Snake bite

By
Dr Biswaranjan prusty
Associate professor
• First aid treatment
• • Transport to hospital
• • Rapid clinical assessment and resuscitation
• • Investigations/laboratory tests
• • Clinical assessment and species diagnosis, if possible
• • Antivenom treatment
• • Observing the response to antivenom
• • Deciding whether further dose(s) of antivenom are needed
• • Supportive/ancillary treatment
• • Treatment of the bitten part
• • Follow-up
• • Rehabilitation
Aims of first-aid
• Attempt to retard systemic absorption of venom.
• Preserve life and prevent complications before the patient can
receive medicalcare
• Control distressing or dangerous early symptoms of envenoming.
• Arrange the transport of the patient to a place where they can receive
medical care.
• ABOVE ALL, AIM TO DO NO HARM!
• The three major families of venomous snakes are the Elapidae, the Viperidae, and the Colubridae
• Hydrophidae (WHO 2010).

• Elapidae (cobra, king cobra, krait, and coral snake): These snakes have heads that are of about the
same width as their necks. The head is covered with large scales but lack laureal shields.

• Viperidae (vipers): The head of a viper is triangular, wider than the neck, and has laureal shields.
• They have vertically elliptical pupils and are ovi-viviparous. Their fangs are long, movable, and
• canalized like hypodermic needles. They are further subdivided into pit viper and pitless viper
• subfamilies.

• Hydrophidae (sea snake): Sea snakes are found in the vicinity of the seacoast. Though venomous,
they seldom bite.
• There are more than 2000 species of snakes in the world and about 300 species are found in India
• out of which 52 are venomou
At community level/village
• Reassure 70% of all snakebites are from non-venomous species.
• Immobilize the limb in the same way as a fractured limb.
• Nil by mouth till victim reaches a medical health facility.
• No traditional remedies.
• Shift the victim to the nearest health facility (PHC or hospital)
immediately.
• Arrange transport of the patient to medical care as quickly, safely and
passively as possible by vehicle ambulance (toll free no. 102/108/etc.),
boat, bicycle, motorbike, stretcher etc.
• Remove shoes, rings, watches, jewellary and tight clothing from the
bitten area as they can act as a tourniquet when swelling occurs.
Clinical features

• Fang mark or their patterns have no role to determine whether the

biting species was venomous or nonvenomous or amount of venom
injected, severity of systemic poisoning and nature of poisoning –
Elapidae or viperidae venom etc. Some species like Krait may leave
no bite marks.
• Asymptomatic as:
• 1. The bite is from a non venomous species (approximately 70% of snakebites are from
non venomous species

• 2. The bite is from a venomous species but has not injected enough venom to cause
symptoms or has injected none at all (dry bites)

• 3. The venom is of a sufficiently high level to cause symptoms but is now progressing
through the tissue without causing swelling to indicate its presence. Envenomation
can take many hours to present signs and symptoms (Very common in Krait bite).
• 4. May be envenomed but no visible signs or immediately detectable symptoms are
visible (The victim may have incoagulable blood or bleeding or renal failure may be
underway but not visible)
• Patients many a times present with nonspecific symptoms related to
anxiety.
• Common symptoms in these patients are: Palpitations, sweating,
tremoulessness, tachycardia, tachypnoea, elevated blood pressure,
cold extremities and paraesthesia, dilated pupils (sympathetic
overactivity).
Dry Bite

• Bites by nonvenomous snakes are common .

• bites by venomous species are not alwaysaccompanied by the injection of venom (dry bites).
• Dry bites ranges from 10–80% for various poisonous snakes.
• Some people who are bitten by snakes (or suspect or imagine that they have been bitten) or
have doubts regarding bite may develop quite striking symptoms and signs, even when no
venom has been injected due to understandable fear of the consequences of a real
venomous bite.
• Even in case of dry bite, symptoms due to anxiety and sympathetic overactivity
• (as above) may be present.
• As symptoms associated with panic or stress sometimes mimic early envenoming
symptoms, clinicians may have difficulties in determining whether envenoming occurred or
not.
Neuroparalytic (Progressive
weakness; Elapid envenomation

• Neuroparalytic snakebite patients present with typical symptoms

within 30 min– 6 hours in case of Cobra bite and 6 – 24 hours for Krait
bite; however, ptosis in Krait bite have been recorded as late as 36
hours after hospitalization.
• These symptoms can be remembered as 5 Ds and 2 Ps.
• • 5 Ds – Dyspnea, Dysphonia, Dysarthria, Diplopia, Dysphagia
• • 2 Ps – Ptosis, Paralysis
• In chronological order of appearance of symptoms – furrowing of forehead, Ptosis
• (drooping of eyelids) occurs first (Figure 3), followed by Diplopia (double vision), then
• Dysarthria (speech difficulty), then Dysphonia (pitch of voice becomes less) followed by
• Dyspnoea (breathlessness) and Dysphagia (Inability to swallow) occurs. All these
• symptoms are related to 3rd, 4th, 6th and lower cranial nerve paralysis. Finally, paralysis of
• intercostal and skeletal muscles occurs in descending manner.
• • Other signs of impending respiratory failure are diminished or absent deep tendon reflexes
• and head lag.
• • Additional features like stridor, ataxia may also be seen.
• • Associated hypertension and tachycardia may be present due to hypoxia
• In chronological order of appearance of symptoms – furrowing of forehead, Ptosis
• (drooping of eyelids) occurs first (Figure 3), followed by Diplopia (double vision),
then Dysarthria (speech difficulty), then Dysphonia (pitch of voice becomes less)
followed by
• Dyspnoea (breathlessness) and Dysphagia (Inability to swallow) occurs.
• All these symptoms are related to 3rd, 4th, 6th and lower cranial nerve paralysis.
• Finally, paralysis of intercostal and skeletal muscles occurs in descending manner.
• Other signs of impending respiratory failure are diminished or absent deep tendon
reflexes and head lag.
• • Additional features like stridor, ataxia may also be seen.
• • Associated hypertension and tachycardia may be present due to hypoxia.
• Bilateral dilated, poorly or a non-reacting pupil is not the sign of
brain dead in elapid envenoming (Figure 3).

• Refer patients presenting with neuroparalytic symptoms immediately

to a higher facility for intensive monitoring after giving Atropine
Neostigmine (AN) injection (schedule of AN injection described
below).
Vasculotoxic (haemotoxic or
Bleeding
General signs and symptoms of Viperine envenomation)
• Vasculotoxic bites are due to Viper species.
• Local manifestations – these are more prominent in Russel’s viper bite followed
by Saw scaled viper and least in Pit viper bite.

• Local swelling, bleeding, blistering, and necrosis.

• Pain at bite site and severe swelling leading to compartment syndrome
• Pain on passive movement.
• Absence of peripheral pulses and hypoesthesia over the fuels of nerve passing
through the compartment helps to diagnose compartment syndrome.
• Tender enlargement of local draining lymph node.
• Visible systemic bleeding from the action of haemorrhagins (Figure 4) e.g. gingival bleeding,
• epistaxis, ecchymotic patches, vomiting, hematemesis, hemoptysis, bleeding per rectum,
• subconjunctival hemorrhages, continuous bleeding from the bite site, bleeding from pre-existing
• conditions e.g. haemorrhoids, bleeding from freshly healed wounds.
• • Bleeding or ecchymosis at the injection site is a common finding in Viper bites.
• • The skin and mucous membranes may show evidence of petechiae, purpura ecchymoses, blebs
• and gangrene.
• • Swelling and local pain.
• • Acute abdominal tenderness may suggest gastro-intestinal or retro peritoneal bleeding.
• • Lateralizing neurological symptoms such as asymmetrical pupils may be indicative of intracranial
• bleeding.
• • Consumption coagulopathy detectable by 20WBCT, develops as early as within 30 minutes
• from time of bite but may be delayed.
Life threatening complications
are due to renal involvement
• . Patient presents with hematuria,
• hemoglobinuria, myoglobinuria followed by oliguria and anuria with acute kidney injury (AKI).
• Bilateral renal angle tenderness.
• Reddish or dark brown urine or declining urine output.
• • AKI e.g. declining or no urine output, deteriorating renal signs >serum creatinine, urea or K+.
• Some species e.g. Russell’s viper (Daboia sp) and Saw scale vipers (Echis sp) frequently causes AKI
• Hypotension due to hypovolaemia or direct vasodilatation or direct cardiotoxicity aggravates AKI.
Parotid swelling, conjunctiva oedema, sub-conjunctival haemorrhage, renal failure, acute
• respiratory distress syndrome [leaking syndrome] and refractory shock.
• Long term sequelae e.g. pituitary insufficiency with Russell’s viper (Daboia sp), Sheehan’s
• syndrome or amenorrhea in females
Painful Progressive Swelling
(PPS)
• PPS indicative of local venom toxicity.
• Prominent in Russel’s viper bite, Saw scaled viper bite and Cobra bite.
• Local necrosis which often has a rancid smell.
• Limb is swollen and the skin is taut and shiny.
• Blistering with reddish black fluid at and around the bite site.
• Skip lesions around main lesion are also seen.
• Ecchymoses due to venom action destroying blood vessel wall.
• Significant painful swelling potentially involving the whole limb and extending onto
the trunk.
• Compartment syndrome will present invariably.
• Regional tender enlarged lymphadenopathy.
Myotoxic

• Sea snakebite.
• Patient presents with: Muscle aches, muscle swelling, involuntary
contractions of muscles.
• Passage of dark brown urine.
• Compartment syndrome, cardiac arrhythmias due to hyperkalaemia,
AKI due to myoglobinuria, and subtle neuroparalytic signs.
Occult snakebite

• Krait bite victims often present in the early morning with paralysis
with no local signs. Krait has nocturnal habitat and has fine slender
teeth. Hence bite marks usually cannot be identified even on close
examination.
• Typical presenting history is that the patient was healthy at night, in
the morning gets up with severe epigastric/umbilical pain with
vomiting persisting for 3 – 4 hours and followed by typical
neuroparalytic symptoms within next 4- 6 hours.
• There is no history of snakebite.Unexplained respiratory distress in
children in the presence of ptosis or sudden onset of acute flaccid
paralysis in a child (locked-in syndrome) are highly suspicious
symptoms in endemic areas particularly of Krait bite envenomation.
Sometimes patients may present with throat pain or chest pain also.
KRAIT
Clinical situations in which snake-bite
victims might require urgent resuscitation
• :
• (a) Profound hypotension and shock resulting from direct cardiovascular effects of the
venom or secondary effects, such as hypovolaemia, release of inflammatory vasoactive
mediators, haemorrhagic shock or rarely primary anaphylaxis induced by the venom itself.
• (b) Terminal respiratory failure from progressive neurotoxic envenoming that has led to
paralysis of the respiratory muscles.
• (c) Sudden deterioration or rapid development of severe systemic envenoming following
the release of a tight tourniquet or compression bandage (see Caution above).
• (e) Cardiac arrest precipitated by hyperkalaemia resulting from skeletal muscle breakdown
(rhabdomyolysis) after bites by sea snakes, certain kraits and Russell’s vipers.
• If the patient arrives late: Late results of severe envenoming such as renal failure and
septicaemia
• complicating local necrosis.
Early clues that a patient has severe
envenoming (WHO):

• • 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
General examination
• : Measure the blood pressure (sitting up and lying to detect a postural drop
• indicative of hypovolaemia) and heart rate.
• Examine the skin and mucous membranes for evidence of petechiae, purpura, discoid
haemorrhages, ecchymoses and, in the conjunctivae, for haemorrhages and chemosis.
• Thoroughly examine the gingival sulci, using a torch and tongue depressor, as these
may show the earliest evidence of spontaneous systemic bleeding.
• Examine the nose for epistaxis.
• Abdominal tenderness may suggest gastrointestinal or retroperitoneal bleeding.
• Loin (low back) pain and tenderness suggests acute renal ischaemia (Russell’s viper
bites).
• Intracranial haemorrhage is suggested by lateralising neurological signs, asymmetrical
pupils, convulsions or impaired consciousness (in the absence of respiratory or
circulatory failure).
Diagnosis Phase: Investigations

• Simple diagnostic test: 20 Minute Whole Blood Clotting Test (20WBCT)

• It is considered as the most reliable test of coagulation and can be carried out,
at the bedside without specialist training. It can also be carried out in the most
basic settings.
• A few ml of fresh venous blood is placed in a NEW, CLEAN AND DRY GLASS
vessel/tube and left at ambient temperature for 20 minutes. The glass vessel
should be left undisturbed for 20 minutes and then gently tilted, not shaken.
• 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 XI– 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) (WHO)
Results Interpretation (20WBCT)

• If the blood is solid i.e. has clotted the patient has passed the
coagulation test and no ASV isrequired at this stage. The patient is
re-tested every hour for the first three hours and then 6 hourly for
24 hours until either test result is not clotted or clinical evidence of
envenomation to ascertain ifdose of ASV is indicated.
• In case test is non-clotting, repeat 6 hour after administration of
loading dose of ASV.
• In case of neurotoxic envenomation repeat clotting test after 6 hours.
20WBCT
At Primary health centre

• Peak flow meter in patients (adolescents and adults) presenting with

neuroparalytic syndrome. If Peak flow meter is not available in PHC
then assess respiratory function using bedside tests – single breath
count, breath holding time and ability to complete one sentence in
one health as described earlier.
• Urine examination for albumin and blood by dipstick.
At District Hospital

• In addition to the above

• Prothrombin time
• Platelet count,
• Clot retraction time
• Liver function test (LFT)
• Renal Function test (RFT)
• Serum Amylase
• Blood sugar
• ECG
• Abdominal ultrasound
• 2D Echo (if available)
 AT TERTIARY CARE
• In neuroparalytic envenomation
• Arterial blood gases. Caution: Arterial puncture is contraindicated in patients with haemostatic
• abnormalities.
• Pulmonary function tests
• In Vasculotoxic venomation
• For coagulopathy- BT, CT, PT, APTT, Platelet, Serum Fibrinogen, FDP D-Dimer assay, LDH,
peripheral blood smear
• Hemolysis -Urine for myoglobin, Urine haemoglobin
• For renal failure- Urine microscopy for RBC, casts, RFT, urinary proteins, creatinine ratio
• Hepatic injury – LFTs including SGOT, SGPT, Alkalien phosphatase, serum proteins
• Cardiotoxicity- CPK-MB, 2D Echo, BNP
• Myotoxic – CPK, SGOT, Urine myoglobin, compartment pressure
• Infection- Serum procalcitonin, culture (blood, urine, wound) and sensitivity
• Arterial blood gases and urine examination should be repeated at frequent intervals during the
acute
• phase to assess progressive systemic toxicity).
• Hemogram: The hemogram may show transient elevation of
hemoglobin level due to hemoconcentration (because of the
increased capillary leak) or may show anemia (due to
• hemolysis, especially in viper bites).
• Presence of neutrophilic leucocytosis signifies systemic absorption of
venom
• Thrombocytopenia may be a feature of viper envenomation.
• 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
• Serum creatinine: AKI after viper and sea snakebite.
• Serum creatinine phosphokinase (CPK): Elevated levels of these markers suggests muscle
damage (caution for renal damage) and raised amylase suggests pancreatic injury
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT): Prolongation may
be present in viper bite (to be repeated 6 hourly, if abnormal).
• Fibrinogen and fibrin degradation products (FDPs): Low fibrinogen with elevated FDP is
present when venom interferes with the clotting mechanism.
• Urine examination for Proteinuria/ RBC/ Haemoglobinuria/ Myoglobinuria: 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.
• Electrocardiogram (ECG): Nonspecific ECG changes such as bradycardia and
atrioventricular block with ST-T changes may be seen
• Late-onset envenoming
• The patient should be kept under close observation for at least 24 hours. Many species, particularly
• the Krait and the Hump-nosed pitviper (Joseph et al, 2006) are known for the length of time it can
• take for symptoms to manifest. Often this can take between 6 to 12 hours. Late onset envenoming
• is a well documented occurrence (Ho et al, 1986) (Warrell et al, 1977) (Reitz, 1989). In many cases
• of Common krait bites in West Bengal, bilateral ptosis appeared after 24- 36 h after admission for
• pain abdomen.
• This is also particularly pertinent at the start of the rainy season when snakes generally give birth to
• their young. Juvenile snakes, 8-10 inches long, tend to bite the victim lower down on the foot in the
• hard tissue area, and thus any signs of envenomation can take much longer to appear
ASV
• If ASV is indicated i.e. signs and symptoms of envenomation with or without evidence of
• laboratory tests, administer full dose. There are no absolute contraindications to ASV. Do not
• routinely administer ASV to any patient claiming to have bitten by a snake as ASV exposes such
• patients to the risks of ASV reactions unnecessarily; besides wastage of valuable and scarce
stocks of
• ASV. However, at the same time do not delay or withhold ASV on the grounds of anaphylactic
• reaction to a deserving case. Do NOT give incomplete dose. Purely local swelling, even if
• accompanied by a bite mark from an apparently venomous snake, is not a ground for
administering
• ASV. Swelling, a number of hours old is also not a ground for giving ASV. However, rapid
• development of swelling indicates bite with envenoming requiring ASV.
• Anti snake venom (ASV) in India is polyvalent i.e. it is effective against
all the four common species;1 Russell’s viper (Daboia russelii),
2Common Cobra (Naja naja),3 Common Krait (Bungarus caeruleus)
and 4 Saw Scaled viper (Echis carinatus).
• There are no currently available monovalent ASVs primarily because
there are no objective means of identifying the snake species, in the
absence of the dead snake. It would be impossible for the physician to
determine which type of Monovalent ASV to employ in treating the
patient.
• ASV comes in two forms lyophilised powdered and liquid. Lyophilised
ASV is simply liquid ASV freeze-dried. There is NO evidence that
clinically one form is better at neutralising venom than the other.
They each have advantages or disadvantages that must be considered
• Liquid ASV requires a reliable cold chain and refrigeration and has a
2 year shelf life. Lyophilised ASV, in powder form, requires only to be
kept cool. This is a useful feature in remote areas where power
supply is inconsistent
• Dose of ASV
• ASV should be given only by the IV route, and should be given
slowly, with the physician at the bed side during the initial period to
intervene immediately at the first sign of any reaction.
• The rate of infusion can be increased gradually in the absence of a
reaction until the full starting dose has been administered (over a
period of ~1 hour
• Epinephrine (adrenaline) should always be drawn up in readiness
before ASV is administered.
• ASV must NEVER be given by the IM route because of poor
bioavailability by this route.
• Also do NOT inject the ASV locally at the bite site since it is not
effective, is extremely painful and may increase intra-compartmental
pressure.
• Take all aseptic precautions before starting ASV to prevent any
pyrogenic reactions to ASV.
• For neuroparalytic snakebite – ASV 10 vials stat as infusion over 30 minutes followed by 2nd dose
of 10 vials after 1 hour if no improvement within 1st hour.
• For vasculotoxic snakebite - Two regimens low dose infusion therapy and high dose intermittent
bolus therapy can be used.
• Low dose infusion therapy is as effective as high dose intermittent bolus therapy and also saves
scarce ASV doses.
• Low Dose infusion therapy – 10 vials for Russel’s viper or 6 vials for Saw scaled viper as stat as
infusion over 30 minutes followed by 2 vials every 6 hours as infusion in 100 ml of normal saline
till clotting time normalizes or for 3 days whichever is earlier.
• Or
• High dose intermittent bolus therapy - 10 vials of polyvalent ASV stat over 30 minutes as
infusion, followed by 6 vials 6 hourly as bolus therapy till clotting time normalizes and/or local
swelling subsides.
• No ASV for Sea snakebite or pit viper bite as available ASV does not contain antibodies against
them.
• ASV Can
• Bind to a venom molecule that it is effective against and neutralise
that venom molecule rendering it unable to bind to the target cell but
only whilst the venom molecule is circulating in the blood or lymph
and is unbound.
• ASV Cannot:
• 1) Reverse necrotic action of the venom on tissue
• 2) Reverse local swelling
• 3) Reverse renal failure
• 4) Reverse coagulopathy; the liver does this.
• 5) Reverse pre synaptic envenoming; the nerve damage is structural and large
quantities of ASV are ineffective, the body must regenerate synaptic vesicles
• 6) Prevent local necrosis; the damage is done too quickly and the venom is in
the tissue and therefore not reachable by the ASV (Gutierrez et al, 2007)
• 7) Prevent local swelling; the damage is done too quickly and the venom is in
the tissue and therefore not reachable by the ASV (Gutierrez et al, 2007
• Monitoring of Patients on ASV therapy
• All patients should be watched carefully every 5 min for first 30 min,
then at 15 min for 2 hours for manifestation of a reaction. At the
earliest sign of an adverse reaction suspend temporarily.
• Maintain a strict intake output chart and note colour of urine to
detect acute kidney injury early.
• Snakes inject the same dose of venom into children and adults.
Children must therefore be given exactly the same dose of
antivenom as adults.

• ASV should be given: IN PREGNANCY

• 1. In the same dose and
• 2. Under the same criteria as standard victims.
Adverse reaction to ASV
• Early anaphylactic reactions occurs within 10–180 min of start of
therapy and is characterized by
• itching, urticaria, dry cough, nausea and vomiting, abdominal colic,
diarrhoea, tachycardia, and fever. Some patients may develop severe
life-threatening anaphylaxis characterized by hypotension,
bronchospasm, and angioedema.
• Any new sign or symptom after starting the ASV in drip should be
suspected as a reaction to ASV such as vomiting, hot or cold feeling;
sudden dry cough, new pain abdomen, dyspnoea; fall of BP and shock,
swelling of face, conjunctiva and protrusion of the tongue due to
angiooedema.
• Pyrogenic reactions usually develop 1–2 h after treatment.
Symptoms include chills and rigors, fever, and hypotension. These
reactions are caused by contamination of the ASV with pyrogens
during the manufacturing process.
• Late (serum sickness–type) reactions develop 1–12 (mean 7) days
after treatment. Clinical features include fever, nausea, vomiting,
diarrhea, itching, recurrent urticaria, arthralgia,
myalgia,lymphadenopathy, immune complex nephritis and, rarely,
encephalopathy
• Administer Epinephrine (adrenaline) (1 in 1,000 solution, 0.5 mg (i e
0.5 ml) in adults intramuscular over deltoid or over thigh; In children
0.01 mg/kg body weight) for early anaphylactic and pyrogenic ASV
reactions.
• Ideally 2 syringes should be drawn up ready if the ASV is known to
cause frequent reactions.
• Administer Chlorpheniramine maleate (adult dose 10 mg, in children
0.2 mg/kg) intravenously.
• Treatment of Late (serum sickness–type) reactions
• Inj. Chlorpheniramine 2 mg in adults (In children 0.25 mg/kg/day) 6
hourly for 5 days
• In patients who fail to respond within 24–48 h give a 5-day course of
Prednisolone (5 mg 6 hourly in adults and 0.7 mg/kg/day in divided
doses in children
Observation to ASV
• If an adequate dose of appropriate antivenom has been administered, the following responses
may be observed.
• General: The patient feels better. Nausea, headache and generalised aches and pains may
disappear very quickly. This may be partly attributable to a placebo effect.
• Spontaneous systemic bleeding (e.g. from the gums): This usually stops within 15-30 minutes.
• 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.
• In shocked patients: Blood pressure may increase within the first 30-60 minutes and arrhythmias
such as sinus bradycardia may resolve.
• 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.
• Active haemolysis and rhabdomyolysis may cease within a few hours and the urine returns to its
normal colour.
• In all cases of neurotoxic envenomation the 'AN challenge Test' will be
administered, Atropine 0.6 mg followed by neostigmine (1.5mg) to be
given IV stat and repeat dose of neostigmine 0.5 mg with atropine
every 30 minutes for 5 doses (In children, Inj. Atropine 0.05 mg/kg
followed by Inj.Neostigmine 0.04 mg/kg Intravenous and repeat dose
0.01 mg/kg every 30 minutes for 5 doses).
• A fixed dose combination of Neostigmine and glycopyrolate IV can
also be used.
• Thereafter to be given as tapering dose at 1 hour, 2 hour, 6 hours and
12 hour. Majority of patients improve within first 5 doses.
• Observe the patient closely observed for 1 hour to determine if the
neostigmine is effective.
• After 30 minutes, any improvement should be visible by an
improvement in ptosis.
• Positive response to “AN” trial is measured as 50% or more recovery
of the ptosis in one hour.
• 1. AKI- Correction of hypovolumia, HD.
• 2 In cases where generalised capillary permeability has been
established a vasoconstrictor such as dopamine can be used. Dosing is
2.5- 5μg/kg/minute.
• 3 INJ TT
• 4. ANTIBIOTICS
• If the patient has oliguria or dipstick positive for blood give a trial of forced alkaline diuresis
• (FAD) within first 24 hours of the bite to avoid pigment nephropathy leading to acute tubular
• necrosis (ATN).
• Delayed FAD has no role. Sequence of FAD in adults is as follows:
• a) Inj. Frusemide 40 mg IV stat
• b) Inj. Normal saline 500 ml + 20 ml of NaHCO3 over 20 minutes
• c) Inj. Ringer’s lactate 500 ml + 20 ml of NaHCO3 over 20 minutes
• d) Inj. 5% dextrose 500 ml + 10 ml of Potassium Chloride over 90 minutes
• e) Inj. Mannitol 150 ml over 20 min
• Whole cycle completes in 2 h 30 min and urine output of 3 ml/min is expected.
• If patient responds to first cycle continue for 3 cycles. FAD converts oliguria into polyuria and
avoid ATN and acute kidney injury needing dialysis in more than 75% patients.
• If there is no response to furosemide discontinue FAD and refer patient immediately to a higher
center for dialysis.
• FIRST HOUR is the Golden hour in Snakebite management” should
always be the Golden Rule in Snakebite Management. In whatever
condition, after whatever hours of the actual bite a venomous bite
patient arrives at a Health Facility, FIRST DOSE of ASV MUST be given
at first contact health centre.
THANK YOU