Prepared by Henry Edward and Liberatus Makenge.(MD4 students)

1. Prepared by:-
Liberatus Makenge MD4
Henry Edward MD4
Snakebites

2. • A snakebite is an injury caused by the bite of a
snake. It often results in two puncture wounds
from the animal's fangs. Sometimes poisoning
from the bite may occur.
• The number of snakebites that occur each year
may be as high as five million. They result in
about 2.5 million poisonings and 20,000 to
125,000 deaths. The frequency of bites varies
greatly among different parts of the world. They
occur most commonly in Africa, Asia, and Latin
America,with rural areas more greatly affected

3. Epidemiology
• 25% are dry bites
• 25-75% of stored venom may be discharged in
a bite
• Replenished in 3 to 4 weeks
• Extremities are most common bite site
• Most common victims:
–Intoxicated males age 15-40yrs.
–Snake handlers and collectors.

4. • In Africa approximately 60% of all bites are
caused by vipers alone. In drier regions of the
continent, the saw-scaled vipers inflict up to 90%
of all bites.
• The puff adder is responsible for the most
fatalities overall,
• The black mamba, although responsible for far
less snakebite incidents, is the species which has
the highest mortality rate in Africa and in the
world.

5. Poisonous snakes
Elapidae
Cobra, Black Mamba,
Kraits. Neurotoxic
Viperidae
(Vipers)
Russell’s Vipers.,
Saw scaled Vipers.,
Pit Vipers.
Haemotoxic
Hydrophidae Sea Snakes
Myotoxic

6. Krait Pit Viper
Cobra
Puff Adda

7. BLACK MAMBA

8. Biochemical composition of Snake
Venoms
• Dried snake venom contains mainly proteins (70-
90%) and small amounts of metals, amino acids,
peptides, nucleotides, carbohydrates, lipids and
biogenic amines
• The protein components include enzymes and
non-enzymatic proteins/polypeptides
• The main toxins in the venoms of elapid snakes
(cobras, kraits and sea snakes) include:
polypeptide postsynaptic neurotoxins,
cardiotoxins and phospholipases A that may
exhibit presynaptic neurotoxicity or myotoxicity

9. • The main toxins of crotalid (pit viper) snake
venoms, on the other hand, are thrombin-like
enzymes, hemorrhagic proteases and platelet-
aggregation inducers

10. Effects of envenomation
• Local effects
• Systemic effects:
- Neurotoxic.
- Haemotoxic.
- Haemotoxic.

11. Local effects
Local necrosis
Increased
vascular
permeability
Swelling and
bruising.
Myotoxins and
cytotoxins
Ischemia/
thrombosis
Venom
ophthalmia

12. Pit Viper Venom Poisoning
(Viperidae)
• The venom of pit vipers causes local swelling,
necrosis and systemic bleeding. Hemorrhage is
the outstanding symptom of systemic pit viper
poisoning
• Clotting defect usually accompanies hemorrhage.
The commonest and earliest hemorrhagic
manifestation is hemoptysis, which may be seen
as early as 20 minutes after the bite
• Bleeding from the gum is less common and
follows later after the bite

13. • Discoid ecchymoses appear in the skin an hour
or so later
• Bleeding into the brain or other vital organ
may be fatal.
• In severe cases, loss of blood may lead to
hypovolemic shock
• In pit viper bite, the clotting defect is
primarily due to thrombocytopenia
aggravated by defibrination syndrome

14. Systemic effects
• Elapid venoms (cobras, kraits and sea snakes)
generally exhibit neurotoxicity and
cardiotoxicity
• The earliest symptom of systemic elapid
poisoning is a feeling of drowsiness or
intoxication, which starts from 15 min to 5 hr
after cobra bites

15. • Difficulty in opening the eyes (bilateral ptosis:
eyelids may remain completely closed though
the patient usually remains conscious until
respiratory failure is advanced), speaking,
opening the mouth, moving the lips and in
swallowing follows within 1 to 4 hrs
• Breathing becomes increasingly difficult. In
severe poisoning, respiratory failure sets in
rapidly

16. Neurotoxicity
Neurotoxins block
transmission at the
NM junction
Flaccid/Respiratory
paralysis
Anticholinesterase
drugs
Unphysiologic
drowsiness

17. • The neurotoxic effects are mainly at the
postsynaptic level of the neuromuscular
junction where the neurotoxins block
acetylcholine receptors, thereby producing
muscular paralysis and respiratory failure
• The major neurotoxins are usually basic
polypeptides

18. cardiotoxicity
• Cardiotoxicity is caused by polypeptide
cardiotoxin that affects both excitable and
non-excitable cells, causing irreversible
depolarization of the cell membrane and
consequently impairing the structure and
function of various cells, thus contributing to
muscle paralysis and leading to circulatory and
respiratory failure and systolic arrest

19. • Cobra venom also causes extensive local necrosis,
which requires treatment
• The local necrosis is presumably caused by the
combine action of cardiotoxin and phospholipase
A2
• Sea snake venoms contain both polypeptide
neurotoxins (homologous to elapid neurotoxins)
and myotoxins, which are basic phospholipase A2.
• The venom causes respiratory failure (neurotoxic
effect), myonecrosis, myoglobinemia and acute
renal failure

20. Renal failure/rhabdomyolysis
ATN: hypotension/hypovolemia,
DIC, direct toxic effect on tubules,
hemoglobinuria, myoglobinuria
Generalized rhabdo: Release of
myoglobin, muscle enzymes, uric
acid, K (presynaptic neurotoxins)

21. Hypotension/shock
Vasodilation
Direct action of
venom on myocardium
Bleeding/hypovolemia
Vipers: profound
hypotension within
minutes (ACE
inhibitors)

22. Haemotoxin effect

23. • Defibrination syndrome is due mainly to the
action of ancrod and partly to the activation of
fibrinolysis causing fibrinogenolysis.
• Ancrod is a thrombin-like enzyme that acts
directly on fibrinogen, releasing only
fibrinopeptide A and fibrin monomers that
form microclots.
• The microclots formed are easily lysed by
plasmin digestion.

24. • Thus, ancrod causes continual
microcoagulation of fibronogen but the
microclots are virtually simultaneously lysed.
• In the presence of sufficient amount of
ancrod, the rate of consumption of fibrinogen
may exceeed its rate of synthesis in the liver,
resulting in defibrination syndrome
characterized by non-clotting blood.

25. • Thrombocytopenia is presumably due to the
actions of platelet aggregation inducers.
• Aggregoserpentin, a non-enzymatic protein
with molecular weight of 28160 has been
purified, it activates platelets through the
activation of endogenous phospholipase A2 or
C.
• Anti-platelet protease may be also be
involved.

26. • Hemorrhage is presumably due to the action
of some metalloproteases that cause damage
to vascular endothelium.
• L-amino acid oxidases and platelet
aggregation inhibitor may also play a role in
the hemorrhagic action of the venom.

27. Coagulopathy
Procoagulants and
anticoagulants
Intravascular coagulation,
consumption coagulopahty
 Thrombocytopenia
Bleeding from old and
recent wounds, gingiva,
epistaxis, hematemesis,
melena

29. DIAGNOSIS OF SNAKE BITE
• FANG MARKS: classically, two puncture
wounds separated by a distance varying from
8mm to 4cm, depending on the species
involved.
• However a side swipe may produce only a
single puncture, while multiple bites could
result in numerous fang marks.

31. Evidence of systemic
envenomation
• CT> 10 MINUTES
• Bleeding manifestations
• Oliguria /haematuria
• Hypotension
• Ptosis
• Circumoral paraesthesia
• Aphonia/Dysarthria

32. Investigations
• Blood grouping
• Hb, elevated PCV
• TC-leucocytosis
• Platelet count- thrombocytopenia
• Peripheral smear – Haemolysis
• BT,CT(20 min)
• Prolonged PT ,aPTT
• BUN
• Serum Electrolytes- hyperkalemia
• Urine Routine-haematuria
• Metabolic /resp acidosis

33. General Snakebite Management
• Calm and reassure the patient.
• Secure and maintain airway
• Do not delay treatment for any first aid/treatment measure or
wait for signs of envenomation to occur.
• Obtain vital signs including O2 saturation
• Oxygen to keep saturation > 90% (method as best tolerated by
patient)
• Remove ALL watches, rings, and jewelry (not just from
affected limb)
• If bite on extremity, immobilize affected extremity at or below
the level of the heart (make sure any immobilization device
and practice does not result in becoming a tourniquet over
time due to swelling)
• Mark the proximal edge of any discoloration or swelling in ink
and write the time on the line (if signs increase during
transport, make new marks with the times)

34. .
ANTIVENOM
• Monospecific (monovalent) antivenoms are more
effective and less likely to cause reactions than
polyspecific (polyvalent) antivenoms.
• Give I/m Epinephrine or I/v chlorpheniramine if allergic
reaction occurs. It rapidly reverses the uncomfortable
flushing and itching as well as the more serious
problem with breathing and dangerous drop in BP.
• Give monovalent if the species of snake is known.
Give polyvalent antivenom if the species is not known.
Follow the directions given on the antivenom
preparation. The dose for children is the same as for
adults.

35. Anti snake venom (Asv)

36. How to give asv ?
• Initial dose: 4-6 vials, dependent upon
patient response. Treatment should begin
within 6 hours of snakebite; monitor for 1
hour following infusion. Repeat with an
additional 4-6 vials if control is not achieved
with initial dose. Continue to treat with 4-6
vial doses until complete arrest of local
manifestations, coagulation tests and systemic
signs are normal. Monitor closely.

37. .Maintenance dose:
• Once control is achieved, administer 2 vials
every 6 hours for up to 18 hours. Optimal
dosing past 18 hours has not been
established; however, treatment may be
continued if deemed necessary based on the
patient’s condition.
• Administer I.V. over 60 minutes at a rate of 25-
50 mL/hour for the first 10 minutes. If no
allergic reaction is observed, increase rate to
250 mL/hour. Monitor closely.

38. Antivenom reactions

40. OTHER TREATMENT
• Surgical opinion
Seek surgical opinion if there is severe swelling
in a limb, if it has palsy or painful or there is
local necrosis.

41. Surgical care will include:-
• Excision of diced tissue from wound
• Incision of facial membranes to relieve
pressure in limb compartments if necessary.
• Skin grafting, If extensive necrosis.
• Tracheotomy (or endotracheal intubation)if
paralysis of muscles involved in swallowing
occur.

42. Monitoring
• Level of consiousness
• Pulse, BP, Resp rate,Capillary refill time
• Clotting time 1/2hr -1hourly
• Urine output
• Muscle weakness

43. Supportive care
• Give fluid orally or by NGT tube according to daily
requirements. keep a close record of fluid intake and
output.
• Provide adequate pain relief
• Elevate limb if swollen.
• Give anti-tetanus prophylaxis.
• Antibiotic treatment is not required unless there is
tissue necrosis at wound site.
• Avoid intramuscular injection.
• Monitor very closely immediately after admission
then hourly for at least 24hrs.

44. Initiate immediate supportive care:
 Secure & maintain airway
 Prepare for immediate transport (do not delay transport for any first aid/treatment
measures or wait for signs of envenomation to occur)
 Calm and reassure the patient
 Obtain vital signs including O2 saturation
 O2 to keep saturation >90% (method as best tolerated by patient)
 Do NOT apply any constricting bands, ice or apply suction to the bite (if
constricting band is in place upon EMS arrival, contact Medical Direction)
Use standing order on patients with complaints of a snake bite or signs/symptoms of
envenomation:
 Local edema, redness, pain, burning sensation, numbness/tingling,
vomiting, weakness and/or hypotension
 Remove ALL watches, rings, and jewelry
Not just from affected limb
 If bite on extremity, immobilize affected
extremity at or below the heart level. Make
sure any immobilization device and practice does
not result in becoming a tourniquet over time due
to swelling.
 Mark the proximal edge of any
discoloration or swelling in ink and write
the time on the line. If signs increase during
transport, make new marks with the times.
 Initiate IV Normal Saline in unaffected
extremity to maintain adequate
peripheral perfusion:
o 20cc/kg bolus
o Reassess patient after each
bolus
 Contact Medical Direction for any
questions, signs/symptoms of allergic
reaction, or deterioration in patient
condition.
SNAKE BITE STANDING ORDER
I
N
C
L
U
S
I
O
N
O
R
D
E
R
S
Special Notes:
1.) There is no need to bring the
snake to the hospital. This practice
actually increases the risk of
secondary bites and can delay
transport. In Arizona all rattle snakes
use the same antivenin. There is no
antivenin for Arizona coral snakes.
2.) Clinical effects of snakebites
range from mild local reactions to
life-threatening systemic reactions,
depending on the species and size of
the snake involved; the location of
the bite(s); the volume of venom
injected; and the age, size, and health
of the victim. Children are more
likely to suffer significant morbidity
and mortality because they receive a
larger envenomation relative to body
size.

45. Remember
• Do NOT use ice or cold packs. It does not slow
the enzyme activity. It slows the immune-
response.

46. .• DO NOT use tourniquets or restricting bands.
All you do is localize all those digestive
enzymes.

47. .• DO NOT lance, or use cut and suck methods.
Snakebite is an IM injection. The venom isn’t
going to be sucked out. Cutting increases
tissue damage to an area already infiltrated
with digestive enzymes.

48. Thank you!