1. SNAKE BITES

2. Case
• 5 year old girl was brought to ED with alleged
snake bite over her left leg
• Occurred at 2pm and arrived to ED at 3pm
• Child was playing near her house in Paya Jaras
when she was suddenly bitten by a small
cobra like snake
• No bleeding or LOC
• Left lower leg becomes painful and tender

3. The Culprit

4. • Upon arrival to ED, child appears alert and
concious
• Not in shock, comfortable
O/E
• Pink, well hydrated, cooperative, not
tachypnoeic
• Systemic examination was normal
• HR 89, BP 110/56, SpO2 100% on air

5. • Noted 2 bite marks over Lt lateral maleolus
with erythematous skin changes surrounding
it measuring 5x5cm
• Her left leg was not oedematous
• Pulses were palpable, able to move her toes,
sensation intact
• The left leg was splinted for immobilization

6. • Admission to ward, noted 6 hours after bite ,
Lt lower foot was swollen and had bluish
discoloration
• Swelling was increasing and has encroached
mid shin, tender++, limited ROM
• FBC TW 9, Hb 12.3, PLT 256,PT/ApTT normal
• She was also having spiking temperature

7. After 8 hours

8. • At 11pm, she was administered 1 vile of
monovalen antivenom
• Subsequenlty started on IV Augmentin
• On the following day, noted that swelling was
static and fever was slowly subsiding
• BP remains stable
• Serial FBC and coagulation profile remains
normal
• Child remains alert and comfortable

9. • At D3 of bite, swelling has reduced and child
was able to move her lower limbs
• She was also able to ambulate
• Currently still in ward awaiting swelling to
resolve
• No systemic involvement subsequently

10. Introduction
• Snakebite is a serious medical problem in
Malaysia
• From 1978 to 2000, there were 55000 cases of
snakebites recorded in the hospitals in Malaysia
• The mortality rate of snakebite in Malaysia is only
0.3 per 100000 population but the local necrotic
effects of some venoms can cause prolonged
morbidity or even crippling deformity

11. Types of snakes
• In Malaysia and the coastal waters of the region, there are
at least 18 different species of venomous front fanged land
snakes and more than 22 different species of sea snakes
• These venomous snakes belong to the following 5
subfamilies:
1. Crotalinae: represented by the two
genera Calloselasma and Trimeresurus.
2. Elapinae: represented by the five genera Naja,
Bungarus, Ophiophagus, Maticora and Calliophis;
3. Laticaudinae, represented by the genus Laticauda
4. Hydrophiini, represented by the six genera Enhydrina,
Kerilia, Hydrophis, Thalassophis, Pelamis and Kolpophis
5. Ephalophiini, represented by the only
genus Aipysurus.

12. • not all snakes are venomous
• In Malaysia there are approximately 40 species of
venomous snakes (18 land snakes, all 22 of sea snakes)
belonging to two families:
- Elapidae – have short, fixed front fangs. The family
includes cobras, kraits, coral snakes and sea snakes.
- Viperidae – have a triangular shaped head and long,
retractable fangs. The most important species in
Malaysia are Calloselasma rhodostoma (Malayan pit
viper) and Trimeresurus genus (green viper)
• The Malayan pit vipers are common in the northern
part of Peninsular Malaysia but are not found in Sabah
and Sarawak

13. • Epidemiological studies showed that in
Malaysia, bites were mainly due to four
species of land snakes :
1)Calloselasma rhodostoma (Malayan pit
viper),
2)Naja naja (Asian common cobra),
3)Trimeresurus purpureomaculatus (shore pit
viper)
4)Trimeresurus wagleri (Wagler’s pit viper)

14. 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

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

17. Elapid Venom Poisoning
• 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

18. • 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

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

20. • 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

21. • 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

22. • 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

23. 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)

24. Local necrosis
Increased
vascular
permeability
Swelling and
brusing
Myotoxins and
cytotoxins
Ischemia/
thrombosis
Venom
ophthalmia

25. 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

26. • 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 Malayan pit viper bite, the clotting defect is
primarily due to thrombocytopenia
aggravated by defibrination syndrome

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

28. • 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.

29. • 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.

30. • 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.

31. • 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.

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

33. Recovery times
• In the absence of necrosis, pain after viper bites
rarely exceeds 2 weeks.
• When necrosis develops (in about 10% of cases)
pain may remain severe for a month.
• Swelling usually resolves completely in 2-3
weeks.
• Healing time of local necrotic lesions varies
greatly according to the extent of the lesion and
the treatment given, but may requires 1-6
months or longer.

34. • In patients who do not receive specific
antivenin, systemic symptoms generally
subside more quickly than local symptoms.
• Neurotoxic symptoms usually resolve in 2-3
days.
• Hemorrhagic effects in viper bites are also
short-lived and rarely exceed a week but the
coagulation defect may persist for 3-4 weeks

35. Management
• The aims are to retard absorption of venom,
provide basic life support and prevent further
complications

36. Management Principles in Snake
Venom Poisoning
General management of snakebite poisoning includes the following
measures:
• adequate reassurance
• immobilize the patient, particularly the bitten limb. If a tourniquet
has been applied, it should be released upon admission to hospital
• Treatment of local lesion: the site of the bite and blisters should be
let strictly alone. Sloughs should be excised when local necrosis is
obvious
• Treatment of shock
• Tetanus prophylaxis: Tetanus antitoxin should be given in victims in
whom local necrosis developed
• Specific antivenom should be given to patient with systemic
poisoning
• All bitten patients, even without symptom of poisoning, should be
admitted to hospital for observation of at least 24 hours.

37. First Aid

38. In Hospital

40. Antivenom treatment
• Antivenom is the only specific treatment for
envenomation.
• Give as early as indicated for best result.
• However, it can be given as long as the signs
of systemic envenomation are still present
• For local eff ect, anti venom is probably not
effective if given more than a few hours after
envenomation

41. • Monospecific (monovalent) antivenoms are
more effective and less likely to cause
reactions than polyspecific (polyvalent)
antivenoms.
• At present, however, monospecific
antivenoms are available only against the
three common types of Malaysian poisonous
snakes (anti-Malayan pit viper, anti-Malayan
cobra and anti-Enhydrina schistosa).

42. When to start antivenom?

45. Precautions

46. Antivenom reactions

48. Anticholinesterase

49. Supportive Treatment