRATION IS A COMMON SEQUELA IN THE SUBACUTE PHASE.
COBRA VENOM PRODUCES CONVULSIONS & PARALYSIS
KRAIT VENOM PRODUCES MUSCULAR PARALYSIS
IN EVENT OF RECOVERY
SKIN AND CELLULAR TISSUE SURROUNDING THE BITE MARK UNDERGO
NECROSIS

FATAL DOSE FATAL PERIOD
15 MG
OF DRIED COBRA VENOM
AMOUNT OF DRIED COBRA
VENOM IN A BITE
= 200 – 350 MG
IN COBRAS
FEW MINUTES TO FEW
HOURS

-Queen Cleopatra was bitten
by the Egyptian cobra
she developed the following
clinical picture:
-She had little swelling and
itching at the site of the bite
where there were 2
puncture wounds each was
half an inch wide and half an
inch deep.

 After 20 minutes signs of
neurotoxic effects of the snake
poison started:
- She had generalised fatigue
 -Then after half an hour
 she was unable to swallow due
to paralysis of her tongue
 -After an hour she had pain
followed by numbness in her
legs then she was unable to
walk, she had salivation and
she couldn't even ask for
help because she had
dysphonia.
 She got disoriented for a
while .

 After 2 hours she was
completely paralyzed but
she was conscious till her
vital centers had been
finally got paralyzed too
 she died mainly due to
respiratory paralysis
 this was the end of the
Egyptian queen
Cleopatra????

THESE ARE FURTHER CLASSIFIED INTO
PIT VIPERS
bamboo snake.
PITLESS VIPERS
Russell viper
Saw scaled viper

The ‘pit’ is a special organ in between the eyes and the
nostrils.
The pit senses body heat from animals and gives the
snake a ‘picture’ of that animal.
This helps these snakes to find prey in the dark, which
is when most snakes like to hunt.

The group of snakes known as Pit Vipers have a triangular head,
wider than the neck.
Pupils are vertical.
Tail is tapering.
FANGS .
These are long movable and canalized like hypodermic needles.
So a viper can bite through the clothes and give a complete dose.
These are easy to see when erected but being too big lie tucked up
by the side of upper jaw.

Some pit vipers will bite and poison the prey and then
release it.
It will follow the dying animal, using its heat sensors,
until it stops and the snake can swallow it.
Most pit vipers hunt at night when the air is cooler and
the heat from rodents and other prey is most obvious to
them.
The ‘heat picture’ from larger animals will tell the snake
that a quick escape is a good idea

COMMON GREEN PIT VIPER
[BAMBOO]
THIS GROWS TO A LENGTH OF 30- 100 CM.
COLOR IS VIVID GREEN/ RARELY YELLOW/ BROWN.
BODY IS FLAT AND BROAD.
HEAD IS TRIANGULAR WITH PIT BETWEEN EYES AND
NOSTRIL.
TAIL IS LONG WITH DIVIDED SCALES.

THIS INCLUDES
RUSSELL’S VIPER
SAW SCALED VIPER

THIS IS THE PITLESS VIPER CATEGORY.
IT GROWS TO A LENGTH OF 1.5 M.
COLOR IS BROWN.
HAS 3 ROWS OF BLACK DIAMOND SHAPED SPOTS OR CHAINS ON THE BACK.
CAN BE IDENTIFIED BY
FLAT TRIANGULAR HEAD WITH A DISTINCT V MARK WITH APEX POINTING
FORWARDS.
SMALL HEAD SCALES.
BROAD UNDIVIDED BELLY PLATES.
NARROW SHORT TAIL WITH SHEILDS DIVIDED INTO TWO ROWS.
BIG NOSTRILS.
MAKES A HIISING SOUND WHEN ATTACKS.

THIS GROWS TO A LENGTH OF 50-75 CM.
COLOR IS BROWN/ BROWNISH GREY/ GREENISH.
IDENTIFIED BY
TRIANGULAR HEAD WITH A WHITE MARK ON RESEMBLING AN ARROW.
A WAVY LINE ON EACH FLANK WITH DIAMOND SHAPED AREA BETWEEN
UPPER CURVES OF TWO WAVY LINES.
SMALL HEAD SCALES.
BROAD BELLY PLATES.
UNDIVDED TAIL SHEILDS.
BODY SCALES ARE SERRATED LIKE SAW.
MAKES A RUSTLING SOUND WHEN IT MOVES ON ACCOUNT OF ROUGH SCALES
OF BACK.

CROTALINE VENOM IS A COMPLEX HETROGENOUS SOLUTION AND
SUSPENSION OF
VARIOUS PROTEINS
PEPTIDES
LIPIDS
CARBOHYDRATES
ENZYMES
NEUMEROUS UNIDENTFIED
PROTEOLYTIC ENZYMES
PROCOAGULANTS
ANTICOAGULANTS
CARDIOTOXINS
HEMOTOXINS
NEUROTOXINS
ABOUND IN VIPER VENOM MAKES IT COMPLEX TO ANALYZE.

VIPER VENOM CAN SIMULTANEOUSLY DAMAGE TISSUES
DIRECTLY
AFFECT BLOOD VESSELS
CELLULAR ELEMENTS OF BLOOD
ALTER THE MYONEURONAL JUNCTION AND NERVE
TRANSMISSION.
VENOM IS PRESENT IN CIRCULATION AS WELL AS FIXED TO THE
TISSUES.
VIPER VENOM CONSISTS OF A NUMBER OF UNIDENTIFIED
NEUROTOXINS
WITH CURARE LIKE EFFECTS
THAT PRODUCE SYSTEMIC NEUROTOXICITY AS OPPOSED TO
LOCAL TISSUE INJURY.

LOCAL TISSUE DESTRUCTION DOMINATES VIPER ENVONOMATION.
PIT VIPERS PRODUCE A CHARACTERISTIC COMPLETE BITE WHEN
THE CHANNEL IS COMPLETE
FANGS ARE MOVABLE
THEY STRIKE AND DISTINCT FANG MARKS CAN USUALLY BE
IDENTIFIED AS
SINGLE
DOUBLE
OCASSIONALLY MULTIPLE
AS A GENERAL RULE
IT MAY BE ASSUMED THAT IF NO SYMPTOMS DEVELOP WITHIN 8-12
HOURS FROM THE TIME OF BITE, IT IS THEN MOST PROBABLY A DRY
BITE.

SEVERE LOCAL SYMPTOMS INCLUDE
INTENSE LOCAL PAIN
SWELLING
ECCHYMOSIS
SEVERE OOZING OF HEMOLYTIC BLOOD
BLISTERS APPEAR

WHEN THE VENOM IS INJECTED SUBCUTANEOUSLY
IT TRAVELS BY
LYMPHATICS
SUPERFICIAL VENOUS CHANNELS
AND SPREADS RATHER SLOWLY TO REACH THE GENERAL
CIRCULATION.
THE SUBCUTANEOUS ENVONOMATION LEADS TO VARIABLE AND
UNPREDICTABLE RESULTS AS IT MAY TAKE A NUMBER OF HOURS
TO PRODUCE SYSTEMIC SYMPTOMS.

THIS PRODUCES SIGNIFICANT SYSTEMIC SYMPTOMS IN A MATTER OF
MINUTES INCLUDING
NON-SPECIFIC
WEAKNESS
MALAISE
NAUSEA
RESTLESSNESS
SPECIFIC
PETECHIAL HAEMORRHAGES
BLEEDING FROM GUMS
HEMOPTYSIS
BLEEDING FROM MUCUS MEMBRANE OF RECTUM AND OTHER ORIFICES OF
THE BODY

CONFUSION
ABDOMINAL PAIN
VOMITING
DIARRHOEA
SWEATING
DYSPNEA
TACHYCARDIA
HYPOTENSION
BLURRED VISION
SALIVATION
METALLIC TASTE IN MOUTH

COLLAPSE SETS IN WITH
COLD CLAMMY SKIN
RAPID FEEBLE PULSE
DILATED PUPILS INSENSITIVE TO LIGHT
THIS IS FOLLOWED BY
COMA
DEATH
IN EVENT OF RECOVERY
LOCAL LESION SUPPURATES
UNDERGOES SUPERFICIAL NECROSIS

VIPER VENOM MAY PRODUCE COMPLEX AND DRAMATIC
HEAMATOLOGIC ABNORMALITIES.
SECONDARY TO THE EFFECT OF VENOM
ON
•BLOOD COAGULATION PATHWAYS
•ENDOTHELIAL CELLS
•PLATELETS .
FIBRINOGEN CONCENTRATION DROPS
PLATELET COUNT FALLS.
PROTHROMBIN TIME AND PARTIAL THROMBOPLASTIN TIME
[PT & PTT]
ARE PROLONGED AND FREQUENTLY UNMEASURABLE.

Name Description
Factor X This factor is one of the initiators in the coagulation cascade.
Complex Xa
This is formed naturally in the body, by activating Factor
X, when coagulation is necessary.
The venom, however, can form this complex when coagulation
is not necessary.
Fibrinogen Fibrinogen is also known as factor I.
It is a plasma protein, synthesized in the liver, which is involved
in blood coagulation as the precursor of fibrin.
Fibrin Fibrin is an elastic, insoluble, whitish protein derived from
fibrinogen by the action of thrombin proteolysis during
clotting of blood
FDP Fibrinogen Degradation Products are proteins which dissolve
the fibrin produced by the body.

[Step 1: Envenomation]
X
[Step 2: Activation]
Xa
Xa 111
[Step 3: Clot Formation]
Fibrinogen
Fibrin
[Step 4: Degradation]
FDP Kidney
Fibrin digestion urea

As the venom diffuses into the blood stream, the steps shown above occur
naturally.
The net effect of the process is for the blood to become incoaguable.
The kidneys perform the essential function of removing waste products from
the blood and regulating the water fluid levels.
The kidneys receive blood through the renal artery.
The blood is passed through the structure of the kidneys called nephrons,
where waste products and excess water pass out of the blood stream.
When the venom induces clotting, the fibrin is deposited in the tubules.
As the tubules are blocked, the kidneys are not able to remove the same
amount of waste products from the blood, and urea and creatinine begin to
accumulate in the blood.
If these chemicals are not removed, the concentrations become lethal.

 20 MG VIPER VENOM
 6 MG KRAIT VENOM
 8 MG SAW-SCALED
VIPER
AMOUNT OF DRIED VIPER
VENOM IN SINGLE BITE
YIELDED IS
150-200 MG VIPER VENOM
20 MG KRAIT VENOM
25 MG SAW-SCALED
VIPER VENOM
 IN VIPERS
 A FEW DAYS

DIFFERENCES BETWEEN ELAPIDS & VIPERS
Elapids Vipers
1. Body Long & cylindrical Short
2. Head Nearly of the same
width as neck
Triangular & wider
than neck
3. Pupils Round Vertical
4. Maxillary
bones
Carries fangs +
other teeth
Only fangs
5. Fangs Short, fixed &
grooved
Long, movable &
canalized
6. Tail Round Tapering
7. Venom Neurotoxic Vasculotoxic
8. Other
Characteristics
Oviparous Ovi-viviparous

The majority of sea snakes are highly venomous.
However, when bites occur, it is rare for much venom to be injected, so
that envenomation symptoms usually seem non-existent or trivial.
Bites in which envenomation does occur are usually painless and
may not even be noticed when contact is made.
Teeth may be left in the wound.
There is usually little or no swelling involved and it is rare for any
nearby lymph nodes to be affected.

This is felt as a sharp initial prick which becomes painless later.
Early symptoms include
headache,
a thick-feeling tongue,
thirst,
sweating,
vomiting.
Symptoms that can occur after 30 minutes to several hours post bite include
generalized aching,
stiffness,
tenderness of muscles all over the body.
Passive stretching of the muscles is also painful,
trismus, which is similar to tetanus, is common.

This is followed later on by
symptoms typical of other elapid envenomations.
A progressive flaccid paralysis, starting with ptosis and paralysis of voluntary
muscles.
Paralysis of muscles involved in swallowing. Eventually respiratory failure can be
fatal.
After 3-8 hours
myoglobin as a result of muscle breakdown may start to show up in the blood
plasma,
which can cause the urine to turn a dark reddish, brown, or black color, and
eventually lead to acute renal failure.
After 6-12 hours
Serum transaminase becomes elevated
Severe hyperkalemia, also the result of muscle breakdown, can lead to cardiac
arrest.

A toxic phospholipase A2 (PLA2-H1),
isolated from the venom of the sea snake
induces myonecrosis.
Induction of myonecrosis occurs by the ability of phospholipase to
release creatine kinase (CK muscular) from damaged muscle fibers.
PLA2-H1 exhibits intense myonecrosis
characterized by the changes including
necrosis and edematous appearance
with cellular infiltrate,
vacuolation ,
degenerated muscle cells,
edema in between the cells.

 1.5 milligrams.
 Most Sea Snakes produce
an average of 10-15 mg of
venom so they should
always be approached with
caution as this venom is
10x more lethal than the
venom of the land based
Rattlesnake or Africa's
deadly Black Mamba.
 24- 48 HOURS

A sensitive and specific assay has been developed known as
optical immunoassay (OIA)
The assay is based on the principle of detection of physical changes in
thickness of molecular thin film resulting from specific binding events
on an optical silicon chip.
The kit can detect venom analyzes in
blood
plasma
urine
wound exudates
blister fluid
tissue homogenates.

A double antibody sandwich Enzyme Linked ImmunoSorbent Assay (ELISA)
was developed to detect venom in various organs
brain
heart
lungs
liver
spleen
kidneys
blood
as well as in the tissue at the site of injection up to 72 h)
after death.
The assay could detect venom levels as low as 100 pg/ml of tissue

How to prevent snake bites?
 A world free of snakes
 Nearly a quarter of us would go hungry
 Snakes are important elements in the food chain
to control the rodent population- Which destroy
all major crops.
The bottom line is we need
snakes to survive

Principle for treatment of snake
bite
 1. Allay anxiety
 2.prevention of spread of venom
 Immobilize
 Tourniquet
 Cleansing of wound
 Incision and suction
 3.use of anti-venom / anti toxic therapy
 4.general measures

Step # 1
Relief anxiety
All the snakes are not poisonous
Even poisonous snakes are not fully
charged
Even a fully charged poisonous
snake cannot always inject a lethal
dose.

EXTENT OF
ENVENOMATION
CLINICAL OBSERVATION ANTIVENOM
RECOMMENDATION
OTHER TREATMENT DISPOSITION
NONE [DRY BITE] FANG MARKS MAY BE SEEN, BUT
NO LOCAL OR SYSTEMIC
SYMPTOMS AFTER 8-12 HOURS.
NONE LOCAL WOUND CARE
TETANUS PROPHYLAXIS
DISCHARGE
AFTER 8-12
HOURS OF
OBSERVATION
MINIMAL MINOR LOCAL SWELLING
DISCOMFORT ONLY
WITH NO SYSTEMIC SYMPTOMS
NO HEMATOLOGIC
ABNORMALITIES
NONE LOCAL WOUND CARE
TETANUS PROPHYLAXIS
ADMIT TO
MONITORED
UNIT FOR 24
HOUR
OBSERVATION
MODERATE PROGRESSION OF SWELLING
BEYOND AREA OF BITE
LOCAL TISSUE DESTRUCTION
HEMATOLOGIC ABNORMALITIES
SYSTEMIC SYMPTOMS
YES INTRAVENOUS FLUIDS
CARDIAC MONITORING
ANALGESICS
FOLLOW LABORATORY
VALUES
TETANUS PROPHYLAXIS
ADMIT TO ICU
SEVERE MARKED PROGRESSIVE
SWELLING AND PAIN
BLISTER FORMATION
NECROSIS
SYSTEMIC SYMPTOMS INCLUDING
VOMITING
FASCICULATIONS
WEAKNESS
TACHYCARDIA
HYPOTENSION
SEVERE COAGULOPATHY
YES INTRAVENOUS FLUIDS
CARDIAC MONITORING
ANALGESICS
FOLLOW LABORATORY
VALUES
OXYGEN
VASOPRESSOR
TETANUS PROPHYLAXIS
ADMIT TO ICU

INITIAL OBJECTIVE
DETERMINE THE PRESENCE OR ABSENCE OF ENVENOMATION.
TO PROVIDE BASIC SUPPORTIVE THERAPY.
TO TREAT THE LOCAL AND SYSTEMIC EFFECTS OF ENVENOMATION.
TO LIMIT OR REPAIR TISSUE LOSS AND OR FUNCTIONAL DISABILITY.
MEDICAL THERAPY
SUPPORTIVE CARE
ANTIVENOM WHEN indicated
CONSERVATIVE SURGICAL TREATMENT
DEBRIDEMENT OF DEVITALIZED TISSUE WHEN INDICATED
HENCE AS A RULE THE FASTER THE TREATMENT IS INSTITUTED THE BETTER IS
THE FINAL OUTCOME.

IMMOBILIZATION OF THE AFFECTED AREA
BITTEN PART SHOULD BE IMMOBILIZED AS ACTIVITY INCREASES SPREAD
OF VENOM.
IMMOBILIZATION ALSO REDUCES PAIN.
CLEANSING OF THE WOUND SHOULD BE DONE WITH
PLAIN WATER
SALINE
RAPID TRANSPORT TO MEDICAL FACILITY
AVOID PHYSICAL ACTIVITY AS IT MAY HASTEN SYSTEMIC ABSORPTION OF
VENOM

PAIN AND ANXIETY
ANALGESICS
ANXIOLYTICS
TETANUS PROPHYLAXIS
IMMOBILIZE THE EXTREMITY IN A WELL-PADDED SPLINT IN
NEAR FULL EXTENSION
AND
ELEVATED TO AVOID DEPENDENT EDEMA.

Neurotoxic envenoming-Examination
•Ask the patient to look up and observe whether the upper
lids retract fully.
•Test eye movements for evidence of early external
ophthalmoplegia .
•Check the size and reaction of the pupils.
•Krait can cause fixed, dilated non reactive pupils simulating
brain stem death – however, it can recover fully
•Ask the patient to open their mouth wide and protrude
their tongue; early restriction often paralysis of pterygoid
muscles.
• The muscles flexing the neck may be paralysed, giving the
“broken neck sign

Local examination
 During the initial evaluation, the bite site
should be examined for signs of local
envenomation (edema, petechiae, bullae,
oozing from the wound, etc) and for the
extent of swelling.
 The bite site and at least two other, more
proximal, locations should be marked and
the circumference of the bitten limb should
be measured every 15 min thereafter, until
the swelling is no longer progressing.

SURGICAL DEBIDEMENT OR EVEN SKIN GRAFTING MAY EVENTUALLY
BE REQUIRED
BUT
THE INITIAL ROUTINE USE OF
TISSUE EXCISION
FASCIOTOMY
OR
EXPLORATION AND DEBRIDMENT
IS NOT RECOMMENDED.

Spread of snake venom through body is mostly by
diffusion
lymph circulation
Therefore efforts are made to reduce lymph circulation which is
achieved by
immobilization
application of tourniquet
cleansing the wound
incision and suction

Application of torniquet is only possible when the bite is on the
limbs.
If the bite is on face, neck, or trunk firm pressure over bitten area
may be applied.
APPLICATION OF THE TORNIQUET.
It should be applied 5 cm proximal to the bite
It should be tight enough to exclude the
Venous circulation lymphatic flow
Without impeding the
Arterial deep venous flow

At a distance of 5 cm proximal to first one is desirable.
It should be released for 1 minute every half an hour.
or
for 30 seconds every 15 minutes.
to
allow escape of small quantity of toxin
to
general circulation where its destroyed.
IT SHOULD BE APPLIED FOR ABOUT 2 HOURS.
LONGER USE CAN LEAD TO AGGRAVATION OF TISSUE DAMAGE.

THIS THERAPY IS GIVEN TO prevent THE EFFECT OF
LOCAL BITE
SYSTEMIC
ENVENOMATION
AND
IT IS CONSIDERED TO BE LIFE SAVING
HOWEVER
PROPHYLACTIC ADMINISTRATION IS NOT RECOMMENDED

Summary
 Snake bites may be by an non venomous snake or a dry
bite
 Not all snake bites require ASV
 ASV is the main stay in the treatment of snake bites
 ASV must be initiated if indicated at the earliest
 Respiratory paralysis can be because of different
reasons-Neurotoxicity, shock, sepsis, ARF…
 MV may be main stay of treatment or just supportive
depending on the cause of failure.

Fasciotomy
 Fasciotomy should not be carried out in snake bite
patients unless or until haemostatic abnormalities
have been corrected.
 Clinical features of an intracompartmental
syndrome are present and a high
intracompartmental pressure has been confirmed
by direct measurement

SPECIFIC ANTIVENIN.
Is prepared by hyper immunizing horses against venom of a specific
snake.
POLYVALENT ANTIVENIN.
Is prepared by hyper immunizing horses against venoms of four common
snakes
Cobra
Common Krait
Russell’s viper
Saw scaled viper

STRENGTH OF POLYVALENT ANTI-VENOM
1 ml of anti-venom will neutralize
0.6 mg of dried cobra venom
0.45 mg of dried krait venom
0.6 mg of dried Russell viper venom
0.45 mg of dried saw scaled viper venom

CROFAB POLYVALENT OVINE-DERIVED ANTIVENOM IS OBTAINED BY
INNOCULATING THE SHEEP WITH THE VENOM OF
RATTLESNAKE
COTTONMOUTH
THE MANUFACTURING PROCESS INCLUDES
PAPAIN DIGESTION OF ISOLATED IgG ANTIBODIES
TO ELIMINATE
THE Fc PORTION OF THE IMMUNOGLOBULIN
AND
TO ISOLATE
SPECIFIC ANTIBODY FRAGMENT [Fab AND Fab2]
AS WELL AS TO INCREASE
AFFINITY PURIFICATION
AND
LYOPHILIZATION.

This is available in
form of powder in an ampoule.
It can retain its potency for 10 years.
It is dissolved in distilled water or normal saline before injection.
INITIAL DOSE
This is determined by
1. Concentration of the serum
2. Size of the patient.
3. Size of the snake.
4. Nature of the serum.
Dose should preferably be large enough to combine with all the venom
present in the body.

Total dose 60 ml in adults
1/3rd S/C.
or
around the bite.
1/3rd 1/m.
1/3rd I/V.
THE INTRAVENOUS DOSE CAN BE REPEATED ANY TIME IF
COLLAPSE APPEARS
OR
EVERY 6 HOURS TILL SYMPTOMS DISAPPEAR.

DESENSITIZATION IS ACHIEVED BY INJECTING
Multiple small doses under cover of
Adrenaline
Antihistamines
corticosteroids

Anti-venom can neutralize the circulating toxin only.
The toxin action at the tissue level[ fixed in tissues] may be
antagonized by
IN ELAPID BITE
Neostigmine-atropine therapy
IN VIPER BITE
Heparin along with supportive fibrinogen transfusion
Sea snake anti-venom can be effective even when started
several hours after onset of poisoning.

IN ELAPID BITE.
Local infiltration of carbolic soap around site of bite is
recommended.
IN VIPER BITE.
Heparin can be locally applied.

STIMULANTS
in paralytic cases
ARTIFICIAL RESPIRATION.
TRANSFUSION OF WHOLE BLOOD
in hemorrhagic cases
STEROIDS
in allergic manifestations of anti-venom therapy
FOR SECONDARY INFECTION
aspirin
short acting barbiturates
antibiotic prophylaxis

 A 25 yr old male with snake bite has signs of
compartment syndrome and the pressure is 60 mmHg
is undergoing surgery has a Hb of 6 gm%, is
hypotensive 100/60, on noradrenalin,
acidotic,coagulation profile is normal
 Blood is started
 After 15 mts of surgical time patient develops
 Dark colored urine
 Bp drops to 80/60
 What are the possibilities ?
Rhabdomyolysis
Mismatched Blood transfusion
Treatment
Fluids, Mannitol,
Alkalinize the urine,
Manage electrolytes
Fasciotomy
RRT

Marks of snake bite
Swelling & cellulitis at the site
NEUROTOXIC VENOM
produces signs of asphyxia
IN VIPER BITE
 Oozing of blood
 Blood is fluid & haemolysed causing early staining of blood
vessels
 Haemorrhage in lungs, serous membranes & left ventricle

 Petechial Haemorrhage in kidney, pelvis and mucosa of urinary
bladder, stomach and intestines.
 Arterioles & capillaries have blurred walls and swollen endothelial
cells
 Necrosis of renal tubules
 Cloudy swelling and granular changes in cells of other organs

Usually accidental
Rarely Homicidal
Very rarely Suicidal

Case scenario…….
 34 yr old male shifted from rural health center with
H/O snake bite 6 hrs back has ptosis, respiratory
distress, RR 35/mt, BP 120/60, oral secretions present,
absent gag and cough reflex shifted to ICU for teritary
care.
 On ASV 100ml stat, & 50ml in NS over 6 hrs
 Oxygen 3l/mt
Patient received
in casualty
Patient is comfortable, vitals stable
No ptosis, distress
Patient is dead –what do you think
went wrong ?

 What could have been done better ?
 Bulbar signs-probably aspirated and died
 Endotracheal intubation can be placed on T-piece
Ambuing or Transport Ventilator
 Anticholienesterases
 Neostigmine with atropine
Patient is dead –what do you think went wrong ?

Case scenario…….
 34 yr old male shifted from rural health center with
H/O snake bite 6 hrs back has ptosis, respiratory
distress, RR 35/mt, BP 120/60, oral secretions present,
absent gag and cough reflex shifted to ICU for teritary
care.
 On ASV 100ml stat, & 50ml in NS over 6 hrs
 Oxygen 3l/mt
Why does
Neurotoxicity occur
What are the Management issues?
ASV, Anticholineesterases,
MV…

Krait- Pre-synaptic action
Beta-bungarotoxin- Phospholipases A2
1) Inhibiting the release of
acetylcholine from the presynaptic
membrane
2) Presynaptic nerve terminals
exhibited signs of irreversible physical
damage and are devoid of synaptic
vesicles
3) Antivenoms & anticholinesterases
have no effect
Paralysis lasts several weeks and frequently requires prolonged MV.
Recovery is dependent upon regeneration of the terminal axon.

Cobra –post-synaptic
 alpha-neurotoxins
“Curare-mimetic toxins’’
Bind specifically to acetylcholine
receptors, preventing the interaction
between acetylcholine and receptors
on postsynaptic membrane.
Prevents the opening of the sodium
channel associated with the
acetylcholine receptor and results in
neuromuscular blockade.
 ASV -rapid reversal of paralysis.
 Dissociation of the toxin-receptor
complex, which leads to a reversal of
Paralysis
Anticholinesterases reverse the neuromuscular blockade

Snake envenomation in a north Indian hospital
Ptosis
RS
involvement
N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120
Ophthalmoplegia

 2 cm long
 Discharge almond green secretion when dry becomes
grayish brown.
 Active principle is Cantharidin
 Can be absorb from any surface, insoluble in water but
soluble in fat, alcohol.
 On skin causes blister formation
 If swallowed causes nausea, abdominal pain, intense
thirst
 Strangury:- Nephrotoxicty, desire to micturate, but
only small amount of blood stained urine passes.
 Priapism:- in males causes persistant but painful
penile erection, in females causes engorgement of
vulva and abortion.

 Medicolegal importance:
Abortificient
Aphrodisiac
Fatel dose 8-10 gm
Postmortem findings:
shiny green wings are resistant to putrefaction
Give special clue in cases where death due to this fly.
GI tract bloody patch appearance
Urinary tract inflamed
Pelvic viscera engorged
Kidneys shows niphritis.

 Neurotoxic
 Haemotoxic
 Cardiotoxin (red scorpian)
 Sign/Sympyoms:-
 Local irritation sever
 Profuse prespiration
 Muscular cramps
 Treatment:-
 Torniquite,
 incised,
 wash with water, ammonia,
 inj calcium gluconate (10ml of 10% slowly i/v)

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