5 :2

Organophosphorus Poisoning:
Current management guidelines

ABSTRACT
NK Sundaray, Ratheesh Kumar J, Trivandrum
Organophosphorus (OP) compounds which are in use since
1940s world wide as insecticides have been a source of poisoning
and continue to pose management problems. Resuscitation, Intoxication by these agents continues to be a therapeutic
Decontamination, Specific antidote, and supportive measures problem. Possibility of exposure during war /terrorist activities
continue to be the main stay of therapy. Different authors have is increasing. Resuscitation, decontamination, early use of specific
prescribed different therapeutic regimens leading to controversies. antidote, close observation and good supportive care form the
This paper aims at offering a comprehensive guideline on these basis of management. Despite large number of cases being
aspects of management. Decontamination of the body by washing reported world wide, the current evidence base is small. (2)
with soap and water is to be thorough and complete. A repeat Text books recommend varied therapeutic antidote regimens
stomach wash in every case is recommended to remove residual leading to controversies and confusion. In this paper it is intended
OP. Atropine is the only life saving antidote and is to be started to offer a comprehensive guideline so that junior physicians can
along with decontamination. Out of 38 protocols prescribed in manage such acute poisoning cases efficiently. Before proceeding
literature a protocol of starting with dose of 1-2 mg followed by to management guidelines it will be proper to review the
bolus doses, every 5 min, with double of previous dose, in case pharmacodyamics of the OP compounds, so that the rationale
of no response, to achieve the target end point is recommended. behind the guidelines will be well appreciated.
Thereafter it is to be maintained through Atropine infusion (at Pharmacodynamics: - Orgnophosphates/carbamates inactivate
a rate of 10-20% of total atropine required to load the patient the enzyme Cholinesterase (ChE) by reacting at the esterase
per hour) for 24-48 hrs and gradually withdrawn over next 3-5 site, which leads to an increase in Acetylcholine (ACh) at the
days. Clearance of chest of secretions and maintenance of BP has muscarinic receptors, nicotinic receptors and in CNS leading to
been given more importance in the target point than size of pupil toxic effects. The phosphorylated/carbamated enzyme complex
and heart rate. Glycopyrrolate is recommended as an adjunct subsequently undergoes hydrolysis spontaneously (carbamated
to atropine to control secretions or when atropine toxicity is complexes within minutes to hours whereas phosphorylated
confused with OP toxicity.The role of Oximes has been questioned enzyme complexes take some 60 minutes to several weeks). The
by different workers both from India and abroad. Though it has reactivation time can be enhanced by oximes. Once OPenzyme
been shown to reactivate RBC cholinesterase the causes of failure complex looses the alkyl group (Ageing) it can not be reactivated.
to benefit have not been properly established. Because the idea (3)
is sound it is appropriate to recommend Pralidoxime to start as
OP compounds can be absorbed through skin, conjunctiva, oral
early as possible with a loading dose of 30 mg/kg IV to be given
mucosa, GI tract, respiratory tract, by direct contact, ingestion,
over 30 minutes to be followed by a continuous infusion of 8-10
inhalation and injection. The hydrocarbon solvent also produces
mg/kg/hr until clinical recovery or seven days whichever is later.
its effects. Most patients become symptomatic rapidly, though
Ventilation is the most useful life saving advance in supportive care.
the onset and severity of symptoms depend on the nature of
Criterias for ventilation have been defined. Use of tranquilizer
the compound, amount, route of exposure and rate of metabolic
has been recommended to be liberal. Poisoning effect of solvent
degradation. After absorption they are rapidly distributed in all
in OP compounds contributing to chemical pneumonitis is to
body tissues. Lipid solubility makes easy access to CNS and
be kept in mind. The need of close observation through OP obs
fat stores. They are intermittently released from fat stores to
sheet has been stressed. Use of fluids, diuretics, antibiotics etc
circulation/secreted to stomach and have been incrimininated for
has been discussed.
the sudden deterioration in a stable patient. Metabolism occurs
Introduction: - Organophosphorus (OP) compounds first principally by oxidation in the liver with conjugation and esterase
synthesized in early 1800s were developed as insecticides hydrolysis producing a half life of minutes to hours. Elimination
in early 1900s and found world wide application by 1941. (I) occurs via urine bile and faeces.Toxic effects of excreted products
 Organophosphorus Poisoning: Current management guidelines

Fig. 1 : Showing pin point pupil in a case of OP poisoning

Table 1 : Grading Severity of Organophosphate soap (OPs are hydrolyzed in an aqueous solution in high PH)
Poisoning .Skin folds and underside of fingernails and long hairs require
Normal serum acetylcholinesterase / RBC Cholinesterase level is 8.0-20.0 particular attention. Ocular decontamination is to be carried
u/l out by washing eyes with water/normal saline. Incontinent
MILD MODERATE SEVERE patient requires repeat wash. Attention should not be diverted
Walks and talks Cannot walk Unconscious, no from ABC of Cardiopulmonary resuscitation. Seizures are to be
Headache, dizzy Soft voice papillary reflex. Muscle controlled by appropriate measures.Two IV lines be secured and
Nausea,Vomiting Muscle twitching twitching, flaccid paraly- blood samples for haematological and biochemical and ChE be
Abdominal pain (fasciculations) sis. Increased bronchial collected.ECG be recorded. Laboured breathing, sweating, pin
Sweating, salivation Anxiety, restlessness secretions. Dyspnoea point pupil would suggest OP/carbamate poisoning. Fig-1 Antidote
Rhinorrhoea Small pupils (miosis) crackles / wheeze. Pos- inj atropine should be started immediately which should not be
sible convulsions withheld even if oxygen is not available.There is no good evidence
serum acetylcholinester- serum acetylcholinester- Respiratory failure
that giving atropine to a cyanosed patient would cause harm. (5)
ase enzyme (AChE) ase enzyme (AChE)
Results: 1.6-4.0 u/l Results: 0.8-2.0 u/l serum acetylcholinester- In case clinical presentation is not clear Inj. Atropine 0.6 mg to
ase enzyme (AChE) 1.0 mg may be given IV. Increase in heart rate by more than 20-25
Results: < 0.8 u/l beats/min and flushing would suggest that the patient does not have
significant cholinergic poisoning and further observation required.
in stool locally in form of burns over gluteal region, natal cleft and While observing effects of atropine give 500- 1000 ml of Normal
thighs have been noted. saline (10-20 ml/kg) over 10-20 min to compensate fluid loss due
Clinical features: - They are due to stimulation of muscarinic, to sweating, diarrhoea and cholinergic hyper-secretion. There is
nicotinic and central receptors. Onset is usually within 30 min no evidence that it will harm the patient with bronchorrhoea as
to 03 hrs. This may be delayed depending on the type of OP, long as atropine is being given. (5)History of alcohol ingestion
route of exposure and amount of systemic poison.The severity of should be enquired as well as possibility of other poison being
poisoning has been graded as mild, moderate and severe. (Table- consumed be ascertained.
1)(4) The end result may be a multi system event. Most fatality Active cooling and sedation: - Cooling is indicated if the patient
occurs within 24 hrs. is febrile and climate is hot & humid. Agitated patient need to be
Diagnosis: - History of exposure and clinical features suggest OP/ sedated with Inj. Diazepam 10 mg IV slowly which can be repeated
Carbamate poisoning. Measurement of ChE in serum and RBC up to 30-40 mg/24 hrs. Diazepam will help in allaying anxiety,
and detection of metabolic products in urine assist in diagnosis. . facilitate gastric lavage, reduce damage to CNS (6), diminish
central respiratory failure (7) and control seizure.
Management: - OP poisoning is a medical emergency. They need to
be nursed in general ICU with adequate ventilation unless specific Gastric Decontamination: - Forced emesis and syrup Ipecac have
complications need Specific ICU care. The health care workers no role.(8)Gastric lavage is indicated once patient is stabilized,
need protection through personnel protecting equipments. calm enough to give consent and in unconscious intubated patient,
Rubber Gloves and gowns are recommended as these compounds which is recommended to be repeated after 2-3 hrs (9).Though it
are known to penetrate latex /vinyl gloves. Charcoal cartridge has been recommended only to be carried out within 1-2 hours
masks are recommended for respiratory protection.The staff may of ingestion of OP/carbamate elsewhere it has been started even
need to be rotated if they can’t stand the noxious order. after 12 hrs of ingestion and repeated thrice at an interval of 4
hrs (10). Repeat stomach wash will remove the residual poison
Decontamination: - Besides, the decontamination at the site,
if any/secreted to stomach subsequently from fat stores. After
in the emergency department all clothing, hair accessories
aspirating the contents of stomach through stomach tube (if food
are to be removed and placed in appropriate waste bags. The
particles are present)/Ryle’s tube, water or normal saline in lots
person is to be washed with copious amount of water and
of 300 ml be given and be aspirated. Continue it till the returning

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Table-2: OP / Carbamate Obs Sheet

Remarks
Bowel
Time Heart rate Clear lung Pupil Dry axilla BP Mental state Fever >37.5c SPO2 Atropine
sounds
dose

Table 3 :Target end points for atropine therapy the paucity of data to drive a guideline it is prudent to start the
Clear chest on auscultation with no wheeze loading bolus dose 1-2 mg depending on severity and then to
Heart rate> 80 beats/min repeat same boluses every five minutes (in doubling doses in
Pupil no longer pin point case no improvement is seen) till atropinisation is achieved. An
Dry axilla atropine infusion titrated to achieve atropinisation is an alternate
Systolic blood pressure > 80 mm of Hg protocol. Atropine administration by nebulisation also improves
respiratory distress and oxygenation (17). It can also be given
fluid is colourless and odourless. Ensure that no fluid is left inside
through endotracheal tube initially before securing a veinous
the stomach by measuring the fluid taken off.
route.
Activated Charcoal: - Though there is no evidence that either
Criteria of Atropinisation: - There are no comparative studies
single dose or multiple dose regimens of active charcoal will
of markers for adequate atropinisation. Since patients usually
result in benefit yet a dose of charcoal (50 gm) can be left in the
die from respiratory or circulatory failure, air entry on chest
stomach (11, 12).
auscultation, heart rate and blood pressure were given more
Transfer to ICU: - Atropine and resuscitation measures are to be importance than dilatation of pupil, rise in body temperature,
continued and vitals recorded while transferring to ICU. Patients dryness of mouth/skin. The target end points for atropinisation
with the following criteria may need ventilator support.(13) are given in Table- 3 (5).
History of intake of large dose Atropine maintenance: - Target end point once achieved is to be
Copious secretions maintained by atropine infusion. Infusion of atropine reduces the
fluctuation in atropine concentration associated with repeated
Disturbed level of consciousness bolus doses. The rate of infusion is set at 10 -20 % of the total
Signs of hypoventilation or respiratory obstruction by secretions atropine required to load the patient every hour.

Hence intubation and ventilation facilities should be ensured to Observation: - Observations made initially after each atropine
be available in ICU. Patient is to be placed on monitor. Parameters dose is entered in the observation sheet. Once atropinisation has
including oxygen saturation are to be observed and recorded in been attained, those five parameters are to be monitored every
OP/Carbamate observation sheet. Table – 2(5) 15 minutes initially which can be gradually increased to 1-2-3
hours depending on the state of atropinisation. Close observation
Antidote: - Anticholinergics are competitive antagonist to Ach and monitoring plays not only a vital role in the management but
and reverse all muscarinic activities both in CNS and peripheral also can contribute to the learning process by gathering new
nervous system. Inj.Atropine is the only life saving antidote. Full symptoms and signs and can anticipate recurring cholinergic crisis
and early atropinisation is an essential and simple part of early which may occur with little notice.
management. Clinical toxicology text books describe varied
atropine regimens.The sum total of 38 regimes found in literature Atropine toxicity: - Confusion, agitation, hyperthermia, ileus,
is to start a Bolus loading dose followed by boluses after a fixed tachycardia etc would suggest over atropinisation which would
time interval varying from 5-15-30 min till atropinisation or Bolus necessitate discontinuation of the atropine infusion, followed by
loading dose followed by infusion (14).The latter regimen showed frequent observation. When they settle down the infusion is to
improved outcome. (15) Although the benefit of infusion is not be started at 70- 80 % of the previous rate. Hyperthermia is a
yet proven this regime saves time, requires less observation, serious complication in hot wards which needs prevention. To
produces less fluctuation in plasma atropine concentration and avoid preservative toxicity powder atropine be reconstituted in
makes weaning easier.(16) The dose of atropine recommended to normal saline and be used.
be low (1-2 mg) so as to cater for milder cases and then rapidly Duration of maintenance atropine therapy: - This depends on
escalated (doubled each time) to achieve atropinisation quite the severity and response to therapy. Usually it is maintained for
fast. Alternatively it started with a bigger dose (5 mg) to ensure 24- 48 hrs or longer in severe cases, and gradually withdrawn
rapid atropinisation. Because of danger of over atropinisation the over 3-5 days. Frequent observation is required to detect early
former practice offers more control by starting with low doses. signs of intermediate syndrome. Tidal volume and blood gases
The peak effect of atropine is seen within three minutes of an IV are to be measured. Indications for ventilation have been spelt
injection. Hence, one need not wait for more than five minutes out. Table-4 (3). .
before giving another bolus. Though the authors acknowledged
Glycopyrolate: - Some studies have shown that glycopyrolate

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 Organophosphorus Poisoning: Current management guidelines

Table 4 : Guidelines for ventilator support Table 5 : Equivalent dosing units of pralidoxine salts
I. Respiratory Gas Tensions Salt Equivalent dose (g)
i Direct Indices Pralidoxine chloride 1.00
Arterial Oxygen Tension < 50 mm Hg on room air Pralidoxine mesilate 1.34
Arterial Co2 Tension > 50 mm Hg in the absence of metabolic Pralidoxine metilsulfate 1.43
alkalosis Pralidoxine iodide 1.53
ii Derived Indices
P a o2/ Fio2 < 250 mm of Hg reactivation of red cell acetylcholinesterase in diethyl OP pesticide
PA-aOo2 ( Pulmonary arterial-alveolar O2 gradient) > 350 mm poisoned patient (ageing in this compound AChE complex takes
of Hg much longer than Dimethyl OPs) the reason for their failure
Vd/Vt> 0.6 to benefit was not apparent.(22) Further studies on different
II. Clinical - Respiratory Rate (RR)> 35 breaths/min regimens or different oximes have been recommended by these
III. Mechanical Indices workers while proposing type of OP and it’s coformulant, poison
Tidal Volume 5 ml/kg load, time to start of therapy and the dose of oxime being the
Vital capacity < 15 ml/kg limiting factors.(23)
Maximum inspiratory force <- 25 cm of H2O
Since the idea is sound and animal experiments suggest it is useful,
is equally effective with fewer central nervous system side it is recommended preferably in moderate to severe cases. (9,
effects and better control of secretions. Since it does not enter 24)It is to be administered as early as possible post ingestion
CNS initial muscarinic signs like coma or drowsiness will not to offer benefit. Delayed presentation is not a contraindication
respond. Hence it’s use is recommended when there is copious (4). There are no definite dose recommendations. However, it
secretion as an adjunct to atropine or when features of atropine has been established that the therapeutically effective oxime
toxicity like delirium etc are confused with CNS effects of concentration in plasma is 4mg/litre though effect has been
poison or when atropine is not available. Ampoules of 7.5 mg demonstrated in lower concentration as well. Elsewhere it has
of glycopyrolate in 200ml of saline is started as infusion and is been used as 2gm loading followed by 1gm/h for 48h by infusion
titrated to the desired effects of dry mucus membranes. (18)It (high dose) with benefit, concluding (25) that administration in
has also been given at a dose of 0.2mg IM stat and repeated 6hrly high dose and constant infusion is better than repeated bolus
if required. Diphenhydramine can be an alternate centrally acting administration. A low dose schedule (1gm bolus) has also shown
anticholinergic agent if atropine is not available (19). lower mortality suggesting that the bolus dose do achieve a
Magnesium Therapy: - Magnesium therapy in addition to atropine therapeutic concentration for a limited amount of time (26).
and oximes has been found to benefit.The mechanism appears to In view of above though guide lines are not definite, it is clear that
be inhibition of AChE and OP antagonism. (20) oximes are effective when given early and in high doses (dose to
Cholinesterase Reactivators: - These agents known as oximes get be adjusted depending on the salt used) that too a bolus dose
attached to the free anionic site of the enzyme ChE. The oxime offers benefit which is to be followed by infusion for a sufficient
end then reacts with the phosphorus atom of OP attached at the duration (therapeutic window for Diethyl AChE complex is 133h)
esteratic site of the enzyme. This oxime phosphate so formed Table-5 (27). Keeping these aspects in mind the guidelines followed
diffuses away leaving the enzyme intact (Reactivated ChE).In addition by Southern Hospitals Network appears most appropriate and
to reactivation they also slow the ageing of the phosphoylated is recommended as Initial bolus dose of 2gm IV(30mg/kg) over
enzyme complex and has a direct action in converting the OP to 30 min(rapid administration leads to complications ) which is
a harmless compound (21). Reactivation of ChE is more marked to be followed by 1 gm IV every 8 hours in mild to moderate
in the skeletal muscle than at autonomic site and not at all in CNS poisoning and in severe poisoning cases 500 mg/hour(8-10mg/
(Do not enter CNS).Thus their use in OP poisoning is secondary kg/h)till clinical recovery(12-24h after atropine no longer required
to that of atropine. Oximes (Pralidoxime, Obidoxime) are widely or the patient is extubated) or 7 days which is later. Repeat bolus/
used since 1955 in OP poisoning along with atropine within 24-48 infusion is to be ceased based on clinical testing or plasma ChE
hours post ingestion as pralidoxime chloride 1 gm every 3-4h for test.(4) Though oximes are not recommended for Carbamate
1-3 days.WHO guidelines recommended giving a 30 mg/kg loading poisoning, their use should not be withheld in case of unknown
dose of Pralidoxime over 10-20 min followed by a continuous cholinergic poisoning as definite harm to human beings has not
infusion of 8-10 mg/kg/hr until clinical recovery or seven days been demonstrated. (5)
have elapsed whichever is later. Where obidoxime is available a Ventilation: - This is the most useful advance in the management of
loading dose of 250 mg is followed by an infusion of 750 mg every Op poisoning and makes all the difference on outcome. Indications
24 hrs.Their efficacy however has been questioned over last two for ventilation have already been tabled above. Regular and
decades by workers from Sri Lanka, South Africa,Taiwan, Iran and close observation in initial course will guide when to ventilate.
India. All these studies have been criticized either on the basis Succinylcholine is to be avoided. Non-depolarising neuromuscular
of non comparable groups of selected patients or inadequate blocking agents require higher doses to show effect.
doses of PAM (9).Though these studies have demonstrated clear

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OP Patients

Vital data monitor

Physical exam
Glasgow Score

ABC resuscitation, Oxygen,

Fluid & Blood sample
Atropine 2 mg if needed

Observation every 5
Prepare the monitor, Pralidoxime 30 mg/Kg
minutes
Gastric lavage bolus in 30 minutes

Aspired water without 8-10 mg/Kg. hr infusion

No improvement Improvement
smell and clean until clinical recovery

Double the dose Repeat with the

Check the vital data, same dose
of Atropine
respiratory exam, etc

Atropinization

Atropine infusion
10%-20% of loading

Atropinization Maintain Atropine toxicity

cannot maintain Atropinisation

Bolus + infusion Keep on infusion Stop until

toxicity resolved

Decrease until
stop atropine

Fig. 2 : Treatment Protocol for OP Poisoned Patient

Furosemide: - It is recommended if pulmonary oedema persists, Summary of treatment protocol is given in figure-2.(10)
even after full atropinisation.
Contraindications: - Drugs like morphine, succinylcholine,
Hydrocarbon Aspiration: - In case of ingestion of liquid theophylline, phenothiazine and reserpine are contraindicated.
concentrates of OP, hydrocarbon solvent aspiration causes Adrenergic amines should be given only if there is specific
chemical pneumonitis. These cases are to be managed as a case indication, such as marked by hypotension.
of Acute Respiratory Distress Syndrome.
Conclusion: - Medical management of Organophosphorus
Antibiotics:- Broad spectrum antibiotics are to be instituted as pesticide poisoning demands close observation, timely institution
per antibiotics policy of the institution, considering the risk of of antidote in adequate doses and duration and good supportive
infection due to frequent and multiple interventions. care. Though available evidence is lacking in many aspects of
different controversies, attempt has been made to define them and
Agitation/Convulsion: - Causes of agitation unrelated to pesticide
offer a pragmatic therapeutic protocol which will enable junior
toxicity like alcohol withdrawal/full bladder unless catheterized/
physicians to manage these patients with confidence and success.
head injury etc are to be excluded. Role of Diazepam has already
been described and is preferred over haloperidol. Intraosseous
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 Organophosphorus Poisoning: Current management guidelines

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