SNAKE BITE

ABHIJA BABUJI.

CRRI.

DEPARTMENT OF PEDIATRICS.

SMIMS.

Out line

INTRODUCTIONEPIDEMIOLOGYTYPES OF SNAKE BITESCLASSIFICATIONIDENTIFICATION FEATURES.CLINICAL FEATURES OF SNAKE BITENATIONAL SNAKEBITE MANAGEMENT PROTOCOL, INDIA.

INTRODUCTION• . Snake bite is one of the major public health problems in the

tropics. It is also emerging as an occupational disease of agricultural workers. In view of their strong beliefs and many associated myths, people resort to magico –religious treatment for snake bite thus,

causing delay in seeking proper treatment.

• Snake bites is a particularly important public health problem in rural areas of tropical and subtropical countries situated in Africa, Asia, Oceania and Latin America.

INTRODUCTION

The venom apparatus Venomous snakes of medical importance have a pair of enlarged teeth, the fangs, at the front of their upper jaw. These fangs contain a venom channel or groove, along which venom can be introduced deep into the tissues of their natural prey. If a human is bitten, venom is usually injected subcutaneously or

intramuscularly.

epidemiology

• The annual number of cases of snakebite worldwide is about 5 million, among which there are some 100 000 to 200 000 deaths.

• In addition to the deaths, there are an estimated 400000 snakebite-related amputations each year around the world .

• Children have both higher incidence rates and suffer more severe effects than do adults, as a result of their smaller body mass

•

SNAKE BITE INCIDENCES

• Papua New Guinea has some of the highest snakebite

rates in the world, with the country’s rural central province

recording an annual incidence of 561.9 cases per 100 000

population

• Snakebites are concentrated in mainly rural areas and

vary considerably by season, with the peak incidence

seen in the rainy and harvesting seasons

Snake bite deaths worldwide

india

• India is estimated to have the highest snakebite mortality in the world.

• World Health Organization (WHO) estimates place the number of bites to be 83,000 per annum with 11,000 deaths

• Males: Female::2:1.

• Majority of the bites being on the lower extremities.

SNAKES IN INDIA

• There are about 236 species of snakes in India, most of which are nonvenomous

• Their bites, apart from causing panic reaction and local injury, do not harm the patient.

• 13 known species that are venomous and of these four, namely common cobra (Naja naja), Russell’s viper (Dabiola russelii), saw-scaled viper (Echis carinatus) and common krait (Bungarus caeruleus) are highly venomous and believed to be responsible for most of the poisonous bites in India

COMMONEST INDIAN venomous snakes

–

The venom is synthesized by the modified salivary glands and injected through special channeled or grooved teeth called fangs

Cobra Krait

Russel’s viper Saw-scaled viper

CLASSIFICATION• Worldwide, only about 15% of the more than 3000 species of

snakes are considered dangerous to humans.

• The family Viperidae is the largest family of venomous snakes, and members of this family can be found in Africa, Europe, Asia, and the Americas.

• The family Elapidae is the next largest family of venomous snakes.

ELAPIDAE

• Elapidae have short permanently erect fangs This family includes the cobras, king cobra, kraits, coral snakes and the sea snakes.

• The most important species, from a medical point of view include the following:

• Cobras: Genus NajaN naja(spectaled cobra –all over in India )N kaouthia (monocled – West Bengal ,MP ,U.P,

Orissa)N oxiana [Black cobra – northern states - patternless]N philippinensisN atraKing cobra: Ophiophagus hannah

Short permanently erect fangs of a typical elapid

KRAITS (genus Bungarus)

KRAITS (genus Bungarus)• B caeruleus common krait [all over India ]

- paired white bands & large hexagonal scales in top

of the snakes

• B fasciatus banded krait [black & yellow band –

W.B,M.P,A.P,BIHAR ,ORRISSA]

• B candidus Malayan krait

• B multicinctus Chinese krait

• Sea snakes (important genera include Enhydrina,

Lapemis and Hydrophis)

• Blue spotted sea snake (Hydrophis cyanocinctus)

Common krait- key identification feature is PAIRED white bands.

VIPERIDAE

Have long fangs which are Normally folded up againstthe upper jaw but,whenthe snake strikes,are erected .

There are two subgroups, • the typical vipers (Viperinae)• and the pit vipers (Crotalinae).

• The Crotalinae have a special sense organ, the pit organ, to detect their warm-blooded prey. This is situated between the nostril and the eye

Russell’s vipers details of fangs.

RUSSELL’S VIPER

.Hemotoxic venom BUT can

also

Present neurotoxic symptoms

Key identification feature is the black

edged almond or chain shaped marks

on the back

Key Identification

Feature- large plate

scales on the head

PIT VIPERHaemotoxic venom.

Causes Renal failure

Late onset envenoming

•Saw-scaled or carpet vipers - Echis carinatus and E sochureki

Most parts of India except Kerala – Arrow shaped mark in head & hoop like markings in flanks

India: Poisonous snakes

Elapidae Cobra, Kraits Neurotoxic

Viperidae (Vipers)

Russell’s Vipers.,Saw scaled Vipers.,Pit Vipers.

Hemotoxic

Hydrophidae Sea Snakes Myotoxic

Krait and russell’s viper is much more toxic than that of cobra

IDENTIFICATION FEATURES

IDENTIFICATION FEATURES

Snake VenomComplex mixture of proteins includingLarge enzymes-local tissue destruction.

Low molecular weight polypeptides-lethal systemic effects-Acidic.-Sp Gravity: 1.030-1.070-On drying Fine needle like crystals.-Water Soluble.-Lethal Dose:

Cobra-0.12gm, Krait0.06gm- Russell’s V-0.15gm

Healthy, angered and hungry snakes unload more venomthan a recently satiated and surprised snake .Due to the venom, there is cell function degeneration and the final outcome depends on the type of venom injected.

Snake bite-venom injected

enters surrounding tissue

direct venom action

blood vessels lymphatics

Target organs-systemic effect

Capillary absorption

PATHOGENESIS

• Snake venom is a mixture of polypeptides, proteolytic enzymes, and toxins, which are species-specific.

Primarily neurotoxic • Hydrophidae - poisonous sea

snakes’

• Elapidae - cobras, kraits, coral snakes

• Venom have a curare-like effect by blocking neurotransmission at neuromuscular junction.

• Death results from respiratory depression.

Neurotoxic venom

• Venoms with neurotoxic activity produce paralysis and respiratory distress by binding the nicotinic acetylcholine receptors, and preventing the depolarizing action of acetylcholine.

• The most important effect of neurotoxins is to prevent the transmission of nerve impulses in cholinergic synapses. ALFA neurotoxins interfere with neurotransmitter release and cause muscle paralysis, respiratory failure and death by asphyxiation.

PATHOGENESIS

• Viperidae – vipers Primarily hemotoxic& cytotoxic• Crotalidae (sub family of

viperidae) :

• Tissue necrosis, vascular leak, and coagulopathies.

• Death from pit viper bites results from hemorrhagic shock, adult respiratory distress syndrome, and renal failure.

• A hemotoxic venom that acts by lysing erythrocytes. Venoms of this kind have a proteolytic action. They produce swelling, cardiovascular damage, and eventual necrosis. They also disrupt blood clotting and, in the process of destroying the blood's functionality, severely damage internal organs and other body tissues, which can be extremely painful. The immediate cause of death in such cases is usually hypovolemic shock.envenomation increases capillary permeability that results in

• blood and plasma loss from the intravascular to the extracellular space, creating edema, which, in case of being sufficiently important, may cause circulatory compromise and hypovolemic shock.

HEMOTOXIC

VENOM

Cytotoxic venom

• snake venom has cytolytic properties, which cause local necrosis and secondary infection, which could result in sepsis and death

CLINICAL FEATURES.

When venom has not been injected;• Out of fearVasovagal attackCollapse Slowing of heart rate• Another source of misleading symptoms caused byFirst aid and traditional treatments.

CLINICAL FEATURES

• Following the immediate pain of the bite-increasing local

pain (burning, bursting, throbbing) at the site of the bite

• Local swelling that gradually extends proximatelly up the

bitten limb and tender, painful enlargement of the regional

lymph nodes draining the site of the bite

• Bites by kraits, sea snakes may be virtually painless and

may cause negligible local swelling. Someone who is

sleeping may not even wake up when bitten by a krait and

there may be no detectable fang marks or signs of local

envenoming

Local symptoms and signs in the bitten

part • Fang marks

• ™ Local pain

• ™ Local bleeding

• ™ Bruising

• ™ Lymphangitis

• ™ Lymph node enlargement

• ™ Inflammation (swelling, redness, heat)

• ™ Blistering

• ™ Local infection, abscess formation

• ™ Necrosis

Fang marksPersistent bleeding from

fang marks 40min after

bite of pit viper

Blistering at

site of bite

SYSTEMIC SYMPTOMS & SIGNS

Generalised (systemic) symptoms and signs

• Nausea, vomiting, malaise, abdominal pain, weakness,

drowsiness, prostration

Cardiovascular (Viperidae)

• Dizziness, faintness, collapse, shock, hypotension,

cardiac arrhythmias, pulmonary oedema, cardiac arrest

Cont.

Bleeding and clotting disorders (viperidae)

• Bleeding from recent wounds (including fang

marks,venepunctures etc) and from old partly-healed

wounds.

• Spontaneous systemic bleeding – from gums, epistaxis,

bleeding into the tears, haemoptysis, haematemesis,

rectal bleeding or melaena, haematuria, vaginal bleeding,

bleeding into the skin (petechiae, purpura, ecchymoses)

and mucosae

Cont.

Neurological(Elapidae, Russells’s viper)

• Drowsiness, paraesthesiae, abnormalities of taste and

smell, “heavy” eyelids, ptosis, external ophthalmoplegia,

paralysis of facial muscles ,difficulty in opening mouth and

showing tongue and weakness of other muscles

innervated by the cranial nerves, aphonia, difficullty in

swallowing secretions, respiratory and generalised flaccid

paralysis

Cont.

Skeletal muscle breakdown(sea snakes, Russell’s

viper)

• Generalised pain, stiffness and tenderness of

muscles, trismus, myoglobinuria hyperkalaemia,

cardiac arrest

Renal(Viperidae, sea snakes)

• Loin (lower back) pain, haematuria,

haemoglobinuria, myoglobinuria, oliguria/anuria,

symptoms and signs of uraemia (acidotic breathing,

hiccups, nausea, pleuritic chest pain etc

Broken neck

sign in a

child

envenomed

by krait

Bleeding from

gingival sulci

Species: Signs and Symptoms

Signs/Symptoms

and Potential

Treatments

Cobra Krait Russell’s

Viper Saw Scaled

Viper

Other

Vipers

Local pain/ Tissue

DamageYes No Yes Yes Yes

Ptosis/Neurotoxicity Yes Yes Yes! NO No

Coagulation No No Yes Yes Yes

Renal Problems No No Yes NO Yes

Neostigmine &

Atropine Yes No? No? NO No

•National snakebite management

protocol, India.

FIRST AID

• The first aid recommended is based around the mnemonic:

• "Do it R.I.G.H.T."• It consists of:

• R. = Reassure the patient. Seventy per cent of all snakebites are from non venomous species. Only 50% of bites by venomous species actually enveno-mate the patient

• I = Immobilize in the same way as a fractured limb. Children can be carried. 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 do not work and can be dangerous!

• G.H. = Get to Hospital immediately. Traditional remedies have NO PROVEN benefit in treating snakebite.

• T = Tell the doctor of any systemic symptoms such as ptosis that manifest on the way to hospital.

•

PRESSURE IMMOBILISATION

Its purpose is to retard themovement of venom frombite site into circulation,

thus buying time for thepatient to reach

medical care.

Cont.

• Be prepared to treat the shock and provide

cardiopulmonary resuscitation (CPR).

• Get the victim to the nearest secondary or tertiary care

hospital where antivenom can be provided

DO NOTS IN FIRST AID

• Do not apply a tourniquet.

• Do not wash the bite site with soap or any other solution to remove the venom.

• Do not make cuts or incisions on or near the bitten area.

• Do not use electrical shock.

• Do not freeze or apply extreme cold to the area of bite.

• Do not apply any kind of potentially harmful herbal or folk remedy. • .

Cont.

• Do not attempt to suck out venom with your mouth.

• Do not give the victim drink, alcohol or other drugs.

• Do not attempt to capture, handle or kill the snake and patients should not be taken to quacks.

SNAKE BITE TREATMENT PROTOCOL

• The initial management includes dealing with airway, breathing and treatment of shock.

• Administer tetanus toxoid

Emergency care

Try to identify the snake responsible.

• Snake colouration, its pupil shape and bitemarks

• Ask the victim relatives to carefully bring the snake to hospital if it has been killed and then use the snake identification material in protocol to identify it.

• Determine if any traditional medicines have been used as they can sometimes lead to confusing symptoms.

• Determine the exact time of bite which helps in determining progression of signs and symptom.

Cont.

• Iv access established in unaffected extremity• CBC, coagulation profile, fibrinogen concentration,

should be assessed.• Tourniquets placed in field should be carefully

removed.• The bitten extremity should be marked at 2 or more

sites proximal to the bite and the circumference at these locations should be assessed every 15min to monitor for progressive edema-indicative of ongoing venom effects.

Cont.

• All the patients should be kept under observation for a minimum of 24 hours.

• Many species, particularly the Krait and the hump-nosed pit viper are known for delayed appearance of symptoms which can develop after 6–12 hours

Investigations

• Twenty-minute whole blood clotting test (20WBCT) reliable test of coagulation which can be carried out by bedside and is considered to be superior to ‘capillary tube’ method for establishing clotting capability in snake bite.

• A few milliliters of fresh venous blood should be placed in a fresh, clean and dry glass vessel preferably test tube and left undisturbed at ambient temperature for 20 minutes.

• After that tube should be gently tilted to detect whether blood is still liquid and if so then blood is incoagulable.The test should be carried out every 30 minutes from admission for 3 hours and then hourly after that.

Other Useful Tests (If Facilities Available• Hb/platelet count/peripheral smear prothrombin time (PT)/activated

partialthromboplastin time•

• Urine examination for proteinuria/RBC/hemoglobinuria

• Myoglobinuria

• Biochemistry for serum creatinine/Urea/Potassium

• • ECG/X-ray/CT/Ultrasound(The use of X-ray and ultrasound, area of unproven benefit, apart from identification of clot in viperine bite)

• Oxygen saturation/arterial blood gas (ABG)

• • Enzyme-linked immunosorbent assay (ELISA) to confirmsnakespecies.

Treatment Phase

• Pain can be relieved with oral paracetamol or tramadol.

• Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) should not be administered

Severity of envenomation.

Anti-snake venom (ASV)

• Anti-snake venom (ASV)is the mainstay of treatment. Antivenom is immunoglobulin [usually pepsin-refined F(ab’)2 fragment of whole IgG] purified from the plasma of a horse, mule or donkey (equine) or sheep (ovine) that has been immunized with the venoms of one or more species of snake.

• In India, polyvalent ASV, i.e. effective against all the four common species; Russell’s viper, common cobra, common Krait and saw-scaled Viper and no monovalent ASVs are available

• ASV is produced both in Liquid and Lyophilized forms.

• There is no evidence to suggest which form is more effective.

• Liquid ASV requires a reliable cold chain and has 2-yearshelf life.

• Lyophilized ASV in powder form,has 5-year shelf life and requires only to be kept cool.

• Only free unbound fraction of venom can be neutralized by anti snake venom.

Antivenom treatment should be given as soon as it is indicated. It may reverse systemic envenoming even when this has persisted for several days or, in the case of haemostatic abnormalities, for two or more weeks. It is,therefore, appropriate to give antivenom for as long as evidence of the coagulopathy persists.

HOW LONG ASV CAN BE GIVEN?

ROUTE?

Freeze-dried (lyophilized) antivenoms are reconstituted, usually with 10ml of sterile water for injection per ampoule.Two methods of administration are recommended:(1) Intravenous “push” injection: Reconstituted freeze-dried antivenom is given by slow intravenous injection(not more than 2 ml/minute). (2) Intravenous infusion: Reconstituted freeze-dried antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg body weight) and is infused at a constant rateover a period of about one hourPatients must be closely observed for at least one hour after starting intravenous antivenom administration, so that early anaphylactic antivenom reactions can be detected and treated early with epinephrine(adrenaline)

Cont.• Local administration of ASV is not recommended as it

is extremely painful and can raise the intracompartmentalpressure.

• Intramuscular inj are not recommended .Antivenoms are large molecules (F(ab’)2 fragments or sometimes whole IgG) which, after intramuscular injection, are absorbed slowly via lymphatics. Bioavailability is poor, especially after intraglutealinjection, and blood levels of antivenom never reach those achieved rapidly by intravenous administration. Other disadvantages are the pain of injection of large volumes of antivenom and the risk of haematoma formation

Anti-snake Venom Administration

INDICATIONSEvidence of systemic toxicity.Hemodynamic or respiratory instability

Hypotension, respiratory distressHemotoxicity

Clinically significant bleeding orabnormal coagulation studies

Neurotoxicity Any evidence of toxicity usually beginning with CN

abnormalities and progressing to descendingparalysis including diaphragm

Evidence of local toxicity Progressive soft tissue swelling

TEST DOSE

• Anti-snake Venom Test Dose• Test doses have not been shown to have predictive value in

predicting anaphylactic reaction or late serum sickness and not recommended

• .

INTIAL DOSE.The recommended dose is often the amount of antivenom

required to neutralize the average venom yield when captive snakes are milked of their venom. In practice, the choice of an initial dose of antivenom is usually empirical.• Each vial is 10 ml of reconstituted ASV

Initial dose is 8-10 vials for both adults and children.

• Common krait- 100ml ASV• Russell’s viper-100ml• Saw scaled viper-50 ml• Indian cobra-100ml

Response to intial dose of ASV: If an adequate dose of appropriate antivenom has been administered, the following responses may be observed.(a) General: The patient feels better. Nausea, headache and generalisedaches and pains may disappear very quickly. .(b) Spontaneous systemic bleeding (e.g. from the gums): This usually stops within 15-30 minutes.(c) Blood coagulability (as measured by 20WBCT): This is usuallyrestored in 3-9 hours. (d) In shocked patients: Blood pressure may increase within the first30-60 minutes and arrhythmias such as sinus bradycardia mayresolve.(e) Neurotoxic envenoming (cobra bites)may begin to improve as early as 30 minutes after antivenom, butusually takes several hours.(f) Active haemolysis may cease within a few hours and the urine returns to its normal colour

REPEAT DOSES

Criteria for giving more antivenom

• Persistence or recurrence of blood incoagulability after 6 hours(measured by 20WBCT) or of bleeding after 1-2 hours.

• Deteriorating neurotoxic or cardiovascular signs after 1-2 hours of administering intial dose of ASV

Range of venom injected is about 5mg-147mgMaximum dose of ASV is around 25 vials.

ASV should be administered over a period of 1hour.

In hemotoxic envenomation;

• Once initial dose has been administered over one hour, no further ASV is given for 6 hours.

• Twenty WBCT test every 6 hours will determine if additional ASV is required. If the blood remains incoagulable (as measured by 20WBCT) six hours after the initial dose of antivenom, the same dose should be repeated. This is based on the observation that, if a large dose of antivenom (more than enough to neutralize the venom procoagulant enzymes) is given initially, the time taken for the liver to restore coagulable levels of fibrinogen and other clotting factors is 3-9 hours

• This reflects the period the liver requires to restore clotting factors.

In Neurotoxic envenomation

• Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis

• Death may result from aspiration, airway obstruction or respiratory failure.A clear airway must be maintained. Once there is loss of gag reflex and pooling of secretions in the pharynx, failure of the cough reflex or respiratory distress,acuffed endotracheal tube or laryngeal mask airway should be inserted

Neostigmine test.• A trial of anticholinesterase (eg “Tensilon test”) should be

performed in every patient with neurotoxic envenoming• Atropine sulphate (0.6 mg for adults; 50 μg/kg for children) or

glycopyrronium is given by intravenous injection followed byneostigmine bromide . in appropriate doses) by intramuscular

injection 0.02 mg/kg for adults, 0.04 mg/kg for Children.• The patient is observed over the next 30-60 minutes

(neostigmine) or 10-20 minutes (edrophonium) for signs of improved neuromuscular transmission. Ptosis may disappear and ventilatory capacity (peak flow, FEV-1 or maximum expiratory pressure) may improve.

• If positive institute regular atropine & neostigmine.

Treatment of hypotension and shock

Snake bite causes of hypotension and shock.

• Anaphylaxis• Vasodilatation• Cardiotoxicity• Hypovolaemia• Antivenom reaction• Respiratory failure• Acute pituitary adrenal insufficiency• SepticaemiaTreatment- a selective vasoconstrictor such as dopamine may be given by intravenous infusion, preferably into a central vein (startingdose 2.5-5mcg/kg/minute).

• Adverse reactions to anti-snake venom

• Fear of potentially life threatening adverse reactions

causes reluctance amongst some to treat snakebite.

• However, if handled early and with the primary drug of

choice, these reactions are easily managed.

• Patients should be monitored closely as there is evidence

that many anaphylactoid reactions go unnoticed

Adverse reactions to anti-snake venom

At the first sign of any of the following:

Urticaria, itching, fever, shaking chills, nausea, vomiting,

diarrhea, abdominal cramps, tachycardia, hypotension,

bronchospasm and angio-oedema:

1. ASV should be discontinued

2. 0.5 mg. of 1:1000 adrenaline should be given

IM

The pediatric dose is 0.01 mg/kg body weight of

adrenaline IM.

Evidence shows that adrenaline reaches necessary blood

plasma levels in 8 minutes via the IM route, but up to 34

minutes in the subcutaneous route.

Adverse reactions to anti-snake venom

100 mg of hydrocortisone and 10 mg of H1 antihistamine will be administered IV.

The dose for children is 0.2 mg/kg of antihistamine IV and 2 mg/kg

. If after 10 to 15 minutes the patient’s condition has not improved or is worsening, second dose of 0.5 mg of adrenaline 1:1000 IM is given.

This can be repeated for a third and final occasion but in the vast majority of reactions, 2 doses of adrenaline will be sufficient.

Once the patient has recoverd

ASV can be restarted

Given slowly for 10-15 minutes (underclose monitoring)

Then the normal drip rate should be resumed

ASV test doses have been abandoned:Have no predictive value in anaphylactoid or late serum reactions.May pre-sensitise the patient to the protein.

FOLLOW-UP

• After discharge from hospital, victim should be followed.

• If discharged within 24 hours, patient should be advised to return if there is any worsening of symptoms such as bleeding, pain or swelling at the site of bite, difficulty in breathing, altered sensorium, etc.

• The patients should also be explained about serum sickness which may manifest after 5–10 days

SUMMARY

• Snake bites is a particularly important public health

problem in rural areas of tropical and subtropical countries

situated in Africa, Asia, Oceania and Latin America

• The annual number of cases of snakebite worldwide is

about 5 million, among which there are some 100 000 to

200 000 deaths.

• common cobra (Naja naja), Russell’s viper (Dabiola

russelii), saw-scaled viper (Echis carinatus) and

common krait (Bungarus caeruleus) are highly

venomous and believed to be responsible for most of the

poisonous bites in India.

REFERENCES

• WHO Fact Sheet On Snake Bite .Geneva.WHO.last accessed on 19th

january 2015.

• National snakebite management protocol, India. (2008). [online] Avaialable at www://mohfw.nic.in (Directorate General of Healthand Family Welfare, Ministry of Health and Family Welfare, India).

• Simpson ID. Snakebite Management in India, the first few hours: A guide forprimary care physicians.J Indian Med Assoc.

2007;105:324-35.

• .Snake Bite Guidelines INDIAN PEDIATRICS, VOLUME 44 -MARCH 17, 2007.

• NELSON TEXTBOOK OF PEDIATRICS

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