2. Some facts about OP Compounds
1. Commonest poisoning seen in INDIA
2. Agriculture based economy
3. OPC’S integral part of modern agriculture
CAUSES OF HIGH MORTALITY
1. High toxicity of available compounds
2. Time gap in transporting patients
3. Paucity of Health care personnel
4. Lack of antidotes
8. Acute O-P poisoning
MUSCARININC FEATURES NICOTINIC FEATURES CNS FEATURES
D iarrhoea Muscle weakness Fatigue
U rination Muscle fasiculations Confusion
M iosis Muscle paralysis Unconsciousness
B ronchorrhea
B ronchospasm Seizues
E mesis Hypertension Ataxia
L acrimation Tachycardia Resp. depression
S alivation
S weating
9. Diagnosis
• History of Exposure.
• Clinical Manifestations.
• Atropine test
Pseudo-cholinesterase-8%
Regenerates more quickly than AChE.
RBC-Cholinesterase- 92%
• Complete recovery of RBC-Cholinesterase may lag
behind enzyme recovery in nervous tissue.
• Depends on its re-synthesis & turnover rate of
RBCs themselves?
10. FATE OF ACETYL CHOLINESTERASE ?
1.Endogenous Reactivation
2.Reactivation – Pralidoxime (P2AM)
3.Irreversible binding and permanent enzyme
inactivation (aging)
Great variability in toxicity and treatment response depending
on OP agent consumed and time delay in presentation
3 hours 12 hours
11. Clinical Features
1. Acute O-P
poisoning Resp distress
Death
- Muscarinic features
- Nicotinic features
- CNS features
2. Intermediate Syndrome
3. Delayed neuropathy (OPIDP)
4. Delayed Organophosphate Encephalopathy (DOPE)
12. Intermediate syndrome (IMS)
• Muscular weakness -Ocular, neck, bulbar,
proximal limb and respiratory muscles with
occasional dystonic posturing,
• Cranial-nerve palsies are common.
• The sensory functions remain normal
• Full recovery is evident in 4-18 days.
Due to a conformational change in the
acetylcholine receptor.
Electro diagnostic criteria -conflicting results.
13. Intermediate syndrome (IMS)
• 1 to 3 days after poisoning, often when acute
cholinergic syndrome signs decreased/gone (Beware!)
• 10-40% of patients
• No clear association between particular OP pesticide
and development of syndrome
• Persists for 14-20 days
• Resolution within 2-3 weeks (with adequate supportive
care eg. ventilatory support)
• Recovery usually without sequelae
Atropine + supportive care
14. Organophosphate induced
Delayed Polyneuropathy– (OPIDP)
• 2-3 weeks after poisoning
• Distal degeneration of axons of both peripheral and CNS
Clinical features
• Transient painful ‘stock & glove’ paraesthesias followed by a symmetrical motor
polyneuropathy characterised by flaccid weakness of lower extremities which
ascends to involve upper extremities
• High-stepping gait associated with bilateral foot drop
• Predominantly distal but can involve proximal in severe neurotoxicity
• Risk of development independent of severity of acute cholinergic toxicity
• Recovery 6-12 months – spastic ataxia may be permanent outcome
Standard therapy plus corticosteroids
15. Delayed Organophosphate
Encephalopathy (DOPE)
• “CNS intermediate”
• New syndrome recognised and described in 2008
• Clinical features
• Normal sensorium then progression to coma days after poisoning
(delayed coma)
• Miosed non-reacting pupils
• Extra-pyramidal signs – dystonia, resting tremor, cog-wheel rigidity,
choreo-athetosis
• Investigations
• EEG – bi hemispheric slow waves (features consistent with
encephalopathy)
• CT brain and CSF analysis normal
• Persistently low pseudo-cholinesterase levels and increasing atropine
requirements during coma
• Prognosis excellent with adequate supportive care
16. The Grading of Clinical severity
Severity AChE
(RBC)
Muscarinic Nicotinic CNS
Mild > 40% nausea, vomiting,
diarrhoea, salivation,
bronchorrhoea and
-constriction,
bradycardia
headache,
dizziness
Moderate 20 - 40% as above, + miosis,
incontinence
Severe < 20%
fasciculations
(fine muscles)
as above, +
fasciculations
as above, +
dysarthria, ataxia
as above, +
coma,
(diaphragm, resp. convulsions
muscles)
17. Case …
• 40 yr old male farmer admitted with OP
poisoning has
• BP 80/60, HR 158/mt, RR 40/mt
• Sweating profusely, has plenty of oral and
bronchial secretions. On 6L of nasalO2, SPo2
90%, Restless and drowsy
• How do we proceed?
18. How do we proceed?
• Intubation ?
• Succinylcholine? For RSI
• Fluids/ Vasopressors?
• Atropine/ HR 158/mt
• Oximes?
• Supportive care
• Pseudocholinesterase levels???
20. Gastrointestinal decontamination
• To be considered only after stabilization, oxygen,
atropine and oximes.
• In patients who can protect the airway or after
intubation
• Forced emesis CI
• Use of Activated charcoal not supported in RCTS
• Gastric lavage decreases absorbption by 42% if
• done at 20 min & 16% if performed by 60 minutes.
• Collection of stomach contents may be mandatory
• in MLC cases
Dermal exposure- disrobing and washing
22. Atropine is the main stay in OP Poisoning
• Dose
• Incremental vs bolus
• Incremental better
• Signs of atropinisation
• Signs over atropinisation
• Is Glycopyrrolate better – no CNS penetration,
may not control CNS side effects, no definitive
evidence.
Atropine does not bind to nicotinic receptors
and cannot relieve nicotinic effects
23. Atropine dosing?
Incremental
• 1.8 to 3 mg Atropine IV
• Double the dose every 5
minutes
• Till atropinisation is
achieved
• Followed by 10 to 20% of
the total dose requires for
Atropinisation as IV
infusion
• Stop once anticholinergic
effects occur.(Absent bowel
sounds, urinary retention,
agitation)
Bolus
• 2-5 mg Atropine every 10 to 15
min
• Till atropinisation is achieved
• Followed by maintenance using
reduced doses or
increasing time duration in
b/w doses
• Various studies clearly found
Incremental doses to be superior
25. 3-5 mg / hour of atropine infusion is
required in most cases
Reduce rate by 20% every 4 hourly once patient
is stable. STOP.
The most sensitive measure of adequate
atropinisation appears to be repeated evaluation
(5 to 30 min) of the quantity of secretions .
Atropine toxicity = absent bowel sounds + fever
+ confusion
26. End Point of Atropinisation
• HR-We keep a HR > 80-90/BPM as baseline.
• Tachycardia may reflect hypoxia caused by
pulmonary hypersecretion and bronchospasm.
The use of atropine is not, contraindicated in a
patient; as the patient’s oxygenation improves the
pulse rate will usually slow down.
• 10% of organophosphate-poisoned patients do
not have miosis
27. Case
• 30 yr old farmer admitted to ICU with Op poisoning,
has HR 54/mt, lot of oral secretions, continously
spitting out, on room air saturations 95%, RR 23/mt.
• Atropine/ glycopyrrolate?
• Nurse starts 100ml infusion finishes
• In 30 min and gives one more in next one hr
• Patients becomes very very restless has to be
deeply sedated and some times even intubated
28. INDIAN JOURNAL OF ANAESTHESIA, FEB. 200240
ORGANOPHOSPHORUS POISONING - STILL A
CHALLENGING PROPOSITION
Dr. N. Krupesh1 Dr. T. R. Chandrashekar2 Dr. A. C. Ashok3
SUMMARY
A prospective study was conducted on patients admitted with organophosphorus (O.P.) poisoning to our unit from May 99 to May’00.
Total number of cases admitted were 62, 37 of them were ventilated. 6 of them died during the course of the treatment. The various
aspects of treatment, complications, drug options and uncommon problems were evaluated.
Keywords : Organophosphorus poisoning, Pancreatitis, Atropine, Pralidoxime (p2am), Glycopyrrolate.
Diaphragmatic Paralysis, Respiratory Failure, Tachycardia,
Hypertension.
(c)CNSeffects
Headache, Tremors, restlessness, ataxia, confusion,
slurred speech, seizures and coma.
Aim
The aim of the present study was to evaluate (a)
cause of death (b) role of Atropine and Glycopyrolate (c)
incidence of other rare complications.
MaterialAndMethods
Introduction
Organophosphorus poisoning is the most common
poisoning in India because of its easy availability.O.P
compounds produce their effects by inhibiting the action
of acetylcholinesterase enzyme, which leads to an increase
in acetylcholine, in preganglionic and postganglionic
parasympathetic receptors (muscarinic action), sympathetic
preganglionic synapses including adrenal medulla and
neuromuscular junctions (nicotinic action). Acetylcholine
is also a transmitter in central nervous system. The O.P.
compounds are divided into two groups phosphates and
carbamates, which binds to the active amino acid site on
the acetylcholinesterase enzyme serine, and phosphorylate
Indian J. Anaesth. 2002; 46 (1) : 40-43 40
About 10% of admissions very because of Atropine toxicity
Pancreatitis was seen in significant number of patients
In Baygon spray poisoning , when ever patient passed first
stools post poisoning, they developed superficial burns on the
buttocks
33. MV and Supportive care
If bronchial secretions
are manageable, MV
with minimal settings
Massive aspiration or
severe bronchorrhea
not responding to
atropine- MV may
require high settings
Avoid narcotics +atropine as both lead to
paralytic ileus. Early Enteral feeding beneficial
If patients have convulsions with atropine, IV Diazepam is the
drug of choice.
Fluid management -loss of fluid through sweating, atropine
fever, oral and bronchial secretions can be substantial.
After the initial cholinergic phase oral secretions are more than
the bronchial secretions in many patients.
34. Take home message
1.Early stabilization and resuscitation.
2. Incremental dose Atropine – Main stay along with
Good supportive care
3.Early institution of Oximes.- Controversial
4.External decontamination, MgSO4, Clonidine, Use of
benzodiazepines and Alklalinization, Early Enteral
feeding were found to be beneficial.
5.FFP, forced emesis were found harmful.
36. OXIMES.
•Oxime catalyses the regeneration of active
AChE by exerting a nucleophilic attack on the
phosphoryl group, transferring it from the
enzyme to itself and making AChE effective
again
•Aged’ AChE with its negatively charged
phosphate can no longer is attacked by a
negatively charged nucleophile, i.e. OH. Or an
oximate group and regeneration is no longer
possible
