The presentation lecture was given in IST online platform on 15 June 2021

1. Dr.Venugopalan P P , Sr.Consultant & Director ,EM - Aster India- 15th June 2021@Indian Society of Toxicology(IST)
KraitEnvenomation
Clinical Presentation & Management

2. Background

3. Snakebite
Snake-bite poisoning is an occupational hazard
Common accident reported in tropical and subtropical countries
Lack of knowledge, improper training regarding early reorganisation of
venomous snake bites and rapid intervention may add to mortality and morbidity.
Prone for snake bite
Farmers, villagers, labourers, hunters, trekkers, snake rescuers,
Migrating population like shepherds,
Scientists working with snakes for milking
Persons who take care of snakes in snake parks
Background

4. More than 20,00,000 snake bite incidences are reported in India and of these >46,900
people die each year, which means that every hour 5 patients lose their lives to snake
bites
More than the 3,000 known species of snakes, only about 300 are venomous and
there are about 216 species of snakes identifiable in India, of which 52 are known to
be poisonous
“Snake bite is a life threatening medical
emergency & time limited which must be
treated in a window period”

5. Krait - about the snake

7. Krait
Bungarus species
Generally nocturnal snakes
Symptomatology is similar to the cobra's
neurotoxic effects
Without local symptoms (ie. necrosis,
bleeding)
Symptoms of envenomation include
drowsiness, neurologic/neuromuscular
manifestations, and abdominal pain
Proximal limb paralysis, ventilatory
failure and/or coma can ensue rapidly

8. Krait
About snake
Averages about 90 cm in length
with males growing longer than
females.
1.5 m specimens are not
unheard of
South India, mating occurs in
December and females lay
between 5-15 eggs in February
Young appear in April

9. Krait
About snake
Krait - tiny ballpoint pen refill thick
hatchlings are brilliantly marked.
They often have a collar around
their necks that fades along with
many of the anterior bands as they
grow older.
Not much is known about what
they might eat at this size
They eat a large number of
insects, worm snakes, and
hatchling lizards

10. Krait
The common krait is regarded as the
most dangerous species of venomous
snake in the Indian subcontinent
Most bites occur during the cooler months
of June to December, when snakes may,
during the course of their hunting activity
Linger on a person’s bedding to take
advantage of the warmth

11. Venom

12. Snakevenom
Most snakes inject 10% of the available venom in single strike except Russell’s
viper injects 75% of stored venom in one bite due to big long sharp curved fangs
Snake venom is a cocktail of 20 or more
components including proteins, enzymes, non-
enzymatic polypeptide toxins, non-toxic nerve
growth factors, hyaluronidase, metals, lipids, free
amino acids, nucleotides carbohydrates, biogenic
amines and various activators and inactivates of
physiological processes.
Venom from both types contains acetylcholine
esterase, phospholipase B and glycerophosphatase

13. Kraitvenom
Krait venom is ten times more lethal than the cobra
Victim report too late due to delayed clinical manifestations.
Krait is nocturnal in habit
Its fangs are small size like that of a 24-
size needle
It injects the venom deep into the skin
Though the venom is of small molecular
size, it is absorbed slowly as skin has poor
circulation
Reflexes are blunted during sleep.
Beta bungarotoxin in the krait venom
bears similarity to botulinum toxin.
Common Indian Krait venom contains
both presynaptic beta bungarotoxin and
alfa bungarotoxin.

14. KraitToxin
What happen exactly ?
Toxins affecting the presynaptic
junction Beta-bungarotoxin (krait)
Toxins have phospholipase A2
activity and are called SPANS
(snake presynaptic phospholipase
A2 neurotoxins)
Catalyze the hydrolysis of
phosphatidylcholine, a major
component of the plasma membrane
Hydrolysis forms lysophosphatides
and releasing both saturated and
unsaturated fatty acids

15. KraitToxin
How does it acts ?
The exact mechanism of toxicity is
undefined
Hydrolysis of these phospholipids
leads to massive release of synaptic
vesicles
Fusion of synaptic vesicles with the
presynaptic membrane is induced,
followed by inhibited reformation of
the vesicles after exocytosis
Further neurotransmitter release is
prevented

16. KraitToxin
What are the additional Risk
Poisoned nerve terminals show an
absence of vesicles , which
causes delayed degeneration of
the motor nerve terminals
Recovery requires nerve terminal
regeneration, a process that may
take weeks.
The presynaptic neurotoxins also
possess myotoxic activity
Lead to degeneration of skeletal
muscle and death from acute renal
failure.

17. Othersnakewithpresynaptictoxins
SPANS
Notexin (tiger snake)
Taipoxin (Taipan)
Crotoxin (Brazilian rattlesnake)

18. Kraitvenom
A. The toxins initially release
acetylcholine at the nerve
endings at the neuromuscular
junction
B. Then damage it subsequently
preventing the release of
acetylcholine
C. Finally receptors are damaged
and destroyed
D. Causes resistance to anti-
cholinesterase.
What we need to understand ?
Initial release of acetylcholine
results in autonomic nerve
stimulation plus Release of
cholecystokinin
Two chemicals causes krait
bite symptoms
Acute abdominal pain, vomiting,
staring look, blurring of vision,
gooseflesh, salivation,
hypertension, pulmonary oedema

19. Clinical presentation

20. Kraitenvenomation
Neuro/ Neuromuscular symptoms
Ptosis
Glossopharyngeal
palsy (dysphagia)
Ophthalmoplegia
Strabismus
Blurring vision
Pupils dilated

21. Krait
Neuro/Neuromuscular symptoms
Proximal limb paralysis
Intercostal &
diaphragmatic paralysis
(respiratory failure)
Increased oral secretion
Ataxia
Headache

22. Krait
Neuro/Neuromuscular symptoms
Drowsiness
Coma
Facial paralysis
(Malayan kraits)
Decreased tendon
reflexes (Malayan
kraits)

23. Krait
General symptoms
These symptoms typically
manifest within one to three hours
Though for Kraits it can be up to
12 hours following the bite.
Abdominal pain is usually
moderate to severe and confined
to the epigastrium, but can be
generalized.
Diffuse muscle tenderness rarely
occurs

24. Krait
Haematology
One may expect a
polymorph leucocytosis
Ranging up to
22x103 WBC with 90%
polys

25. Krait
Cardiotoxicity
A small amount of
cardiotoxin is present in
Indian Krait snake venom
Usually do not cause much
heart manifestations.
A transient (5-15 minutes)
decrease in arterial pressure
without further changes has
been reported.

26. Krait
Local Symptoms
Rarely if ever does local
tissue destruction and
necrosis appear
One can find minimal edema
and pain at the bite site

27. Krait
Fang marks
May be present as one or more well defined
punctures
A series of small lacerations or scratches
There may not be any noticeable or obvious
markings where the bite occurred
The absence of fang marks does not
preclude the possibility of a bite
(especially if a juvenile snake is involved)

28. Krait
Fang marks
In general, the fang marks from a Krait are
made from a quick, snapping motion.
Multiple bites inflicted by a single snake or
by more than one snake are also possible
The presence of fang marks does not
always imply that the injection or
deposition of venom into the bite wound
(envenomation) actually occurred

29. Kraitbitepattern
Important Observations

30. Kraitbitepattern
Important Observations

31. Kraitbitepattern
Important Observations

32. Kraitbitepattern
Important Observations

33. Practical points

34. Kraitbite
Few practical points
Because of negligible or absent local
manifestations
• Envenomation is neglected
• Falsely initially attributed to ant or rat bite or
no bite at all
The venom stimulates the autonomic
nervous system within 20 to 30 minutes of
the bite
Clinical effects are seen within 30 minutes or
sometimes too late in around 18 hours

35. Kraitbite
Few practical points
A. The victim wakes up to transient
abdominal colicky pain, vomiting (once
or twice), and chest pain
B. Relatives and even an inexperienced doctor
could neglect these vital symptoms
C. Attributing them to indigestion or
acidity or an acute appendicitis or ACS
D. Minimum T wave inversion due to hypoxia
E. Pts may get admitted wrongly in
Cororanary Care Unit

36. Kraitbite
Few practical points
1.The tissues having a high
concentration of acetylcholine
receptors are affected earlier.
2.Sphincter pupillae, Elevator palpebral
superior, Neck muscles, Bulbar and
Limbs are affected initially
3.Diaphragm and Intercostal muscles are
affected last in the sequence

37. Kraitbite
Few practical points
1.Quadriplegia with aphasia and dilated pupils
may be diagnosed as Brain death or Locked
in syndrome [pseudo coma] or GB
syndrome.
2.Venom-induced paralysis of pupillary muscle
resulting in non-reacting pupils, but this is
not the sign of irreversible brain damage.
3.After recovery, few patients have signs and
symptoms of peripheral neuropathy.
4.Many times, patients succumb to iatrogenic
respiratory infection or adult respiratory
distress syndrome
Broken neck
sign
Locked in
syndrome
Ptosis

38. Kraitbite
Few practical points
At times, krait-bite victims
even bring the killed snake
but do not develop any clinical
manifestations, local fangs
marks without urticaria,
indicated bite without
envenomation or “Dry bite”

39. Kraitbite
Few practical points
An inexperienced treating doctor may
diagnose a krait bite envenoming even if a
patient brings a specimen of wolf snake
To confirm or identify the venomous krait
it is best to look at the tail which is covered by
white bands till its end. This feature is absent
in wolf snake - a non-venomous species which
apparently looks like krait
Krait
Wolf snake

40. Krait bite : First Aid

41. Krait
•Reassure the patient as around 70% of all snake
bites are from non-venomous species
•Immobilize the limb in the same way as a fractured
limb
•Recovery position (prone, on the left side)
•Protect airway to minimize the risk of aspiration of
vomitus
First aid in any snake bite
Apply splint extending to the entire length of the limb, immobilizing all of the joints of the limb

42. Krait
•Use any rigid object as a splint
e.g. spade, piece of wood or tree
branch, rolled up newspapers etc
•Do NOT block the blood supply
•Don't apply pressure
First aid in any snake bite

43. Kraitbite
•Nil by mouth till victim reaches a medical
health facility
•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
•Vehicle ambulance (toll free no. 102/108/etc.)
•Boat, bicycle, motorbike, stretcher etc can be
used
First Aid in any snake bite

44. KraitBite
Motorbike may be a feasible
alternative for rural India where no other
transport is available but third person
must sit behind the patient.
Victim must not run or drive himself
to reach a Health facility
First aid in any Snake bite

45. Kraitbite
•Remove shoes, rings, watches,
jewellary and tight clothing from
the bitten area
•It can act as a tourniquet when
swelling occurs
•Leave the blisters undisturbed.
First aid in any snake bite
Inform the doctor if progress of swelling, ptosis or new symptoms that manifest on the
way to hospital.

46. Kraitbite:Management
1.If one succeeds to locate the bite site, the surface-
deposited venom should be removed by a clean cloth
or cotton.
2.The bitten part should be kept below heart level
3.Elastic-Crepe bandage should be used from the
distal end of the bite site with the right amount of
pressure so that one can easily put and remove the
finger from underneath the bandage
First Aid

47. Kraitbite:Management
1.The crepe bandage carries no benefit if the
victim cannot reach the hospital within 30
minutes, and a delay of more than 4 hours is
expected.
2.The victim should not be allowed to walk.
3.Mouth-to-mouth / Artificial ventilation
should be started if the victim is in
respiratory arrest
First Aid

49. Kraitbite
Whenever possible medical officer can accompany
with patient
1.To know the progress,manifestation of the new
symptoms(such as progress of swelling, ptosis or new
symptoms)
2.Management of respiratory arrest
3.Management and treatment of shock
4.Cardiopulmonary resuscitation (CPR)
When referring to a higher center

50. Krait bite : Hospital
Mangement

51. Hospitallevelmanagement
Emergency Room
1.Collect details and patient history, and
patient activity at the time of the bite
2.Initial clinical signs such as bulbar palsy,
muscle power, tendon reflexes, respiratory
rate, oxygen saturation, one-minute
counting, pooling of saliva, broken neck
sign should be noted in detail.
3.Blood pressure and ECG changes should
be monitored
4.WBCT-20 , Baseline RFT, LFT , ABG,
Coagulation profile
A
C
B
D
E
Assess & Manage Airway
OPA,NPA, Head tilt , Chin
lift ,Suction, Intubation
Assess & Manage
Breathing ,Oxygenation ,
Mechanical ventilation
Assess & Manage circulation
IV line , Fliuds ,Monitors , Labs
and tests
Assess & Manage Disability
Neurological status, Muscle
power , GCS ???
Assess & Manage
Exposure , Bite mark

52. Krait
Airway and Ventilation
• Endotracheal intubation
• To buy time - LMA , Combitube ,
Kings airway

53. Kraitbite
Bedside tests
Peak flow meter in patients (adolescents
and adults) presenting with neuroparalytic
syndrome
Peak flow meter is not available in PHC
then assess respiratory function using
bedside tests -
A. Single breath count
B. Breath holding time
C. Ability to complete one sentence

54. Kraitbite
Emergency room
Glasgow Coma scale cannot be used
to assess the level of consciousness
of patients paralyzed by neurotoxic
venom
“Arterial blood gases and urine examination should be repeated at frequent intervals
during the acute phase to assess progressive systemic toxicity”

55. Krait
Antidotes
• Prevention
• Pharmacological-
Physiological - Drugs ?
Neostigmine /Atropine
• Immunological - Anti-venom
• Mechanical : Ventilator

56. Kraitbite
Emergency management
1.Serum electrolytes and renal profiling
should be done every few hours till
clinical improvement is seen.
2.On arrival 100 ml (10 vials) of anti-
snake venom (ASV) should be added
to 200 cc of normal saline and should
be run over 30 to 50 minutes.
3.One should sit by the side of the victim
for early diagnosis and treatment of
anaphylaxis.
4. Crash cart and Loaded adrenaline
is a good practice

57. ASV Concerns

58. Kraitbite
Repetition of ASV
Within 30 minutes after the initial dose
of ASV, if there is no improvement of
neurological manifestations, one can
repeat dose of ASV
Maximum dose : Not more than a
total of 20 vials of ASV
ASV only neutralizes circulating
venom and it has no action once the
venom is attached to the receptor
site

59. Krait
ASV repetition
In krait bite there is a destruction of
receptors, thus neurological
manifestations may persist for weeks
till there is a regeneration of
receptors.
At this stage administration of ASV
is merely a waste
No contraindication to give ASV for pregnant and
lactating mother
Children - Same dose as in adults

60. 10generalrules
1.ASV is indicated i.e. signs and symptoms of envenomation with or without
evidence of laboratory tests, administer FULL dose without any delay.
2.Do NOT wait for any test report
3.History of Bite; known or unknown, if there is spontaneous abnormal bleeding
beyond 20 minutes from time of bite, start ASV, Do NOT wait for 20 WBCT
report
4.No absolute contraindications to ASV
5. Do not routinely administer ASV to any patient claiming to have bitten by a
snake
ASV administration

61. 10generalrules
6.Do not delay or withhold ASV on the grounds of anaphylactic reaction to a
deserving case
7. Do NOT give incomplete dose.
8. Local swelling, accompanied by a bite mark from an apparently venomous
snake, is not an indication for administering ASV.
9. Swelling, a number of hours old is also not an indication for giving ASV
10. Rapid development of swelling indicates bite with envenoming requiring
ASV.
ASV administration

62. ASV reactions

82. Atropin -Neostigmine
AN

90. Krait bite

91. Krait
Acetyl choline inhibitors ?
Indian common krait venom
contains both pre- and post-
synaptic blockers.
?? Whether the victim responds to
AChI or not can be confirmed by
placing an ice-filled glove finger
over the eyelids.
Hypothermia sensitises the AChl
receptors of acetylcholine. If there
is a slight improvement in ptosis
one can try AChI???
Expert opinion

92. Critical Care Management

93. Krait
Clinical signs to initiate Ventilation
•Pooling of saliva in the victim is
noticed
•Unable to lift the neck from
the pillow
•Reduction in SpO2 saturation
•Respiratory failure is noticed
•Abdominal-thoracic respiration
occurs
•Signs of hypoxia
•Signs of Carbon dioxide retention
The last to recover is ptosis and the proximal muscles of lower limbs.

94. Respiratoryfailurein
Kraitbite
A ventilator is the “mechanical
antidote” for Krait venom

95. Krait
Severe uncontrolled hypertension
This is attributed to the blocked
presynaptic receptors and unblocked
post-synaptic receptors which
release epinephrine into circulation
At times the victim may land up with acute
myocardial failure with pulmonary oedema
Need intravenous nitroglycerine drip and
BIPAP ventilation
Severe hypertension with tachycardia and
pulmonary oedema recover with
nitroglycerine drip
Non-invasive ventilation

96. Nut shell

100. Thanks a lot …