SNAKE BITE INJURY

- PRESENTOR-Dr Varsha N Shetty

- Moderator-Dr Nagaraj Shetty
INTRODUCTION
• Snake bite envenomation is a common acute life-threatening medical
emergency.
• More than 200,000 snake bites are reported in the country and an
estimated 35,000 to 50,000 people die each year.
• Majority of snake bite deaths go unreported as many victims go to
traditional healers and many deaths occur before reaching hospital.
Classification of poisonous snakes
• 1. Elapidae (neurotoxic) examples
• Common cobra/ or Naja naja
• King cobra : Naja bangarus
• Krait : a)common krait or bangarus caeruleus b) banded krait or
bangarus fasciatus c) coral snake d) tiger snake e) mambas f) death
adder
• 2. Viperidae (vasculotoxic)
• Pitless vipers :russel viper and saw scaled viper
• Pit viper : pit viper - crotalidae b) common green pit viper
• Hydrophidae: (myotoxic)
• 20 types of sea snakes found in India . All are poisonous
• Most snakes inject 10% of available venom in a single strike except
Russell’s viper which injects 75% of stored venom in one bite and is
responsible for high morbidity and mortality in India.
Pathophysiology
• Snake venoms are not single toxins but a cocktail of many
components: enzymes, polynucleotide toxins, nontoxin proteins,
carbohydrates, metals, lipids, free amino acids, nucleotides and
biogenic amines.
ELAPIDAE
Cobra
• Dorsal scales of the Indian cobra may have a hood mark or colour
patterns. The most common visible pattern is a posteriorly convex light
band at the level of the 20th to 25th ventrals.

• The fangs of a cobra are small and sharp.Its venom is small molecular
size hence rapidly absorbed into the circulation.

• Cobra venom is a cardiotoxic, neurotoxic, haematotoxic and cytotoxic.

KRAIT
• Krait is the most poisonous snake, its venom being 10 times more
poisonous than cobra venom.

• It is 1 to 4 feet long, with enlarged hexagonal vertebral scales,

uniform white or red belly and narrow white crossbars on the back,
more or less distinctly in pairs, the crossbars are typically absent near
the head and neck region.
ELAPIDAE (NEUROTOXIN)

• Presynaptic neurotoxins (Kraft venom)are phospholipids A2 that

damage nerve endings, initially releasing acetylcholine transmitter,
then interfere with its release.
• Postsynaptic neurotoxins(cobra venom) are polypeptides which
compete with acetylcholine for receptors in the neuromuscular
junction and lead to curare-like paralysis .
 Cobra Neurotoxin
Neurological and Neuromuscular: These signs and symptoms will usually
manifest earliest. Not all of these will necessarily develop, even with severe
envenomation
• Drowsiness 
• Eyelid drooping (Ptosis)
• Respiratory paralysis or Dyspnea Ophthalmoplegia 
• Palatal paralysis 
• Glossopharyngeal paralysis
• Limb paralysis Convulsions 
• Head drooping (Cervical muscle paresis or paralysis)
• Headache sudden loss of consciousness
• Stumbling gait (Ataxia)
Cardiotoxicity: Increased Blood Pressure and increased Cardiac
Output followed by Myocardial Depression and Asystole.
Local Symptoms:
• Gangrene requiring amputation can occur.
• Localized discoloration of skin 
Vesiculation (usually small and localized) 
Necrosis (can be extensive, but is characteristically localized to the
bite site) 
Local edema (usually minimal)
KRAIT
ENVENOMATION
 Krait bites often present in the early morning with paralysis that can be
mistaken for a stroke.
It’s Venom is a presynaptic neurotoxin causing
• 1) Acute Abdominal pain, goose flesh, hypersalivation, Sweating ( due to
cholecystokinin release)
• 2)Neurological manifestations( Same as in cobra) : Ptosis, pooling of saliva,
aphasia, respiratory muscles involvement leading to respiratory failure.
Rapidly progressing Neuro paralysis lasting for days to weeks needing
prolonged ventilator support.
• 3) Envenomation by Kraits can cause: Resistent neuroparlysis,
hyponatremia, hyperkalemia causing arrhythmias, Renal failures.
ELAPIDAE envenomation common features

• Rapid ptosis and bulbar palsy accompanied with respiratory

depression can occur. Blurring of vision and loss of accommodation
are the earliest neurological signs of envenomation

• Descending paralysis, initially of muscles innervated by the cranial

nerves, commencing with ptosis, diplopia, or ophthalmoplegia.
• Numbness around the lips and mouth, progressing to pooling of
secretions, bulbar paralysis, and respiratory failure.
• Paradoxical respiration, as a result of the intercostal muscles
becoming paralysed is a frequent sign.
•
• Locked-in syndrome: Phenomenon is due to blocked post-synaptic
acetylcholine receptors including pupillary muscle which are rich in
acetylcholine receptors.
• This may be seen in few cases, but such victims recover totally within
3 to 4 days if treated properly by maintaining oxygen saturation with
proper ventilator support, maintaining electrolytes and nutrition and
prevent iatrogenic infection.
Viperidae
ECHIS CARINATUS OR SAW-SCALED
VIPER OR CARPET VIPER
• It is 1 to 3 feet long, head is sub-ovate with short rounded snout,
body is cylindrical, short and covered with rough, serrated flank
scales,neck is distinctly constricted.It is pale brown or tawny with dark
brown. A cruciform or trident or arrow type or just like the bird foot
print shaped mark is seen on head.
Russell’s viper

• It is a 3 to 5 feet long snake; the head is covered with small scales and
without shields.
• The body is massive and cylindrical, narrowing at both ends; the head is
flat, triangular with short snout, large gold flecked eyes with vertical
pupils and large open nostrils. Its belly is round with constricted neck.
Typical rows of oval arranged in two rows is characteristic of Russell’s
viper.
Viperidae( Hemotoxins)

• Procoagulant enzymes are the major factor in viper venom, which

stimulates blood clotting and consumption of fibrinogen, causing
disseminated intravascular coagulation (DIC).
 General signs and symptoms of Viperine
envenomation
• Swelling and local pain.
• Tender enlargement of local lymph nodes as large molecular
weight Viper venom molecules enter the system via the lymphatics
• Bleeding from the oral cavity (gingival sulci) and other
orifices,Epistaxis
• Vomiting , abdominal tenderness which may suggest gastro-
intestinal or retro peritoneal bleeding .
• The skin and mucous membranes may show evidence of
petechiae, purpura, and ecchymoses .
• Hypotension resulting from hypovolaemia or direct vasodilation.
• Low back pain, indicative of early renal failure,
• The passing of reddish or dark-brown urine, or diminishing/ nil urine
output.
• Lateralising neurological symptoms such as asymmetrical pupils
may being indicative of intra-cranial bleeding. Muscle pain indicating
rhabdomyolysis.
Sea Snakes
• Sea snake is accidentally handled by fishermen during fishing. Its
venom is neurotoxic, myotoxic and haematotoxic.
• Soon after a bite, the victim experiences severe muscle pain, marked
tenderness all over the muscles, trismus, muscular paralysis,
respiratory arrest, without local manifestations at the site of bite.
• Myotoxic effects of venom causes hyperkalemia and myoglobinuria
causing acute tubular necrosis.
•MANAGEMENT OF SNAKE
BITE
FIRST AID-

• It consists of the following: “DO IT RIGHT”

• Reassure the patient. 70% of all snakebites are from non- venomous
species. Only 50% of bites by venomous species actually envenomate the
patient
• Immobilise in the same way as a fractured limb. Use bandages or cloth to
hold the splints, not to block the blood supply or apply pressure. Do not
apply any compression in the form of tight ligatures; they don’t work and
can be dangerous!
• Get to Hospital immediately.
• Traditional remedies have NO PROVEN benefit in treating snakebite.Tell the
doctor of any systemic symptoms such as ptosis that manifest on the way to
hospital.“
Traditional methods to be discarded
TOURNIQUETS
Was initially done to stop venom flow into the body.
However discarded due to drawbacks
Risk of ischemia and loss of limb
Increased risk of necrosis
Increased risk of massive neurotoxic blockade release
• For the above reason tourniquet use is contraindicated in India
INSCISION AND SUCTION
INCREASES RISK OF BLEEDING
WASHING OF THE WOUND
Discouraged as increases flow of venom into the system.
INDIAN SNAKE BITE TREATMENT
PROTOCOL

Patient Assessment Phase:

• On Arrival deal with any life threatening symptoms on presentation,
i.e., attend to Airway, Breathing and Circulation.If there is evidence
of a bite, where the skin has been broken, give Tetanus Toxoid Routine
use of antibiotic is not necessary.
DIAGNOSIS PHASE :General Principals
1. PAIN-Adequate pain relief with mild opioids like Tramadol is
preferred.
2. Tourniquet release- Sudden removal can lead to a massive surge of
venom leading to neurological paralysis, hypotension due to
vasodilation, etc. Be prepared to handle complications such as
sudden respiratory distress or hypotension. If the tourniquet has
occluded the distal pulse, then a blood pressure cuff can be applied
to reduce the pressure slowly.
Diagnosis Phase: Investigations
• 20 Minute Whole Blood Clotting Test (20WBCT)
• The test should be carried out every half hour for a period of 3 hours
from admission and then every 6th hourly thereafter for 24 hours.
Other Investigations
• Haemoglobin/ Packed Cell Volume/ Platelet Count/
• Bleeding parameters:Prothrombin time/ APTT / FDP/ D-Dimer
• Peripheral Smear
• Urine Tests for Proteinuria/ RBC/ Haemoglobinuria/ Myoglobinuria
• Biochemistry for Serum Creatinine/ Urea/ Potassium
• ECG/ X-Ray/ Ultrasound.
ANTI SNAKE VENOM
• ASV is the only definitive treatment of snake bite. It acts by
neutralizing, circulating venom in the blood and tissue fluid.
• Anti venom is immunoglobulin usually enzyme refined f(ab)2
fragments of IgG purified from the serum or plasma of a horse or
sheep that has been immunized with the venom of one or more
species of snakes.
• Polyvalent anti venom neutralizes the venom of several different
species of snakes. In India only polyvalent antisnake venom is
available.

• India antivenoms are produced against 4 most important venomous

snakes of India – naza naza (cobra);B.caeruleus (Indian common
krait);Russell’s viper (daboi Russelli) and saw-scaled viper (Echis
carinatus). It is raised in horse serum.
• (1) lyophilized form which will be reconstituted with 10 ml water to
10 ml of ASV
• (2) liquid form of ASV – each vial contains 10 ml of ASV. It should be
preserved in +20 to 80 C.
WHEN TO USE ANTI VENOM
• When there is no systemic envenomation the case should be
observed for 24 hrs clinically and with repeated 20WBCT and then
discharged
• WHO has recommended which has been accepted by others, that the
initial dose of Indian polyvalentASV is 100 ml.
• In 200 ml NS add 10 vials of ASV and administer over 1hr.
Dose of ASV
• Dosage :ideally administer within 4 hours but effective if given within
24 hours
• Mild cases: 5 vial (50 ml)
• Moderate cases : 5 to 10 vials
• Severe cases : 10 to 20 vials
• Additional infusion containing 5 to vials are infused until progression
of swelling ceased and systemic symptoms are disappeared.
Mode of administration
• ASV is given slowly as IV injection or infusion at rate of 2 ml/ minute

• AVS dilute 5-10ml/kg body weight of normal saline or 5% dextrose

and infused over 1 hour.

• ASV should never be given locally at site of snake bite.

• Adverse reaction of ASV : It May develop in 20% patients.

• In neurotoxic bites ASV can not reverse the paralysis that has already
occurred, and can neutralise the circulating venom only.
• Elapidae with improvement in neuroparalysis is seen after 30 minutes of
ASV administration.
• To reverse respiratory paralysis and the cases should be kept in I.C.U for
consideration of artificial ventilation when the need arise.
• Hence reversal occurs only with Neostigmine over a period of 2-5 days.
• Neostigmine is an anticholinesterase which is helpful only in cases of
post synaptic paralysis that occurs in cobra bites and not presynaptic
paralysis with Krait bites.
Reactions to Anti Snake Venom
• It usually occurs in 10-180 min of starting antivenom.
• They develop urticaria, itching, cough, nausea, vomiting, abdominal colic, diarrhea,
tachycardia.
• Minority of cases develop fatal anaphylaxis – hypotension, bronchospasm and angioneurotic
oedema.

MANAGEMENT
Stop ASV
Adrenaline 0.5 mg (1:1000 dilution) to be given intra muscularly for adult and 0.01 mg/kg for
children.
Injection hydrocortisone
Then Restart ASV at a slower rate.
• Late serum sickness
• Develops in 1-12 days . Characterised by fever ,nausea ,vomiting,
diarrhoea , arthritis , nephritis , myoglobinuria .
• Treatment consists of oral antihistaminic - 5 day course of oral
antihistamines . Adults - CPM 2mg/ 6 hours
• Children - 0.25mg /kg/ya in decided doses
• Prednisolone - 5mg in 6 hours in adults and 0.7mg /kg/day in decided
dose in children.
• General measures:
Antibiotic coverage: Preferred is B Lactam antibiotics to reduce the
risk of infection from bite site.
Keep a watch on the affected limb for signs of Compartment
syndrome due to excessive limb edema.
References
• Guidelines for the managment of snake bite - WHO
• API textbook of medicine
• Uptodate
• THANKYOU