This pptx is on recognition of different snakes, snake bite management particularly in children. At the end of the slide show you will definitely able to recognize and manage snake bites.

1. SNAKE BITE IN CHILDREN
Presenter: Dr. Ashwini. B. S
Moderator: Dr. Hiremath
Sagar

2. CONTENTS
1. Snakes-
 Classification & Identification
 Venom composition
 Pathophysiology of envenomation
2. Burden of Snake bite
3. Clinical effects and patterns
4. Management-
 First aid
 Clinical assessment
 Labs
 ASV
 Management of different envenomations

4. SNAKES- CLASSIFICATION &
IDENTIFICATION
There are three families of venomous snakes in South East Asia,
1. Elapidae- cobras (Naja), kraits (Bungarus).
2. Viperidae- typical vipers (Viperinae) and pit-vipers
(Crotalinae)
 Russell’s vipers , saw-scaled vipers , Malayan pit viper
3. Hydrophidae- Sea- snakes.

5. ELAPIDAE
Cobras, King cobras and the Kraits
Description: long, thin, uniformly-coloured, large smooth
symmetrical scales on the top of the head.
Cobras: raise the front part of their body off the ground and
spread a hood, the defensive behaviour of the cobras is well known: they
rear up, spread a hood, hiss and make repeated strikes towards the
aggressor.
Kraits: Have alternating colored bands on their dorsum.

6. COMMON SPECTACLED
COBRA

7. Narrow white dorsal bands
Pure white ventrals
COMMON

8. BANDED
KRAIT

9. VIPERIDAE
Description: short, thick-bodied, short-tailed snakes with many
small rough scales on the top of the head.
characteristic patterns of coloured markings on their backs

10. PIT VIPER

11. RUSSELL’S
VIPER

12. SAW SCALED
VIPER

13. HYDROPHIDAE
Flattened Paddle-like tails and many have laterally compressed
bodies that give them an eel-like appearance.
Most have nostrils located dorsally

14. SEA SNAKE

15. SNAKE VENOM
CONTENTS: >100 different proteins: enzymes, non-enzymatic
polypeptide toxins, and non-toxic proteins. Enzymes are digestive
hydrolases, hyaluronidase (spreading factor), yellow L-amino acid
oxidases, phospholipases A2 , and peptidases.
Snake venom metalloproteases (SVMPs): damage basement
membranes, causing endothelial cell damage and spontaneous
systemic bleeding.
Procoagulant enzymes: thrombin-like, splitting fibrinogen, or
activators of factors V, X, prothrombin cause DIC
Phospholipases A2: presynaptic neurotoxic activity, cardiotoxicity,
myotoxicity.
50% OF VENOMOUS SNAKE BITES ARE DRY BITES

16. VENOM GLAND

17. BURDEN OF SNAKE BITE
Only 7.23% snakebite deaths were officially reported (Majumdar,
2014 and Mohapatra 2011).
Mostly in rural areas, and more commonly among males than females
Peak age group 15–29
About 45,900 annual snakebite deaths nationally
An annual age-standardized rate of 4.1/100,000, with higher rates in
rural areas

18. CLINICAL FEATURES
WHEN VENOM IS
INJECTED
WHEN VENOM IS NOT
INJECTED
• fear of consequences of a
real venomous bite
• pins and needles
(paraesthesiae) of the
extremities,
• stiffness or tetany of
their hands and feet and
dizziness.
• vasovagal shock
• highly agitated and
irrational
• Increased HR, Sweating
• Local effects
• Hemotoxicity
• Neurotoxicity
• Myotixicity
• Shock

19. LOCAL SWELLING
Swelling and bruising
increased vascular
permeability and ischemia
by
1.Venom- endopeptidases,
metalloproteinase
hemorrhagins,
2.Thrombosis,
3.Tight tourniquets
4.Swollen muscle within
tight fascial compartments
KOBRA &
VIPERS
SYSTEMIC
BLEEDING & DIC
1. Venom phospholipases
are anticoagulant
2. Platelet
activation/inhibition
and sequestration
3. Zn metalloproteases
hemorrhagins-
Spontaneous systemic
bleeding
4. Elapid- Alternate path-
cobra venom factor
5. Viperidae- Classical
path
VIPERS
Local swelling, bleeding,
blistering, and necrosis.
Pain at bite site
compartment syndrome
Tender enlarged LNs
Visible systemic bleeding
petechiae, purpura
ecchymoses
gastro-intestinal or retro
peritoneal bleeding
Consumption
coagulopathy
IC bleed

22. NEUROTOXICITY
Post synaptic(α)
neurotoxins bind to
acetylcholine
receptors at the
motor endplate.
Presynaptic (β)
neurotoxins are
phospholipases that
damage nerve
endings irreparably
blocking transmission
at the neuromuscular
junction
By prolonging
activity of ACh at
neuromuscular
junctions,
anticholinesterase
drugs may
improve paralytic
symptoms
COBRA &
KRAIT
ONSET: within 30
min– 6 hours in case
of Cobra bite and 6 –
24 hours for Krait
bite
5 Ds – dyspnea,
dysphonia,
dysarthria, diplopia,
dysphagia
2 Ps – ptosis,
paralysis

24. HYPOTENSION
AND SHOCK
1. Vasodilatation
2. Leakage of plasma or
blood into the bitten
limb
3. Massive GI hemorrhage
4. Myocardial damage.
5. Oligopeptides and
vasodilating autacoids
6. DIC and consumption
coagulopathy.
MYOTOXICITY
AND AKI
PLA2 myotoxins and
metalloproteases (sea
snakes)
1. Rhabdomyolysis,
2. Myoglobinaemia,
myoglobinuria and
3. Acute kidney injury.
VIPERS
SEA
SNAKES
Muscle aches,
involuntary contractions
of muscles.
Passage of dark brown
urine.
Compartment syndrome
Cardiac arrhythmias due
to hyperkalaemia
Acute kidney injury due
to myoglobinuria

25. CLINICAL EFFECTS
SYNDROME 1:
Local envenoming (swelling etc) with bleeding/clotting disturbances
= Viperidae (all species)
SYNDROME 2:
Local envenoming (swelling etc) with bleeding/clotting disturbances,
shock or acute kidney injury with conjunctival oedema (chemosis) and
acute pituitary insufficiency = Russell’s viper

26. CLINICAL EFFECTS
SYNDROME 3:
Local envenoming (swelling etc) with paralysis = cobra or king cobra
SYNDROME 4:
Paralysis with minimal or no local envenoming: Bitten on land while
sleeping on the ground with/without abdominal pain = krait

27. CLINICAL EFFECTS
SYNDROME 5:
Paralysis with dark brown urine and acute kidney injury: Bitten on
land (with bleeding/clotting disturbance) = Russell’s viper,

28. LIMITATIONS OF SYNDROMIC
APPROACH
1. The range of activities of a particular venom is very wide.
2. Some elapid venoms, such as those of Asian cobras, can cause
severe local envenoming, formerly thought to be an effect only of
viper venoms.
3. In Sri Lanka and India, Russell’s viper venom causes paralytic signs
(ptosis etc.)

29. COBRA SPIT OPHTHALMIA
If the “spat” venom enters
the eyes, there is immediate
and persistent intense
burning, stinging pain,
followed by profuse
watering of the eyes with
production of whitish
discharge, congested
conjunctivae, spasm and
swelling of the eyelids,
photophobia, clouding of
vision and temporary
blindness.

30. LONG TERM COMPLICATIONS
(SEQUELAE) OF SNAKEBITE
Necrotic areas or amputation: chronic ulceration, infection,
osteomyelitis or arthritis may persist causing severe physical
disability.
Malignant transformation may occur in skin ulcers after a number of
years (Marjolin’s ulcer)
Chronic kidney disease (renal failure) may occur after bilateral cortical
necrosis (Russell’s viper and hump-nosed pit viper bites)
Chronic panhypopituitarism or diabetes insipidus- pituitary
hemmorrhage after Russell’s viper
Chronic neurological deficit is seen in patients who survive
intracranial haemorrhages and thromboses (Viperidae)
Abnormalities of electrophysiological tests can persist for over 12

31. MANAGEMENT OF SNAKE BITE-
STEPS
 First-aid treatment
Transport to hospital after immobilization.
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 & Advising how to avoid
future bites

32. FIRST- AID
"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
envenomate the patient
I = Immobilise 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.
Dry bites of
venomous
snakes- 10-
80%
Avg- 50%
70%- Non
venomous
30%-
Venomous

33. SPLINTIN
G
Remove shoes, rings, watches, jewellery and tight clothing from the bitten
area as they can act as a tourniquet when swelling occurs.

34. DON’T’S
1. Do not attempt to kill or catch the snake as this may be dangerous.
2. Discard traditional first aid methods (black stones, scarification)
and alternative medical/herbal therapy.
3. Do not wash wound and interfere with the bite wound (incisions,
suction, rubbing, tattooing, vigorous cleaning, massage,
application of herbs or chemicals, cryotherapy, cautery)
4. Do NOT apply or inject anti- snake venom (ASV) locally.
5. Do not tie tourniquets as it may cause gangrenous limbs.

35. RAPID PRIMARY CLINICAL
ASSESSMENT AND RESUSCITATION
@ MEDICAL FACILITY
Airway- Patency
Breathing (respiratory movements)
Circulation (arterial pulse)
Disability of the nervous system (level of consciousness)
Exposure and environmental control
The Glasgow Coma Scale cannot be used to assess the level of
consciousness of patients paralysed by neurotoxic venoms
Conventional tests of brain death can prove misleading
Profound
hypotensi
on &
shock
Cardiac
arrest
Terminal
respirator
y failure
Admit all victims of snakebite confirmed or suspected and keep under observation
for 24 hours.

36. TO IDENTIFY IMPENDING
RESPIRATORY FAILURE BEDSIDE
LUNG FUNCTION TEST
1. Single breath count – number of digits counted in one exhalation -
>30 normal
2. Breath holding time – breath held in inspiration – normal > 45 sec
3. Ability to complete one sentence in one breath.
4. Cry in a child whether loud or husky can help in identifying
impending respiratory failure.

37. PRECISE HISTORY
Where- Which part of the body was bitten?
When and How- At what time were you bitten and what were you
doing?
Where is the snake that bit you? – description or a photo
How are you feeling now?- Symptoms.
Night
-
krait
Sea-
sea-
snake
Paddy
field-
Cobra/
viper

38. PHYSICAL EXAMINATION
LOCAL
• Fang mark
• Swelling-
tenderness
• Bleeding at site
• Lymphnodes
• Pulses of
affected limb
• Early signs of
necrosis
VITALS
• HR, RR, SpO2
• BP
• Skin and mucus
membrane
• Muscle
tenderness,
trismus
SYSTEMS
• Abdominal
tenderness/
loin tenderness
• CNS deficits-
above
downwards
including
respiratory
sufficiency
• Lateralizing
signs
Krait
may
leave no
fang
mark
Bleeding
from fang
mark-
Russells
viper

39. SPECIES DIAGNOSIS
BASED ON SCENARIO- HISTORY, CLINICAL PRESENTATION AND ALSO
DESCRIPTON/ PHOTO OF SNAKE.
Since crotalids can
envenomate even
when dead, bringing
the killed snake into
the emergency
department should be
discouraged.

40. INVESTIGATIONS
1. 20WBCT- 20 Minute whole blood clotting time.
Take 2ml venous
blood in a clean,
dry glass vial
Keep it aside
undisturbed for
20mins
Gently tilt to look
for clotting
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-
FALSE NEGATIVE

41. 20WBCT
How often?
If clotted- every 1h from admission for three hours and then 6 hourly
for 24 hours.
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.
In case of doubtful results?
repeat the test in duplicate, including a “control” (blood from a
healthy person)

42. OTHER INVESTIGATIONS
Hematocrit: Capillary leak/ systemic bleed in viper bite.
Platelet count: Falls in consumptive coagulopathy.
Neutophilic leukocytosis: evidence of systemic envenoming.
Peripheral smear: fragmented RBCs- schistocytes- HUS (induced by
snake venom)
Blood urea and S. Creatinine: Deranged in AKI
AST and CPK elevated: Rhabdomyolysis
PT/ INR: Deranged in hemotoxic snake bite
Urine: Hematuria and hemoglobinuria- AKI/ Rhabdomyolysis.

43. OTHER INVESTIGATIONS
CXR- Pulmonary edema
ECHO- Cardiac function
ECG- Hyperkalemia/ arrhythmia
USG- DVT
CT/MRI Brain- IC bleed/ Infarct/ Pituitary shrinkage

44. ANTI- SNAKE VENOM (ASV)
Immunoglobulin [usually pepsin-refined F(ab’)2 fragments of whole
IgG] purified from plasma of horses or sheep- hyperimmunised with
venoms of one (to make monospecific antivenom) or more (to make
poly-specific antivenom) species of snake
Indian “polyvalent anti-snake venom serum” is made against the “BIG
FOUR”
1. Spectacled cobra (N. naja);
2. Common krait (B. caeruleus),
3. Russell’s viper (D. russelii),
4. Saw-scaled viper (E. carinatus)

45. WHEN TO GIVE ASV
Systemic envenoming: haemostatic abnormalities [spontaneous systemic
bleeding, coagulopathy (+ve non-clotting 20WBCT, INR >1.2, or
prothrombin time >4-5 seconds longer than control), or thrombocytopenia.
Neurotoxicity bilateral ptosis, external ophthalmoplegia, paralysis.
Cardiovascular abnormalities hypotension, shock, cardiac arrhythmia,
abnormal ECG
Acute kidney injury
Generalized rhabdomyolysis
Local envenoming: local swelling involving more than half bitten limb (in
absence of tourniquet) within 48 hr of the bite; swelling after bites on digits;
rapid extension of swelling beyond wrist/ankle within few hours of bites on
hand/foot); enlarged tender lymph node draining bitten limb
There are no absolute contraindications to
ASV.

47. HOW TO GIVE ASV?
1. ASV supplied in dry powder form has to be reconstituted by
diluting in 10 ml of distilled water/normal saline. Mixing is done by
swirling and not by vigorous shaking. 10 vials= 100ml diluted in 5-
10 ml/kg of normal saline NS to give as a slow drip.
2. ASV should be given only by the IV route, and should be given
slowly.
3. Physician at the bed side during the initial period to intervene
immediately at the first sign of any reaction.
4. 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)
5. Epinephrine (adrenaline) should always be drawn up in readiness
Never give ASV as IM injection

48. HOW MUCH ASV TO GIVE?
Neuroparalytic snakebite – ASV 10 vials stat as infusion over 60
minutes followed by 2nd dose of 10 vials after 1 hour if no
improvement within 1st hour. (MAX=20vials)
Vasculotoxic snakebite - once the 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. This
reflects the period the liver requires to restore clotting factors.

49. HOW MUCH ASV IT TAKES TO
NEUTRALIZE?
The range of venom injected is 5 mg-147 mg.
The total required dose range between 10 and 30 vials as each vial
neutralizes 6 mg of Russell’s Viper venom.

50. ASV REACTIONS
Early anaphylactic reactions: 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.
Skin/conjunctival hypersensitivity testing does not reliably predict early or late
antisnake venom reactions and is not recommended.

51. PYROGENIC (ENDOTOXIN)
REACTIONS:
1. Usually develop 1-2 hours after treatment.
2. Symptoms include shaking chills (rigors), fever, vasodilatation and
a fall in blood pressure.
3. These reactions are caused by contamination of the ASV with
pyrogens during the manufacturing process.

52. LATE (SERUM SICKNESS TYPE)
REACTIONS:
1. Develop 1-12 (mean 7) days after treatment.
2. Clinical features include fever, nausea, vomiting, diarrhoea,
itching,
3. Recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
periarticular swellings,
4. Mononeuritis multiplex, proteinuria with immune complex
nephritis and rarely encephalopathy
Mx
Inj. Chlorpheniramine 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 0.7 mg/kg/day in divided doses.

53. MONITORING
1. 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.
2. Epinephrine premedication is not given as routine
3. However, epinephrine should be kept handy

54. MANAGEMENT OF REACTION TO
ASV
1. Stop ASV temporarily
2. Oxygen
3. Start fresh IV normal saline infusion with a new IV set
4. 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.
5. Administer Chlorpheniramine maleate (adult dose 10 mg, in children 0.2
mg/kg) intravenously.
6. Role of Hydrocortisone in managing ASV reaction is not proved.
7. Once the patient has recovered, re-start ASV slowly for 10-15 minutes
keeping the patient under close observation. Then resume normal drip
rate.

55. NEUROTOXIC ENVENOMATION
1. Oxygen
2. Assisted ventilation
3. Administer ‘Atropine Neostigmine (AN)
4. 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
5. A fixed dose combination of Neostigmine and glycopyrolate IV can
also be used
6. Thereafter - tapering dose at 1 hour, 2 hour, 6 hours and 12 hour.
7. Majority of patients improve within first 5 doses
8. Positive response to “AN” trial is measured as 50% or more
recovery of the ptosis in one hour.
ADULT DOSE
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.

56. Stop Atropine neostigmine (AN) dosage schedule if:
1. Patient has complete recovery from neuroparalysis. Rarely patient
can have recurrence, carefully watch patients for recurrence.
2. Patient shows side effects in the form of fasciculations or
bradycardia.
3. If there is no improvement after 3 doses.
Improvement indicates- Cobra bite or Nilgiri Russel’s viper bites.
No improvement after 3 doses indicates probable Krait bite.
Krait affects pre-synaptic fibres where calcium ion acts as
neurotransmitter.
Give Inj. Calcium gluconate 10ml IV (in children 1-2 ml/kg (1:1
dilution) slowly over 5-10 min every 6 hourly and continue till
neuroparalysis recovers which may last for 5-7 days.
Give one dose of “AN” injection before transferring to the
higher centre.

57. MANAGEMENT OF VASCULOTOXIC
SNAKEBITE
1. Strict bed rest to avoid even minor trauma
2. Screen for hematuria, hemoglobinuria, myoglobinuria
3. Closely monitor urine output and maintain 1 ml/kg/h urine output
4. Volume Replacement – If the patient has intravascular volume
depletion
5. 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).
6. If there is no response to furosemide discontinue FAD and refer
patient immediately to a higher center for dialysis.

58. MANAGEMENT OF SEVERE LOCAL
ENVENOMING
1. Tetanus toxoid
2. Inj. Amoxiciilin clavulanic acid/ Inj Ceftriaxone + Inj.
Metronidazole (Broad spectrum)
3. Clean the bitten site with povidone-iodine solution, but do not
apply any dressings.
4. Leave blisters alone
5. Limb elevation
6. Pain management
7. Debridement of necrotic tissue

59. COMPARTMENTAL SYNDROME
Clinical features of a compartmental
syndrome - 5 ‘P’
• Pain (severe)
• Pallor
• Paraesthesia
• Pulselessness
• Paralysis or weakness of compartment
muscle.
confirmed by vascular Doppler and rising
CPK in thousands.
Intra-compartmental
pressure >40 mmHg
of normal saline (in
adults). Measured by
Inserting a 16 no.
needle in the
suspected
compartment at a
depth of 1 cm and
connect to a simple
tubing irrigated with
normal saline.

60. CRITERIA FOR FASCIOTOMY IN
SNAKEBITE LIMB
• Haemostatic abnormalities have been corrected
• Clinical evidence of an intracompartmental syndrome
• Intra-compartmental pressure >40 mmHg of normal saline (in
adults).
• This can be confirmed by vascular Doppler and rising CPK in
thousands. Timely fasciotomy decreases the need for repeated
dialysis.

61. REFERENCES
1. Management of snake bite, quick reference guide, january 2016,
ministry of health & family welfare government of india.
2. Guidelines for the management of snakebites, 2nd edition, WHO,
regional office for south-east asia.
3. The Pediatric Management of Snakebite: The National Protocol,
Indian Pediatrics 2007; 44:173-176