SNAKE AND SCORPION ENVENOMATION

EPIDEMIOLOGY
• 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.
• Worldwide between 1.2 million to 5.5 million snakebites each year,
with 421,000-1,841,000 envenomations and 20,000-94,000 deaths.
• Epidemiology of snake-bite has not been adequately studied. One
reason is that many snake-bite victims are treated not in hospitals
but by traditional healers.
• WHO Recommendation: To remedy the deficiency in reliable snake-
bite data, it is strongly recommended that snake-bites should be
made a specific notifiable disease in all countries in the WHO
South-East Asia Region and that death certification should use the
specific International Classification of Diseases code.

SYMPTOMS AND SIGNS OF SNAKE-BITE
WHEN VENOM HAS NOT BEEN INJECTED-
Anxious people may
1.over-breathe
2. vasovagal shock
3. collapse
4.Blood pressure and pulse rate may increase
5.sweating and trembling.
• Constricting bands or tourniquets may cause pain, swelling and congestion
that suggest local envenoming.
• Ingested herbal remedies may cause vomiting. Instillation of irritant plant
juices into the eyes may cause conjunctivitis. Forcible insufflation of oils into
the respiratory tract may lead to aspiration pneumonia, bronchospasm,
ruptured ear drums and pneumothorax.
• Incisions, cauterization, immersion in scalding liquid and heating over a fire
can result in devastating injuries.

WHEN VENOM HAS BEEN INJECTED
• Increasing local pain (burning, bursting, throbbing) at the site of the bite,
• local swelling that gradually extends proximally up the bitten limb and
tender, painful enlargement of the regional lymph nodes draining the site
of the bite.
• However, bites by kraits, sea snakes and Philippine cobras may be virtually
painless and may cause negligible local swelling

COBRA BITE : SIGN AND SYMPTOMS
Local symptoms: start within 6 to 8 min.
• Small reddish wheal develop at site of bite.
• Tenderness, radiating burning pain,oozing of bloodstained fluid.
• Swelling may be minimal or absent.
Systemic symptoms: appear after 30 mins.
• Patient feels sleepy , intoxicated , weakness of leg.
• Nausea , vomitting.
• Ptosis is the earliest neuroparalytic manifestation followed by
ophthalmoplegia.
• Extraocular muscle weakness and strabismus.
• Paralysis of lower limb followed by trunk, head

• Eyelids also hangdown.
• After half to one hour there is excessive salivation, vomitting , headache ,
vertigo ,paraesthesias around the mouth and myalgia.
• Followed by paralysis of facial muscles, palate, jaws, tongue, vocal cord,
neck muscles, muscles of deglutition(difficulty in speech and swalowing).
• After 2 hours paralysis is complete.
• Respiratory arrest may occur due to obstruction of upper airway by
paralysed tongue,inhaled vomitus or due to paralysis of intercostal
muscles and diaphragm.

KRAITBITE : SIGNS AND SYMPTOMS
• Similar to cobra-bite but no swelling or pain at the site of bite.
• Convulsions are milder.
• Drowsiness and intoxication are more.
• Albumin appears in urine.

RUSSELL’S VIPER AND SAW SCALED VIPER-BITE : SIGN AND SYMPTOMS
• Severe pain at site of bite within 8 minutes.
• Local redness and tenderness.
• Swelling starts within 15 minutes, bloodstained discharge from wound.
• Persistent bleeding from bite site .
• Blisters appear in about 12hours at bitesite and progress to involve entire
limb.
• Intense pain, vomitting, giddiness, sweating, abdominal pain, dilatation of
pupils, getting insensitive to light and in about one to two hours there is
marked collapse and often complete loss of consciousness.
• Skin temperature is raised.
• Tingling, numbness over tongue, mouth and paresthesias around wound.
• Swelling spreads as far as trunk in 1 to 2 days.
• Though limb is swollen and red it is usually not tender.

• Extensive necrosis of skin, s.c. and muscles may may occur f/b epistaxis,
hemoptysis, ecchymoses, intracranial bleed , subconjunctival bleed , G.I,
G.U, intraperitoneal, retroperitoneal bleed.
• In severe cases main feature is persisting shock.
• Blood may show hemoconcentration early, then a decrease in red cells
and platelets and urine contains blood, sugar and protein.
• Bleeding and clotting time are usually prolonged.
• Intravascular hemolysis may lead to hemoglobinuria.
• Renal failure is frequent in russell’s viper and humpnosed viper.
• Petechial hemorrhages.
• In systemic poisoning, blood becomes defibrinated and will not clot.
Increasing respiratory distress, blurring of vision occur.
• Extensive suppuration and sloughing, f/b malignant edema of bitten area.
• Paralysis does not occur.
• Death is usually due to shock and hemorrhage.

CLINICAL SYNDROMES OF SNAKE-BITE
Syndrome 1
Local envenoming with bleeding/clotting disturbances = Viperidae (all
species)
Syndrome 2
Local envenoming with bleeding/clotting disturbances, shock or acute kidney
injury = Russell’s viper with conjunctival oedema (chemosis) and acute
pituitary insufficiency = Russell’s viper, Myanmar with ptosis, external
ophthalmoplegia, facial paralysis etc. and dark brown urine = Russell’s viper
Syndrome 3
Local envenoming with paralysis = Cobra or King Cobra.

Syndrome 4
Paralysis with minimal or no local envenoming Bitten on land while sleeping
on the ground = krait .Bitten in the sea, estuary and some freshwater lakes =
sea snake
Syndrome 5
Paralysis with dark brown urine and acute kidney injury: Bitten on land (with
bleeding/clotting disturbance) = Russell’s viper, Bitten on land while sleeping
indoors = krait (B. niger, B. candidus, B. multicinctus), Bitten in sea, estuary
and some freshwater lakes (no bleeding/clotting disturbances) = sea snake

Algorithm for diagnosis of the snake responsible for a bite

MANAGEMENT OF SNAKE-BITE
• First aid treatment
• Transport to hospital
• Rapid clinical assessment and resuscitation
• Detailed clinical assessment and species diagnosis
• Investigations/laboratory tests
• Antivenom treatment
• Observing the response to antivenom
• Deciding whether further dose(s) of antivenom are needed
• Supportive/ancillary treatment
• Treatment of the bitten part
• Rehabilitation
• Treatment of chronic complications

Recommended first-aid methods
1.Reassure the victim
2.Immobilize the whole of the patient’s body by laying him/her down in a
comfortable and safe position.
3.Especially, immobilize the bitten limb with a splint or sling. Any movement
or muscular contraction increases absorption of venom into the bloodstream
and lymphatics.
4.Avoid any interference with the bite wound (incisions, rubbing, vigorous
cleaning, massage, application of herbs or chemicals) as this may introduce
infection, increase absorption of the venom and increase local bleeding.
5.Tight (arterial) tourniquets are not recommended.
6.Release of tight bands, bandages and ligatures: Ideally, these should not be
released until the patient is under medical care in hospital, resuscitation
facilities are available and antivenom treatment has been started.
• MOST TRADITIONAL FIRST AID METHODS SHOULD BE DISCOURAGED
• THEY DO MORE HARM THAN GOOD !

EARLY CLUES OF SEVERE ENVENOMING
• Snake identified as a very dangerous one.
• Rapid early extension of local swelling from the site of the bite.
• Early tender enlargement of local lymph nodes, indicating spread of
venom in the lymphatic system.
• Early systemic symptoms: collapse (hypotension, shock), nausea, vomiting,
diarrhoea, severe headache, “heaviness” of the eyelids, inappropriate
(pathological) drowsiness or early ptosis/ ophthalmoplegia.
• Early spontaneous systemic bleeding. Passage of dark brown/black urine.
Do not assume that snake bitten patients are unconscious or even
irreversible “brain dead” just because their eyes are closed, they are
unresponsive to painful stimuli, are areflexic, or have fixed dilated pupils.
They may just be paralysed!

INVESTIGATIONS/LABORATORY TESTS
• 20-minute whole blood clotting test (20WBCT) *
• This very useful and informative bedside test requires very little skill and
only one piece of apparatus – a new, clean, dry, glass vessel (tube or
bottle).
• Place 2 mls of freshly sampled venous blood in a small, new or heat
cleaned,dry, glass vessel.
• Leave undisturbed for 20 minutes at ambient temperature.
• Tip the vessel once.
• If the blood is still liquid (unclotted) and runs out, the patient has
hypofibrinogenaemia (“incoagulable blood”) as a result of venom-induced
consumption coagulopathy.

• In the South-East Asia region, incoagulable blood is diagnostic of a viper
bite
• rules out an elapid bite.
• If the vessel used for the test is not made of ordinary glass, or if it has
been cleaned with detergent, its wall may not stimulate clotting of the
blood sample (surface activation of factor XII – Hageman factor) and test
will be invalid
• If there is any doubt, repeat the test in duplicate, including a “control”
(blood from a healthy person such as a relative)

OTHER TESTS
• Haemoglobin concentration/haematocrit: A transient increase indicates
haemoconcentration resulting from a generalized increase in capillary
permeability (e.g. in Russell’s viper bite).
• More often, there is a decrease reflecting blood loss or, in the case of
Indian, Thai and Sri Lankan Russell’s viper bite, intravascular haemolysis.

• Platelet count: This may be decreased in victims of envenoming by vipers
• and Australasian elapids.
• White blood cell count: An early neutrophil leucocytosis is evidence of
• systemic envenoming from any species.
• Blood film: Fragmented red cells (“helmet cell”, schistocytes) are seen
when
• there is microangiopathic haemolysis.
• Plasma/serum: May be pinkish or brownish if there is gross
haemoglobinaemia
• or myoglobinaemia.

BIOCHEMICAL ABNORMALITIES:
• Aminotransferases and muscle enzymes(creatine kinase, aldolase etc) will be
elevated
• Mild hepatic dysfunction is reflected in slight increases in other
serum enzymes. Bilirubin is elevated following massive extravasation of
blood.
• Potassium, creatinine, urea or blood urea nitrogen levels are raised in the
renal failure .

Early hyperkalaemia may be seen following extensive rhabdomyolysis
in sea snake-bites.
• Bicarbonate will be low in metabolic acidosis (e.g. renal
failure).
• Hyponatraemia

ARTERIAL BLOOD GASES AND PH
• May show evidence of respiratory failure
(neurotoxic envenoming) and
• Acidaemia (respiratory or metabolic
acidosis).

• Desaturation: Arterial oxygen saturation can be assessed non-invasively
in patients with respiratory failure or shock using a finger oximeter

URINE EXAMINATION
• The colour of the urine (pink, red, brown, black) should be noted and the
urine should be tested by dipsticks for blood or haemoglobin or
myoglobin.
• Standard dipsticks do not distinguish blood, haemoglobin and myoglobin.
• Haemoglobin and myoglobin can be separated by immunoassays but there
is no easy or reliable test.
• Microscopy will confirm whether there are erythrocytes in the urine.
• Red cell casts indicate glomerular bleeding.
• Massive proteinuria is an early sign of the generalized increase in capillary
permeability in Russell’s viper envenoming and an early indicator of acute
kidney injury.

ANTI VENOM TREATMENT
• Antivenom is the only specific antidote to snake venom. A most important
decision in the management of a snake-bite victim is whether or not to
administer antivenom.
• First introduced by Albert Calmette at the Institut Pasteur in Saigon in the
1890s.
• 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.

• “Specific” antivenom, implies that the antivenom has been raised against
the venom of the snake that has bitten the patient.
• Monovalent (monospecific) antivenom neutralizes the venom of only one
species of snake. Polyvalent (polyspecific) antivenom neutralizes the
venoms of several different species of snakes, usually the most important
species, from a medical point of view, in a particular geographical area.

• Indian antivenom manufacturers’ “polyvalent anti-snake venom serum” is
raised in horses using the venoms of the four most important venomous
snakes in India (Indian cobra, Naja naja; Indian krait, Bungarus caeruleus;
Russell’s viper, Daboia russelii; saw-scaled viper, Echis carinatus).
• Antibodies raised against the venom of one species may have Antivenom
treatment cross-neutralizing activity against other venoms, usually from
closely related species. This is known as paraspecific activity.

MECHANISM OF ACTION OF ANTIVENOM
• Antivenoms bind to and neutralize the venom, halting further damage, but
do not reverse damage already done.
• Thus, they should be administered as soon as possible after the venom
has been injected, but are of some benefit as long as venom is present in
the body.

INDICATIONS FOR ANTIVENOM
Antivenom treatment is recommended if and when a patient with proven or
suspected snake-bite develops one or more of the following signs:
1. Systemic envenoming
• Haemostatic abnormalities: Spontaneous systemic bleeding (clinical),
coagulopathy (20WBCT or other laboratory tests such as prothrombin
time) or thrombocytopenia (<100 x 109/litre or 100 000/cu mm)
• Neurotoxic signs: ptosis, external ophthalmoplegia, paralysis
• Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia,
abnormal ECG.

• Acute kidney injury (renal failure): oliguria/anuria (clinical), rising blood
creatinine/urea (laboratory).
• (Haemoglobin-/myoglobin-urea:) dark brown urine, urine dipsticks, other
evidence of intravascular haemolysis or generalised rhabdomyolysis
(muscle aches & pains, hyperkalaemia).

2. Local envenoming
• Local swelling involving more than half of the bitten limb (in the absence
of a tourniquet) within 48 hours of the bite. Swelling after bites on the
digits (toes and especially fingers).
• Rapid extension of swelling (for example, beyond the wrist or ankle within
a few hours of bite on the hands or feet).
• Development of an enlarged tender lymph node draining the bitten limb

• Antivenom should be given only to patients in whom its benefits are
considered likely to exceed its risks. Since antivenom is relatively costly
and often in limited supply, it should not be used indiscriminately. The
risk of reactions should always be taken into consideration.

It is appropriate to give antivenom for as long as evidence of the
coagulopathy persists.

ADMINISTRATION OF ANTIVENOM
• Epinephrine (adrenaline) should always be drawn up in readiness before
antivenom is administered. Antivenom should be given by the intravenous
route whenever possible.
• Freeze-dried (lyophilized) antivenoms are reconstituted, usually with 10 ml of
sterile water for injection per ampoule. If the freeze-dried protein is difficult
to dissolve, it may have been denatured by inadequate freeze-drying
technique (WHO, 2010).

TWO METHODS OF ADMINISTRATION ARE RECOMMENDED:
(1) Intravenous “push” injection: Reconstituted freeze-dried antivenom or
neat liquid antivenom is given by slow intravenous injection (not > 2
ml/minute).
(2) Intravenous infusion: Reconstituted freeze-dried or neat liquid
antivenom is diluted in approximately 5-10 ml of isotonic fluid per kg
body weight (i.e. 250-500 ml of isotonic saline or 5% dextrose in the case
of an adult patient) and is infused at a constant rate over a period of
about one hour.

Patients 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).
Local administration of antivenom at the site of the bite is not
recommended.

INTRAMUSCULAR INJECTION OF ANTIVENOM:
Anti-venoms 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 intra-gluteal injection, and blood levels
of antivenom never reach those achieved rapidly by intravenous
administration..
The only situations in which intramuscular administration might be
considered:

• At a peripheral first aid station, before a patient with obvious envenoming
is put in an ambulance for a journey to hospital that may last several hours
On an expedition exploring a remote area very far from medical care.
• When intravenous access has proved impossible.

DOSE OF ANTIVENOM
• Manufacturers’ recommendations are usually based on assays in which
venom and antivenom are incubated in vitro before being injected into the
test animal. This may not reflect the dose required to cure a human
patient.
• 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.
• Snakes inject the same dose of venom into children and adults. Children
must therefore be given exactly the same dose of antivenom as adults

OBSERVATION OF ANTIVENOM RESPONSE
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 generalised
aches 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 usually restored
in 3-9 hours. Bleeding from new and partly healed wounds usually stops
much sooner than this.

(a) In shocked patients: Blood pressure may increase within the first 30-60
min. &arrhythmias such as sinus bradycardia may resolve.
(b) Neurotoxic envenoming of the post-synaptic type (cobra bites) may
begin to improve as early as 30 minutes after antivenom, but usually
takes several hours. Envenoming with presynaptic toxins (kraits and sea
snakes) will not respond in this way.
(c) Active haemolysis and rhabdomyolysis may cease within a few hours
and the urine returns to its normal colour.

REPEATING INITIAL DOSE OF ANTIVENOM
Criteria for giving more antivenom
Persistence or recurrence of blood incoagulability after 6 hours or of bleeding
after 1-2 hours.
• Deteriorating neurotoxic or cardiovascular signs after 1-2 hours.

• If the blood remains incoagulable (as measured by 20 WBCT) 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 is given
initially, the time taken for the liver to restore coagulable levels of
fibrinogen & other clotting factors is 3-9 hours In patients who continue
to bleed briskly, the dose of anti-venom should be repeated within 1-2
hours
• In case of deteriorating neurotoxicity or cardiovascular signs, the initial
dose of antivenom should be repeated after 1-2 hours, and full supportive
treatment must be considered.

TREATMENT OF NEUROTOXIC ENVENOMING
• Antivenom treatment alone cannot be relied upon to save the life of a
patient with bulbar and respiratory paralysis.
• Artificial ventilation.

ANTIVENOM REACTIONS
Usually more than 10%, develop a reaction either early (within a few
hours)/late (five days or more) after being given antivenom.
(1) Early anaphylactic reactions:
Usually within 10-180 minutes of starting antivenom, the patient begins to itch
(often over the scalp) and develops urticaria, dry cough, fever, nausea,
vomiting, abdominal colic, diarrhoea and tachycardia. Complement activation
by IgG aggregates or residual Fc fragments or direct stimulation of mast cells or
basophils by antivenom protein are more likely mechanisms for these
reactions.

2) Pyrogenic (endotoxin) reactions:
Usually these develop 1-2 hours after treatment. Symptoms include shaking
chills (rigors), fever, vasodilatation and a fall in blood pressure. Caused by
pyrogen contamination during the manufacturing process & are commonly
reported.
(3) Late (serum sickness type) reactions:
Develop 1-12 (mean 7) days after treatment. Clinical features include fever,
nausea, vomiting, diarrhoea, itching, recurrent urticaria, arthralgia, myalgia,
lymphadenopathy, periarticular swellings, mononeuritis multiplex,
proteinuria with immune complex nephritis and, rarely, encephalopathy.

Prediction of antivenom reactions
• Skin and conjunctival “hypersensitivity” tests will reveal IgE mediated Type
I hypersensitivity to horse or sheep proteins.
• However, since the majority of early (anaphylactic) or late (serum sickness
type) antivenom reactions result from direct complement activation
rather than from IgE mediated hypersensitivity, these tests are not
predictive.
• Since they may delay treatment and can in themselves be sensitising,
these tests should not be used.

• Since no prophylactic drug regimen has proved effective in reducing the
incidence or severity of early antivenom reactions, these drugs should
not be used except in high risk patients .
• All patients should be watched carefully for two hours after the
completion of antivenom administration and should be treated with
epinephrine/adrenaline at the first sign of a reaction

TREATMENT OF ANTIVENOM REACTIONS
Early anaphylactic and pyrogenic anti-venom reactions:
• Epinephrine (adrenaline) is given intramuscularly in an initial dose of 0.5
mg (adults) & 0.01 mg/kg body weight (children).
• Because severe, life-threatening anaphylaxis can evolve so rapidly,
epinephrine (adrenaline) should be given at the very first sign of a
reaction, even when only a few spots of urticaria have appeared/at start
of itching, tachycardia or restlessness.
• Dose can be repeated every 5-10 minutes if patient condition is
deteriorating.

ADDITIONAL TREATMENT:
• After epinephrine (adrenaline), an antihistamine anti-H1 blocker such as
chlorphenamine maleate (adults 10 mg, children 0.2 mg/kg by intravenous
injection over a few minutes) should be given followed by intravenous
hydrocortisone (adults 100 mg, children 2 mg/kg body weight).
• In pyrogenic reactions the patient must also be cooled physically and with
antipyretics. Intravenous fluids should be given to correct hypovolaemia.

TREATMENT OF LATE (SERUM SICKNESS) REACTIONS
 Late (serum sickness) reactions may respond to a 5-day course of oral
antihistamine. Patients who fail to respond in 24-48 hours should be given
a 5-day course of prednisolone.
Doses
 Chlorphenamine: adults 2 mg six hourly, children 0.25 mg/kg / day in
divided doses.
 Prednisolone: adults 5 mg six hourly, children 0.7 mg/kg/day in divided
doses for 5-7 days

TRIAL OF ANTICHOLINESTERASE
• Anticholinesterase drugs have a variable, but potentially very useful effect
in patients with neurotoxic envenoming, especially those bitten by cobras.
• A trial of anticholinesterase (eg “Tensilon test”) should be performed in
every patient with neurotoxic envenoming.
• However, this should not delay antivenom treatment or endotracheal
intubation.

Procedure- Trial of anticholinesterase
1. Baseline observations or measurements are made against which to
assess the effectiveness of the anticholinesterase.
2. Atropine sulphate (0.6 mg for adults; 50 µg/kg for children) or
glycopyrronium is given by intravenous injection followed by neostigmine
bromide by intramuscular injection 0.02 mg/kg for adults, 0.04 mg/kg for
children.
Short acting edrophonium chloride (Tensilon) is ideal.It is given by slow
intravenous injection in an adult dose of 10 mg, or 0.25 mg/kg for children.

(3) 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.
(4) Patients who respond convincingly can be maintained on
neostigmine methylsulphate, 0.5-2.5 mg every 1-3 hours up to 10
mg/24 hours maximum for adults or 0.01-0.04 mg/kg every 2-4
hours for children by intramuscular, intravenous or subcutaneous
injection together with atropine to block muscarinic side effects.

DETECTION OF KIDNEY INJURY
• dwindling or no urine output.
• rising blood urea/creatinine concentrations.
• clinical “uraemia syndrome”:
 nausea, vomiting,
 hiccups, fetor,
 drowsiness, confusion, coma,
 flapping tremor, muscle twitching, convulsions pericardial
friction rub,
 signs of fluid overload

OLIGURIC PHASE OF RENAL FAILURE
• Most, but not all, patients with acute renal failure are oliguric, defined as a
urine output of less than 400 ml/day or less than 20 ml/hour. Conservative
management may avoid the need for dialysis.
• If the patient has intravascular volume depletion, indicated by supine or
postural hypotension, or empty neck veins, proceed as follows:
I. Establish intravenous access.

I. Give fluid challenge.
II. Insert a urethral catheter.
III. Furosemide (frusemide) challenge.
IV. Conservative management: If the urine output does not improve,
despite these challenges no further diuretics should be given. The
diet should be bland, high on calories (1700/day), low in protein (less
than 40g/day), low in potassium.

VI. Biochemical monitoring: Serum potassium, urea, creatinine
and, if possible, pH, bicarbonate, calcium and phosphate should
be monitored frequently.
VII. Detection and management of hyperkalaemia: ECG
evidence of hyperkalaemia: tall peaked T waves, prolonged P-R
interval, absent P waves, wide QRS complexes.
VIII. If the patient is hypotensive & acidotic sodium
bicarbonate be given.

IX. Dialysis – Indications for dialysis
Clinical uraemia
Fluid overload.
Blood biochemistry-one or more of the following:
 creatinine >4 mg/dl (500 μmol/l)
 urea >130 mg/dl (27 mmol/l)
 potassium >7 mmol/l (or hyperkalaemic ECG changes)
 symptomatic acidosis

To minimize the risk of renal damage from excreted myoglobin
and/or haemoglobin.
• Correct hypovolaemia and maintain saline diuresis.
• Correct severe acidosis with bicarbonate.
• Give a single infusion of mannitol (200 ml of 20% solution
over 20 minutes) (not of proven benefit)

Diuretic phase of kidney injury
 Urine output increases to 5-10 litres/24 hours following the
period of anuria.
 The patient may become polyuric and volume depleted so
that salt and water must be carefully replaced.
 Hypokalaemia may develop, in which case a diet rich in
potassium (fruit and fruit juices) is recommended.

Renal recovery phase
• The diuretic phase may last for months after Russell’s viper bite.
• In Myanmar and South India, hypopituitarism may complicate
recovery of Russell’s viper bite victims.
• Corticosteroid, fluid & electrolyte replacement may be needed.
Persisting renal dysfunction
• In India, 20%-25% of patients referred to renal units with acute
renal failure following Russell’s viper bite suffered oliguria for
more than four weeks suggesting the possibility of bilateral
renal cortical necrosis. This can be confirmed by renal biopsy or
contrast enhanced CT scans of the kidneys.

TREATMENT OF THE BITTEN PART
Bacterial infections
• Interference with the wound creates a risk of secondary bacterial
infection and justifies the use of immediate broad spectrum
antibiotics and tetanus prophylaxis

CLINICAL FEATURES - COMPARTMENTAL SYNDROME
• Disproportionately severe pain.
• Weakness of intra-compartmental muscles.
• Pain on passive stretching of intra compartmental muscles.
• Hypo-aesthesia of areas of skin supplied by nerves running
through the compartment.
• Obvious tenseness of the compartment on palpation.

CRITERIA FOR FASCIOTOMY IN BITTEN LIMBS
• Haemostatic abnormalities have been corrected (antivenom
with or without clotting factors)
• Clinical evidence of an intracompartmental syndrome.
• Intracompartmental pressure >40 mmHg (in adults

Infusion pump, saline manometer system in use for
measuring the tissue pressure inside the anterior tibial compartment

Stryker pressure monitor in use for measurement of
intracompartmental pressure

Management of cobra spit ophthalmia
Management of venom ophthalmia consists of:
(1) urgent decontamination by copious irrigation.
(2) analgesia by vasoconstrictors with weak mydriatic activity
(e.g. epinephrine) and limited topical administration of local
anesthetics (e.g. tetracaine)
(3) exclusion of corneal abrasions by fluorescein staining with a
slit lamp examination & application of prophylactic topical
antibiotics.
(4) prevention of posterior synechiae, ciliary spasm and
discomfort with topical cycloplegics.
(5) antihistamines in case of allergic keratoconjunctivitis.

INSTITUTES PRODUCING ASV
• Haffkine institute, mumbai
• King institute, chennai
• Serum institute,pune.

Scorpion sting- C. exilicauda
• Scorpions have a world-wide distribution.
• Highly toxic species are found in the Middle East, India, North Africa,
South America, Mexico, and the Caribbean island of Trinidad.
• There are more than 1250 species of scorpions. About 100 species
are found in india.
• These are eight-legged arthropods and have a hollow string in the
last joint of their tail, which communicates by means of a duct
with the poisonous glands, which secrete poison on stinging.
• Colour of scorpions varies from light yellow to black.most scorpion
string occur on the extremities.
• The venom is a clear, colourless toxalbumen, and can be classified
as either haemolytic or neurotoxic.

Mechanism of action
• Venom can open neuronal sodium channels and cause
prolonged and excessive depolarization
• The venom is a potent autonomic stimulator resulting in
release of massive amounts of catecholamines from the
adrenals.
• It has also some direct effect on the myocardium.
• Its toxicity is more than that of snakes, but only a small
quantity is injected.
• The mortality, except in children is negligible.

Symptoms and sign
• Somatic and autonomic nerves may be affected
• Initial pain and paresthesia at the stung extremity that
becomes generalised
• Cranial nerve- abnormal roving eye movements, blurred
vision, pharyngeal muscle incoordination and drooling and
respiratory compromise

• Excessive motor activity
• Nausea, vomiting, tachycardia, and severe agitation can also
be present.
• Cardiac dysfunction, pulmonary edema, pancreatitis, bleeding
disorders, skin necrosis, and occasionally death can occur

• If the scorpion has haemolytic venom, the reaction is mainly local and
simulates the viper snake bite, but the scorpion sting will have only one hole
in the centre of the reddened area.
• The extremity will have oedema, pain and reddening.

This usually lasts for one to two hours.
The symptoms produced by a neurotoxic venom is similar to
cobra bite.
There is usually no marked reaction in the local area.
Nausea, vomiting, extreme restlessness, fever, various type of
paralysis, cardiac arrhythmias, convulsions, coma and cyanosis,
respiratory depression, and death may occur within hours from
pulmonary oedema or cardiac failure.
The diagnosis is confirmed by ELISA testing.

Treatment
• Pain Management
• Ice pack
• Immobilization of limb
• Local anaesthetics are better than opiates
• Tetanus prophylaxis, wound care and antibiotics
• Benzodizepines for motor activity.

Newer modality
• Insulin has shown to improve cardiopulmonary status in case
of scorpion envenomation

THANKS FOR LISTENING
PATIENTLY

SNAKE AND SCORPION ENVENOMATION

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SNAKE AND SCORPION ENVENOMATION