- Poisoning is an important cause of morbidity and mortality in India, though exact estimates are not available. Hospital studies show up to 10% of admissions are due to poisoning. - Common poisons in India include organophosphates and carbamates (50% of poisonings) as well as other compounds like medications and industrial chemicals. - Accurate history regarding type and amount of poison ingested is important for proper management, which generally involves decontamination, supportive care, and antidotes when available. Prevention focuses on education and addressing social factors contributing to suicidal attempts.

2. • Poison: any substance which produces
adverse effects in a living organism

3. • Important cause of morbidity and mortality in
India
• Exact estimate not available
• Hospital studies- up to 10% of admissions in
medical emergency
• OP & carbamates- ~ 50% of these
• Other compounds- Alphos, methanol, hypnotics
and sedatives, TCAs etc

4. • Urban areas- hypnotics and sedatives, TCAs
• Rural areas- Insecticides and Alphos
• Methanol- Hooch tragedies, where ever they
occur
• Accidental poisoning- common in younger
children
• Suicidal intent- teenagers, adults

5. • Accurate history- may be difficult
• Type of poison, amt ingested/exposed to,
time interval b/w exposure & treatment
• Suspect when there is unexplained, sudden
illness in a healthy individual, h/o psy illness,
h/o strained relationship, onset of illness
while working with insecticides, chemicals or
after ingestion of food.

6. • Quick, careful initial assessment to assess
the need for immediate supportive care
• Certain characteristic features in some

7. • Coma- Narcotics, Benzodiazepines, barbiturates,
alcohol etc
• Delirium- atropine, Datura, LSD, amphetamines,
cocaine, alcohol
• Cyanosis- MethHb eg nitrates, CO, Aniline
• Jaundice- PCM, Phosphorus, ATT, EDB

8. • Cherry red skin- CO
• Bullous rash- barbiturates
• Breath odour- OP, ethanol, Alphos

9. Management …
• General principles
– Pretoxic phase- prior to onset of poisoning
• Decontamination- top priority
• Treatment- solely based on history
• Maximum potential toxicity based on greatest
possible exposure should be assumed
• Establish IV access, cardiac monitoring esp
with unclear history and potentially serious
ingestion

10. • Toxic phase- time b/w onset of poisoning and peak
effect
– Based primarily on clinical exam & lab findings
– Effects of overdosage begin sooner , peak later
& last longer than they do after therapeutic dose
– Resusc & stabilization- top priority
– Decontamination as started in pretoxic phase

11. • Initial therapy-
– Support to vital functions
• Decontamination-
– Skin- removal of clothing, thorough wash
– Gastric-
• Emesis- effective upto 3-4 hrs of ingestion,
only in fully conscious
• Physical stimulation of pharynx, NaCl(200-
400 ml fully saturated), ipecac(10-30ml)

12. • Gastric lavage
– Wide bore NG tube
– First aspirate to be saved for chemical analysis
– 3-5L of tap water ( 200-300ml aliquots)
– C/i- corrosives, petroleum distillates
• Activated charcoal
– To prevent further absorption
– dose- 10 times the dose of poison or as much as
possible if dose unknown (50 gm q 2-6 hrly)

13. Prevention of recurrence
– ~10% of pt with unsuccessful suicidal
attempt are sufficiently depressed and
make another attempt
– Psy counselling, social factor exploration

14. SNAKEBITE

15. Introduction
In the world
3000 species, 500 poisonous
In India
216 species, 52 poisonous
Annual mortality in India
5.6 to 12.6 per 100000

16. Venomous Snakes in India
Elapidae
Cobra
Common Krait
Viperidae
Russell’s viper
Saw-scaled viper
Crotalidae
Pit viper
Hydrophidae
Sea snakes

17. Recognition of Poisonous snakes
1. Fangs

18. 2. Head

19. 3. Pupils

20. 4. Belly scales

21. 5. Body design
Cobra

22. Russell’s viper

23. Saw-scaled viper

24. Krait

26. Snake Venom
Common components
Procoagulant enzymes
Haemolytic toxins
Cytolytic / necrotic toxins
Myolytic toxin
Pre-synaptic neurotoxin
Post-synaptic neurotoxin

27. Snake venoms
Cobra Krait Viper Sea
snakeR SS
Local effect ++ - +++ -
Vasculotoxic - - +++ -
Neurotoxic +++ +++ - ++
Cardiotoxic ++ ++ - +
Myotoxic - - - +++
Dose/bite (mg) 200 22 15
0
4.6
Fatal dose (mg) 120 60 15
0
80

28. Clinical Features
Dry bites
20% pit viper and 43% cobra bites
Local features
Fang marks
Pain
Swelling
Blistering & necrosis
Lymphangitis, lymphadenopathy
Venom ophthalmia
Secondary infection

29. Local effects of pit-viper bite

31. Local effects of a viper bite

32. General features
Flushing
Sweating
Breathlessness, palpitation
Tightness in chest
Nausea, vomiting (in all severe envenoming)
Acroparaesthesiae
Hyper salivation, blurring of vision (cobra)
Abdominal colic, diarrhoea, collapse ( krait)

33. Systemic Features – Elapid / Krait bite
Neurotoxicity
• Onset as early as 15 min with ptosis &
external ophthalmoplegia
• Rapid descending paralysis
• Life-threatening respiratory paralysis
• Effects completely reversible with antivenin /
anticholinesterases
• Spontaneously wears off in 1 – 7 days
Cardiotoxicity
• Direct myocardial toxicity

34. Systemic Features – Viper bite
Clotting defect & haemolysis
• Persistent bleeding from puncture sites
• Spontaneous systemic bleeding (gingival
sulci commonest site) #
•Nephrotoxicity
Commonest with Russell’s viper
Cause - hypovolemia & ischaemia

36. Systemic Features – Sea snake bite
Myotoxicity
• Pain & tenderness in muscles develop 0.5
to 3.5 hours after bite
• Trismus common
• Rhabdomyolysis
Nephrotoxicity
Neurotoxicity
Generalized flaccid paralysis
Cardiotoxicity

37. Management
First aid
• Reassure
• Immobilize
• Move to hospital as soon as possible
• Tourniquet / pressure immobilization
in severe elapid envenoming
(to delay onset of respiratory paralysis)
remove only after 1st
dose of antivenin
• Treat shock with colloids
• Maintain patent airway

38. Pressure immobilization

39. Evaluation in hospital
• Look for fang marks
• Monitor vitals, local swelling &
muscle weakness hourly
• Look for bleeding
• Platelet count q 12 h
• 20 min WBCT , PT, FDP q 6h
• Serum electrolytes q 6 h
• LFT, RFT, CPK, ECG daily
• Monitor urine output, myoglobinuria

41. Antivenin
Lyophilized, polyvalent equine anti - serum
Effective against cobra, common krait, Russell’s
viper & saw-scaled viper
Dilute in 10ml of DW,
then mix with 5ml / kg of NS / 5% D
Give slow i/v over 1 – 2 h
Dose
For viper bite
local swelling, no systemic signs 50ml
mild systemic signs 50 – 100 ml
severe poisoning 150 – 200ml
For cobra bite 100 – 200ml

42. Response to antivenin
• Rapid & dramatic
• Neurotoxic signs may improve within 30 min
spontaneous bleeding stops in 15 – 30 min
• Repeat antivenin q 6 h till progression of
paralysis stops / clotting profile normalizes
• Adverse reactions: early, pyrogen, & late

43. Supportive therapy
• Tetanus prophylaxis
• Antibiotics in severe local envenoming
• Fasciotomy for compartment syndrome
• Respiratory paralysis managed with assisted
ventilation, Neostigmine & Atropine
• FFP, cryo-precipitates & platelet concentrate
for haemostatic disturbances

44. Avoid
Arterial tourniquet
Incision and suction
Electric shock
Cryotherapy
Local heat
Corticosteroids, EDTA, Heparin

45. Thank you