Clinical Vignette

You are posted as a CMO, casualty in the month of June.

A 30 year old housewife from a nearby village is
brought in the afternoon in an unconscious state.
There is h/o domestic violence. Patient’s clothes are
wet and are soiled with urine and feces.
O/E pupils are constricted with BP= 80/60mmHg. You
check patient’s blood sugar level which is 480 mg%.
You order an ABG which is s/o metabolic acidosis.
ECG is done and it shows bradycardia. Routine blood
workup reveals normal serum electrolytes with a
raised amylase level of 300.
Diagnosis ??? ??
Organophosphorus Poisoning

Presenters : Dr Lohit Chauhan

: Dr Dhananjay Gupta
Moderator : Dr. Gurmeet Kaur
 INTRODUCTION
• OP are a group of insecticides or ‘nerve-
agents’ which act at acetyl-cholinesterase

• Have been used as insecticides, petroleum

additives and chemical warfare agents

• Carbamates are another group of insecticides

which act at the same site, with a slight
different MOA
 WHO CLASSIFICATION (simplified)

HIGHLY TOXIC MODERATELY TOXIC

1. Phosphamidon (Dimecron) 1. Malathion
2. Ethyl parathion 2. Fenthion (Baytex)
3. Methyl parathion 3. Temephos (abate)
4. Chloro-thiophos 4. Fenitrothin (tik-20)
5. Carbo-phenothion 5. Diazinon (spectacide)

* Shivakumar S, Ishaq RM. Management of Organophosphorus compounds

(OPC) Poisoning : Current Status 2008. taken from drshivkumar.org
 Epidemiology (WHO)
• Acute OP poisoning is one of the common and
serious medical emergencies

• Asia : 3 million cases/ year of acute

pesticide poisoning

• 3 lakh deaths per year (CFR =10-15 %)

• 99% cases are seen in developing world

 Indian Data
• Poisoning is 4th MC cause of deaths annually

• OP poisoning is the MC poisoning

• Pattern of poisoning is region-dependant

• OP poisoning is more common in south India

• North India- aluminium phosphide > OP

RML Data
Why is OP poisoning common ??
• India is an agarian country
• routinely used in farming

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 training facilities
5. Lack of antidotes
 Why is OP poisoning common ??

Limited resources and infrastructure for

health care delivery
 1. Mode of poisoning

15%

SUICIDAL
ACCIDENTAL
85%

* Banerjee I, Tripathi SK, Roy AS. Clinico-Epidemiological Characteristics of Patients

Presenting with Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch 2012
 2. Occupation

5%
9%

HOUSE WIVES
10%
42% FARMERS
SHOPKEEPERS
LABOURERS
34% STUDENTS

* Maharani B, Vijayakumari M. Profile of poisoning cases in a tertiary care hospital in

Tamil Nadu, India. J of App Pharma Sc. Vol 3(01), Jan 2013
 3. Seasonal distribution

21%
35%
SPRING
WINTER
12% RAINY
SUMMER

32%

* Maharani B, Vijayakumari M. Profile of poisoning cases in a tertiary care hospital in

Tamil Nadu, India. J of App Pharma Sc. Vol 3(01), Jan 2013
 4. Type of Poison

16%

36%
Me Parathion
19%
Diazinon
Chlorpyriphos
Dimecron

29%

* Banerjee I, Tripathi SK, Roy AS. Clinico-Epidemiological Characteristics of Patients

Presenting with Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch 2012
 5. Relative human Toxicity

Eddleston M et al. Differences between organophosphorus insecticides in human self-

poisoning: a prospective cohort study. Lancet. 2005 Oct 22-28;366(9495):1452-9
Mechanism Of Action
 Clinical Features
1. Acute O-P poisoning
- Muscarinic features Resp distress
- Nicotinic features Death
- CNS features

2. Intermediate Syndrome

3. Delayed neuropathy (OPIDP)

4. Neuro-psychiatric disorder (COPIND)

 1. 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
2. Muscarinic / Wadia type 1 syndrome

1. Excessive Sweating

2. Miosis

3. Bronchorrhoea / spasm

4. Bradycardia

5. Hypotension
 3. Bronchorrhoea
• Early cause of morbidity and mortality

• Excess fluid is from airway secretions

• Obstruction of upper and lower airways

• Pulmonary edema - - hypoxia - - death

 The Grading of Clinical severity
Severity AChE Muscarinic Nicotinic CNS
(RBC)
Mild > 40% nausea, vomiting, headache,
diarrhoea, salivation, dizziness
bronchorrhoea and
-constriction,
bradycardia

Moderate 20 - 40% as above, + miosis, fasciculations as above, +

incontinence (fine muscles) dysarthria, ataxia
Severe < 20% as above, + as above, +
fasciculations coma,
(diaphragm, resp. convulsions
muscles)
 4. Intermediate syndrome
• Described in 1987 (Karalliedde and Senanayake)

• Occurs 24-96 hours after resolution of acute

cholinergic crisis

• Most imp. factor responsible is

quantum of exposure of OPC

• May occur from inadequate oxime therapy

 IMS - pathophysiology
• Incidence = 10-50 %

• Prolonged effects on Nicotinic receptors

• Primary motor end plate degeneration

• Leads to muscle weakness

 IMS- muscle weakness of
• Muscles innervated by cranial nerves : III-VII and X

• Neck flexors
- a constant feature
- one of the earliest signs
- inability of patients to raise heads off pillow

• Proximal limb muscle weakness

- typically involve shoulder abductors, hip flexors

• Respiratory muscles - death

 IMS – other features
• Deep tendon Reflexes :
Usually absent / decreased

• Sensory system usually intact

• Muscarinic symptoms :
absent
rarely short relapses may occur
 IMS- complications
• Weakness -- Frank paralysis

• Respiratory distress -- Death

• Main cause of morbidity and mortality

in Indian patients.
 5. OPIDP
• OP induced Delayed Polyneuropathy

• Delayed, rare, neurotoxic effect

• 1-5 weeks after severe acute poisoning, due to

slow release of OP from body fat

• symmetrical sensory-motor axonal degeneration

of the peripheral nerves and SC
 5. OPIDP - C/f
Motor
1. Sharp cramp like pain in calf
2. High stepping gait (initially)
3. Shuffling gate in severe cases
4. Quadriplegia / paraplegia
5. Wrist and foot drop
6. Mild pyramidal signs

Sensory
1. Glove-stocking anesthesia
2. Cerebellar signs +/-
 6. COPIND
• Chronic OP induced Neuro-psychiatric disorder

• Chronic low-dose exposure to OP compounds

• 40 hours/week, 9 months/ year

• No cholinergic symptoms

• Non responsive to levodopa

• Plasma cholinesterase levels are normal

 6. COPIND – c/f
Neurological Symptoms Psychiatric Symptoms
1. Impairment in memory 1. Anxiety
2. Impairment in concentration 2. Dysthymia
3. Impairment in leaning 3. Depression
4. Chronic fatigue
5. EPS : dystonia
6. Resting tremor, bradykinesia
7. Rigidity of face Parkinson-like
8. Postural instability

Non responsive to levodopa

Diagnosis and Management
 Diagnosis of OP poisoning
Diagnosis is mainly clinical, Based on :

1. H/o Ingestion of poison

2. Characteristic clinical features
3. Clinical improvement after atropine/ oxime
4. Inhibition of cholinesterase activity
 1. Inhibition of cholinesterase
• Demonstrating a decrease in cholinesterase

• Definitive or gold standard method

• Theoretically RBC/ true cholinesterase is more

accurate than plasma/ pseudo

• But plasma / pseudo-cholinesterase is more easily

available test
 Diagnosis :
Plasma / SChE :
- easy to measure
- easily available
- more useful in acute exposure

1. 50 % reduction in normal values : diagnostic

(baseline values usually NA)

2. Progressive increase in SChE with treatment

 2. Cholinesterase levels
Useful in monitoring clinical course of illness

persistent Low levels are a predictor of IMS

(Intermediate syndrome)

SChE activity is < 20 % during onset of IMS

* Tajune J, Robert J. Organophosphoric poisoning. Ann Emerg Med 1987 ; 16:193.

 3. Electro-neuro-myogram (ENMG)

• 30 Hz rapid nerve stimulation - decremental

responses correlate best with clinical weakness

• Most useful diagnostic test of IMS *

* Senanayake N et al. Neurotoxic effects of OP insecticides : an intermediate

syndrome. NEJM. 1987 ; 316 :761-63.
4. Other tests of prognostic value
a. Hyperglycemia
b. Neutrophilic leucocytosis
c. Proteinuria / glycosuria
d. ECG changes (QTc prolongation)
e. Blood pH (acidosis)
f. Hyper amylasemia
g. Serum CPK levels
 5. Hyperglycemia in OP-poison
a. Oxidative stress
b. Renal tubular damage
c. Stimulation of adrenals
d. Release of catecholamines

Transient hyperglycemia and glycosuria are

often seen in acute OP-poisoning
* Namba T, Nolte CT, Jackrel J, Grob D. Poisoning due to organophosphate
insecticides: Acute and chronic manifestations. Am J Med. 1971;50:475–92.
 6. Blood pH
• Metabolic Acidosis develops in patients of OP
poisoning, more common with hypotension*1.

• Unknown mechanism.

• If pH < 7.20, treatment with sodium

bicarbonate beneficial*2.
1. *Prakash O.et al. Low ph predicts mortality in OPP and carbamates poisoning, JAPI
2002; 50:857.
2. *Roberts DM, Buckley NA. Alkalinisation for treating organophosphorus pesticide
poisoning. Cochrane Database of Systematic Reviews 2005;1:CD004897.pub2.
 7. QTc prolongation
• Indicates poor prognosis in OP- poisoning

1. Cholinergic stimulation of heart : M2

a. negative ionotropy
b. negative chronotropy

2. Oxidative stress causes conduction problems

* Shadnia S, Okazi A, et al. Prognostic value of long QTc interval in acute
and severe OP poisoning. J of Med Toxico 2009 ; 5(4).
 8. Hyper- amylasemia

• Cholinergic stimulation of salivary glands

• Cholinergic stimulation of pancreas
• Acute pancreatitis (rare)

Raised amylase levels correlate with severity

and presence of shock in acute OP poisoning *

* Lin CL, Yang CT, Pan KY, Huang CC. Most common intoxication in nephrology
ward organophosphate poisoning. Ren Fail 2004 ;26:349-54. .
 9. Acute Pancreatitis
• d/t Excessive cholinergic stimulation and
ductular hypertension

• Painless Ac. Pancreatitis has been reported

• Amylase (>300) : low Sn, low Sp

• Lipase (>300) : useful for diagnosis
* Hsiao CT, Yang CC, Deng JF, Bullard MJ, Liaw SJ. Acute Pancreatitis following
Organohosphate Intoxication. J Toxicol Clin Toxicol. 1996 ;34(3):343-7.
Management
 What to do ??
1. Call AIIMS poison cell : (NPIC)

- National Poisons Information Cell

- Toll free no. 1800 116 117
- Other : 011 - 26589391
- Open 24 X 7 , 365 days a year
 The Paradox of Poisoning….

“The only thing I know is

that I don’t know anything”

- Socrates
 1. Identification of poison
• History by patient/ attendant
• Clinical presentation.
• By showing photographs.
• WHO colour code on container.
Poison :Identification

WHO colour code on container.

Red label Extremely toxic Monocrotophos, zinc phosphide, ethyl mercury acetate,
and others.

Yellow Highly toxic Endosulfan, carbaryl, quinalphos, and others.

label

Blue label Moderately toxic Malathion, thiram, glyphosate, and others.

Green label Slightly toxic Mancozeb, oxyfluorfen, mosquito repellant oils and
liquids, and most other household insecticides.
 Identification of poison
• Signs of cholinergic excess or developing

intermediate syndrome Organophosphosphate

• Disparity between history and clinical presentation,

follow, clinical judgment.

• After identification classify as Organophosphorus

and non-Organophosphorus.
Management :Immediate, Protocol
Assess and record 15-point Glasgow Coma Scale.

Pulse rate, BP and auscultate

Patient : left lateral position- head lower than the feet.

Oxygen, Intubate if respiratory distress.

Start atropine : reduce bronchorrhoea.

0.9% normal saline, Aim SBP > 80 mm Hg & urine output >30 ml/h
When not sure about the poison..??

• ‘Atropine test‘ : Inject 0.6- 1 mg IV

atropine.

• If pulse rate goes up by 25 per minute or

skin flushing develops patient has mild or

no toxicity for OP’s.

 Management : Specific
General Principles of Therapy :

• Decontamination, Resuscitation, Stablization.

• Muscarinic antagonists
• Fluids.
• Acetylcholinesterase reactivators.
• Gastric Decontamination.
• Miscellaneous.
 Decontamination
• Healthcare workers and OP Poisoning.
• Few western hospitals, reported such poisoning.
• None shows inhibition of Acetyl/Butyryl
cholinesterases.
• Cases from Asia : Health-care workers take no
special precautions , No cases of secondary
poisoning reported.
 Decontamination
• Guidelines : Universal Precautions, Maximum
Ventilation, Frequent rotation of staff to keep exposure
minimum.
• PPE should not consist Latex / Vinyl.
• Patient : All clothing to be removed, discard in
ventilated area.
• Thorough irrigation with water.
• Wash with soap and water.
• Soaps containing 30% ethanol advocated.
• Ocular decontamination : water only.
 Initial Stabilisation
• Patent Airway, adequate Breathing and Circulation.
• Oxygen at first opportunity.
• Little evidence, Atropine not to be given until oxygen
availability*1.
• However, in hospitals where oxygen not available, Atropine to
be started early*2.
• Patient Position : Left Lateral, Neck Extended.
 Reduce aspiration risk.
 Keeps airway patent.
 Decrease pyloric emptying and absorption of poison.

*1 Erdman AR. Insecticides. In: Dart RC, Caravati EM, McGuigan MA, et al, eds. Medical toxicology, 3rd edn. Philadelphia:
Lippincott Williams & Wilkins, 2004: 1475–96.

*2 Aaron CK. Organophosphates and carbamates. In: Shannon MS,Borron SW, Burns M, eds. Clinical management of
poisoning and drug overdose, 4th edn. New York, Elsevier Science, 2006.
Initial Stabilisation
 Gastrointestinal decontamination
• Often first intervention

• To be considered only
after stabilization,
oxygen, atropine and
oximes.
• Lavage only if patient
arrives within 1 hour.
• Only consider if patient
Not beneficial, rather increases chances of
intubated or conscious Aspiration Pneumonia & Deaths*
and willing to
cooperate. * The Hazards of Gastric Lavage for Intentional Self Poisoning
in a Resource Poor Location Clin Tox 2007;45(2):136-43
 Gastrointestinal decontamination
• Induced emesis : Ipecacuanha induced ,
Contraindicated.
• Activated charcoal : Studies failed to
find any benefit ( Why..??)
 It binds in vitro, but not in gut due to
NO evidence suggests that
rapid absorption. patients
with pesticide poisoning
 Ingested benefit
dose too large for thewith
amount of *charcoal.
activated charcoal.

* Eddleston M, Juszczak E, Buckley NA, et al. Randomised controlled trial of routine single or
multiple dose superactivated charcoal for self-poisoning in a region with high mortality. Clin
Toxicol 2005; 43: 442–43.
 Muscarinic antagonist
Atropine
Muscarinic Antagonist
Good CNS penetration, cause Anticholinergic delirium, agitation and
psychoses.

Glycopyrrolate
Less CNS penetration, Less CNS side effects.
Lesser respiratory complications
Ineffective in countering Coma and reduced respiration.

Hyoscine methobromide and Hyoscine

Hyoscine has the best CNS penetration
Methbomide form not permeable to BBB.
 Muscarinic antagonist
• A small RCT found no difference in mortality or
ventilator rates, comparing Atropine and
Glycopyrrolate.
• Hyoscine : best for severe Extra-pyramidal features
with few peripheral signs
• In animal studies, found more effective than Atropine
for control of seizures induced by inhaled nerve gas
agents.
• However, Atropine remains mainstay of therapy.
 Easy and wide availability.
 Affordability .
 Moderate ability to penetrate CNS.
 Muscarinic antagonist
AIM OF THERAPY : ATROPINE
• To reverse cholinergic features.
• To improve Cardiac and Respiratory functions.
• Target Endpoints of Atropinization.
1. Drying of Pulmonary secretions, ie. Clear lung fields on
auscultation. (Most reliable)
2. Heart rate > 80 beats / min.
3. SBP > 80 mmHg.
4. Pupils : No longer pinpoint.
5. Dry Axillae.
6. Bowel sounds : just present.
 End points of atropinisation

A 1. Clear Chest
1. Lung secretions
T 2. SBP > 80mmHg
2. Hypotension R
3. HR > 80/min
3. Bradycardia O
4. Sweating P 4. Dry Axillae

5. Miosis I 5. Pupils no longer pinpoint.

6. Bowels : Hyperactive
N 6. Bowel sounds : Just present
E
 Atropine Dosing
Incremental Dosing V/S Bolus Dosing

1.8 to 3 mg Atropine (i/v) 2-5 mg Atropine every 10 to 15 min.

Various studies clearely found

Repeat every 5 minutes with doubling the dose
each time.

Incremental Dosing far superior

Endpoint : Atropinization.
Endpoint : Atropinization.

to bolus dose administration

Followed by : 10 to 20 % of total dose required Followed by maintenance using reduced doses
for atropinization every hour via i/v infusion or increasing time duration in b/w doses.

To be held once anticholinergic effects

occur.(Absent bowel sounds, urinary retention,
agitation).
 Atropine Monitoring
• Patient to be assessed every 15 min to check adequacy of
dosages.
• If clinical features recur, further increment in boluses and
doubling.
• Once parameters reached, Monitoring hourly for atleast 6
hours to check effectiveness of infusion.
OP / Carbamate Observation Sheet

Bowel mental Atropine

Time heart rate Clear lung Pupil Dry SBP Fever SPO2
sounds state infusion
axilla > 80 >37.5c
dose
mm
Hg
 Atropine : When to stop..??

Bronchorrhoea : most important, for titrating dose.

• Atropine toxicity = absent bowel sounds + fever +
confusion.
• Stop infusion for 60 min, if toxicity.
• Re-start infusion at 80% of initial rate, once the temp.
comes down and patient calms.
• Most do not need >3-5 mg (5-9 ml) / hour of atropine
infusion.
• Reduce rate by 20% every 4 hourly once patient is
stable. STOP.
 Oximes
• Reactivate Acetyl cholinesterase, remove phosphoryl group.
• Discovered in 1950’s by Wilson et al.
• Among various oximes (obidoxime and trimedoxime)
Pralidoxime (PAM) remains, most widely used.
• Prevent continued toxicity by Scavenging and detoxifying
enzyme.
• Also endogenous anticholinergic effects.
• Available in four Salts : chloride, iodide, metilsulfate, and
mesilate.
• Chloride and iodide most widely used in developing countries.
• Chloride salt better than iodide.
 More active compound per gram of salt.
 No risk of thyroid toxicity.
 Oximes
Therapeutic effectiveness depends on
1. Concentration of poison consumed (Poison load).
2. Time lapse between poisoning and administration
3. Type of OPC. (More effective on diethyl than dimethyl).
Dimethyl compound reactivate and “age” at slower rate.
4. Lipid solubility of OPC.
5. Concentration of Oxime in blood.
 Oximes
The Controversies
• Two RCT’s in Vellore, India in early 1990’s noted,
Harm from low dose PAM infusion.
• A Cochrane review ( included two RCT’s , 2005) &
two other meta-analysis reported no clear benefit or
harm.
• An RCT in Baramati, India studying very high dose of
PAM in 200 patients with moderate OP poisoning
showed reduced Case fatility. (1% vs 8%).
 Oximes
The consensus
• Oximes will not be effective in very severe (large
dose) poisoning.
• Treatment with oximes should be started as early as
possible, no role if started after 48 hours.
• Less effective in severe complications such as
aspiration pneumonia or hypoxic brain injury before
treatment.
• Less or no effectiveness with dimethyl compounds
and atypical organophosphates.
• Not effective in carbamates but are not
contraindicated either.
 Oximes
Dosing
• PAM : 1-3 gm/day, no role after 48 hrs.
• Serum levels of > 4 mg/lit is necessary for effective
treatment.
• To achieve this, administered as bolus 20-40mg/kg
followed by continuous infusion at 500mg/hr.
• WHO recommendations : Loading dose 30mg/kg,
followed by infusion of 8mg/kg/hr.
 Oximes
Therapeutic end point
• Resolution of muscle fasciculation and weakness,
Reactivation and Increment in SChE levels.
• Use longer than 24 hours indicated if unaged OP’s
release from fat tissue.
• Infusion continued until patient remains symptom
free for atleast 12 hours without additional atropine.
• Or until extubated.
 Role of Benzodiazepines
• Control agitation.
• Sedation in ventilated patients.
• Many opioids, metabolized via SChE, so use for
sedation in pulmonary edema can worsen CNS
manifestation.
• Control of seizures : First line therapy in OP
poisoning, phenytoin not recommended d/t
membrane stabilizing effects.
• Seizures uncommon in oxygenated patients, more
common in nerve gas agents (soman and tabum).
• Diazepam reduce neural damage and prevent
respiratory failure (animal studies).
 Role of Magnesium Sulphate
• MgSO4 (4g) i/v in first day after admission,
decrease hospitalization period and mortality.
• It blocks Calcium channels and reduce
acetylecholine release from presynaptic
terminals.
• Also reduces CNS overstimulation from
NMDA receptor activation.
 Role of Clonidine
• Centrally acting α2-adrenergic receptor
agonists.
• Reduces acetylcholine synthesis and release
from presynaptic terminals
• Animal studies, shown benefit in combination
with atropine. Effect in humans unknown.
Advanced Neuroprotective Drugs

1. Ketamine : Noncompetitive NMDAR

antagonist, within 1 hour of nerve gas agent
induced seizures along with
Midazolam/diazepam.
2. Tezampanel : Glutamate receptor antagonist
specific for kainate subtype Rc, useful in
soman(nerve gas) induced seizures and
neuropathy.
3. Gacyclidine : Another antiglutamatergic
compound found beneficial in conjunction to
standard therapy in nerve gas poisoning .
 Advanced Neuroprotective Drugs

4. For OPIDN : standard therapy plus

corticosteroids.
5. Protease inhibitors : target esterase and
prevent delayed neuropathy.
6. Intermediate syndrome resistant to standard
treatment, artificial respiration.
7. Antioxidants : lipid peroxidation and
thiobarbituric formed in OP poisoning,
Antioxidant beneficial.
Vitamin E reported to have therapeutic effect
Intermediate syndrome : Management
• Usually presents 12 to 96 hours after exposure.
• Early signs : action tremors and pharyngeal
weakness (difficult deglutition , pooling of
secretions).
• Later : inability to flex neck, DTR’s lost, cranial
neuropathies, proximal muscle weakness and
respiratory muscle paralysis.
• Not all require intubation and ventilation, but
patients with tremors and pharyngeal weakness, at
increased risk.
• Treatment : totally symptomatic. Ventilator support if
respiratory muscle paralysis.
 Ventilatory Support
Indicated in stupor / coma, Hypoxemia (PaO2 <60
mmHg) and profound muscle weakness.

Predictors for need of mechanical ventilation.

1. Delay in the initiation of specific treatment.
2. Low level of sensorium at admission
3. Pinpoint pupils and generalized fasciculations.
4. Presence of convulsions
5. Presence of respiratory failure at admission.
6. High initial atropine requirement for atropinization.
 Weaning off Ventilator
• Asses respiratory muscle performance before
weaning off patient.
• Reduce slowly and gradually pressure support level
in CPAP with PSV mode.
Parameter Weaning threshold
PaCO2 <50 mmHg
Minute ventilation (spontaneous) <10-15 L/min
Tidal volumes >5 mL/kg
Maximum voluntary ventilation >20 L/min
Respiratory frequency <35 breaths/min or >6 breaths/min

• Extubate if :
 spontaneous breathing with no distress.
 generates VT >5 mL/kg at Pressure of 3-5 cm of H2O.
 Role of Alkalinization
• IV infusion of Soda. Bicarbonate produce moderate
alkalinization (pH : 7.45 to 7.55) in OP poisoning.

• Infusion of higher dosages (5mEq/Kg) in 60

minutes followed by 5-6 mEq/kg/day was shown
useful.(In dogs)

• More beneficial in Nerve agent poisoning.

• Cochrane review : Insufficient evidence to establish

use of NaHCO in human OP Poisoning.
 Role of Early Enteral Feeding.
• Early enteral feeds associated with improved
outcomes in critically ill because it prevents
enterohepatic circulation.

• Early nutritional supplementation in OP poisoning

assumes importance as these patients may require
prolonged ventilatory support.
 Role of Fresh Frozen Plasma.
• FFP contains important components like
Current evidence not strong enough to clotting
make clear
factors, conclusion
proteins, regarding
enzymes, etc.
bioscavenger role of FFP
• It is hypothesized that butyrylcholinesterase present

in FFP sequester free poison in blood and remove it

from circulation.

• Two trials, both unfavourable to FFP intervention.

 For the future…..
• Removal of OP’s from blood : Hemodialysis,
Hemoperfusion or hemofiltration.
• Hemofiltration after dichlorovos poisoning revealed
beneficial therapeutic effects.
• Military research aims at : Injecting
Butyrylcholinesterase after cloning into soldiers
before exposure to nerve gases.
 Not practical for prophylaxis in self-poisoning as one cannot
predict when a person is going to ingest pesticide.
• Use of recombinant bacterial phosphotriesterases, or
hydrolases to break down OP’s enzymatically.
 Take home message
1. Early stabilization and resuscitation.
2. Incremental dose Atropine.
3. Early institution of Oximes.
4. External decontamination, MgSO4, Clonidine, Use
of benzodiazepines and NMDA receptor antagonists,
Alklinization, Early Enteral feeding were found to
be beneficial.
5. FFP, forced emesis were found harmful.
6. Activated charcoal, Gastric lavage were found to
have no benefit or harm.
7. Gastric lavage : easily performed, cheap could be
used as an adjunct if performed within one hour.
Thank You