16. • All OP are absorbed through
bronchi
intact skin
gut.
• Toxicity between different compounds varies
considerably and onset may be delayed after skin
exposure.
22. 1. Land - line phone
2. Old used and broken surgical table
3. Unwanted Poisoning patients ( Nobody’s patients)
23. GASTRIC LAVAGE
• Most commonly used method of removal poisons
from the stomach. Overall mortality ---- <1 %.
• Gastric lavage should not be considered a routine
management procedure.
• Gastric Lavage should be performed only if a potentially
life-threatening amount of toxin has been ingested
within preceding 1-2 hrs.
European Association of Poison Centres
Clinical Toxicologists/American Academy of Clinical Toxicology
24. • In a busy emergency room, a self-poisoning
patient does not always get a priority.
• The attitude of the health care provider towards
them may not be optimal.
• Should not be used as a mean of a punishment
to the patient.
25. MECHANISM OF ACTION OF OP
OP compounds inactivate
acetylcholinesterase( AChE) resulting in the
accumulation of acetylcholine (Ach) in
cholinergic synapse.
26. • Parasympathetic system muscarinic
• Sympathetic system nicotinic
• CNS nicotinic
muscarinic
• Neuromuscular junction nicotinic
27. Clinical features of OP pesticide poisoning
• Features due to overstimulation of muscarinic
acetylcholine receptors in the PARASYMPATHETIC system
• Bronchospasm
• Bronchorrhoea
• Miosis
• Lachrymation
• Urination
• Diarrhoea
• Hypotension
• Bradycardia
• Vomiting
• Salivation
28. Clinical features of OP pesticide poisoning
• Features due to overstimulation of nicotinic
acetylcholine receptors in the SYMPATHETIC system
• Tachycardia
• Mydriasis
• Hypertension
• Sweating
29. Clinical features of OP pesticide poisoning
• Features due to overstimulation of nicotinic and muscarinic
acetylcholine receptors in the CNS
• Confusion
• Agitation
• Coma
• Respiratory failure
• Features due to overstimulation of nicotinic acetylcholine
receptors at the NEUROMUSCULAR JUNCTION
• Muscle weakness
• Paralysis
• Fasciculations
30. • Patients with severe OP poisoning typically present
with
Pinpoint pupils
Excessive sweating
Reduced consciousness
Poor respiration
33. Check Airway, Breathing, and Circulation
Place patient in the left lateral position
head lower than the feet
(reduce risk of aspiration of stomach contents)
High flow oxygen, if available
Intubate the patient --- compromised airway
breathing
34. • IV access
• IV 1–3 mg of atropine as a bolus depending on severity.
• IV 0·9% normal saline . Aim systolic BP > 80 mm Hg
urine output >0·5 mL/kg/h
• Record PR, BP , pupil size, presence of sweat, and
auscultatory findings in chest at time of first atropine dose
• Remove contaminated clothing and wash with copious
amounts of soap and water
35. • 5 min after giving atropine, check pulse, blood
pressure, pupil size, sweat, and chest sounds.
• If no improvement has taken place, give double the
original dose of atropine
36. Target end points
• Clear chest
• HR >80/min
• Pupils no longer pin-point
• Dry axillae
• Systolic BP >80mmHg
• Tachycardia is not a contraindication to atropine
(can be caused by many factors.)
• Dilated Pupils are not useful endpoint for initial atropinizaion.
delay exists before maximum effect.
• Very dilated pupils are an indicator of atropine toxicity
37. • Once the patient is stable, start an infusion of atropine
Dose-
10–20% of the total dose needed for stabilization / hour
• Check the patient often for adequacy of Atropinization
• Too little atropine
cholinergic features will re-emerge
• Too much atropine
agitation pyrexia
absent bowel sounds urinary retention
-stop the infusion
-wait 30–60 min for these features to settle
-starting again at a lower infusion rate.
38. • OXIME
-IV Pralidoxime chloride 2 g (or obidoxime 250 mg) in
20–30 min into a second cannula; follow with
-Infusion pralidoxime 0·5–1 g/h (or obidoxime 30
mg/hr) in 0·9% normal saline
• Continue the oxime infusion until
atropine has not been needed for 12–24 h
extubation of the patient
39. Oximes reactivate acetylcholineesterase inhibited by OP
Reactivation is limited by ageing of acetylcholineesterase and
high concentration of pesticides
Ageing of acetylcholineesterase takes longer with diethylOP
(120 hours) than with dimethylOP (12 hours)
Oximes may be effective for people presenting after 12 hours
if he has been exposed to diethylOP
40. • Monitor frequently for recurring cholinergic crises due
to release of fat soluble organophosphorus from fat
stores.
• Such crises can occur for several days to weeks after
ingestion of some organophosphorus.
• Patients with recurring cholinergic features will need
retreatment with atropine and oxime
• Severe hypotension might benefit from vasopressors.
41. • Indications for Intubation and ventilation
-Tidal volume is below 5 mL/kg
-Vital capacity is below 15 mL/kg,
-Apnoeic spells
-PaO2 is less than 8 kPa (60 mm Hg) on FIO2 of
more than 60%
42. • Agitated delirium in OP patients
DUE TO
pesticide itself
atropine toxicity
hypoxia
alcohol ingested with the poison
medical complications.
• management
prevention or treatment of underlying causes
IV. diazepam.
43. 19 year- old school girl admitted for taking
Polo insecticide
Features of OP poisoning
Treated with IV atropine
Recovered
CLINICAL SCENARIO
44. • CLINICAL SCENARIO
• Day 3 of hospitalization
While having lunch
Sudden onset of shortness of breath
Unconscious
• Moved to the ICU
Respiratory support with ET tube
Mechanical ventilation
later needed Tracheotomy
45. CLINICAL SCENARIO
• ICU care >20 day
• Gradual weaning of Mechanical ventilator
• Complete recovery
• Discharged after Counseling
47. Intermediate syndrome
• Sudden development of peripheral respiratory
failure in conscious patients with OP poisoning after
seemingly recovering from cholinergic crisis.
• Important cause of death in patients who have been
resuscitated and stabilized on admission to hospital.
48. Intermediate syndrome
• 20% of patients
• 1-4 days post-exposure
• Weakness of ocular muscle
head and neck
proximal limbs
respiratory muscle
• No sensory symptoms
• May last for 2-3 weeks
• Supportive treatment – airway maintenance
Ventilation
49. Intermediate syndrome
Assess flexor neck strength regularly in conscious patients by
asking them to lift their head off the bed and hold it in that
position while pressure is applied to their forehead.
Any sign of weakness is a sign that the patient is at risk of
developing peripheral respiratory failure (intermediate
syndrome).
Tidal volume should be checked every 4 h in such patients.
Values less than 5 mL/kg suggest a need for intubation and
ventilation
51. Organophosphate-induced delayed polyneuropathy
• Muscle cramps followed by numbness
• Paraesthesiae
• Flaccid paralysis of the lower and subsequently the
upper limbs
• Foot and wrist drop
• High-stepping gait, progressing to paraplegia
• Tendon reflexes are reduced or lost
• Mild spasticity may develop later
52. Organophosphate-induced delayed polyneuropathy
• Recovery often incomplete
• May be limited to the hands and feet
• Substantial functional recovery after 1-2 years may
occur, especially in younger patients
53. LEARNING POINTS
- Early use of sufficient dose of atropine is potentially life-saving
in patients with severe toxicity. IV bolus atropine ASAP.
- Repeated IV atropine bolus doses until targets for atropinization
are reached.
- Continued monitoring of patients for the targets of
atropinization.
- Gastric lavage should only be done after the patient has been
stabilised and treated with oxygen, atropine, and an oxime.
- Hospitalization for at least 96 hours post-ingestion especially in
severe patients.
54. CARBAMATE PESTICIDES
Atropine therapy
Pralidoxime –
Not usually required as the duration of toxicity is short
May be given if inadequate response to atropine
poisoning by mixed organophosphate & carbamate
55. References
• Management of acute organophosphrous pesticide
poisoning ;THE LANCET .Michael Eddleson, Nick A
Buckley, MD. Prof Peter Eyer, MD. Prof Andrew H
Dawson,FRACP (August 2007)
• BNF March-September 2017
• Davidson’s Principles and Practice of Medicine 23rd
Edition 2018 Poisoning ;SHL Thomas