Journal of Toxicology

CLINICAL TOXICOLOGY
Vol. 42, No. 6, pp. 865–875, 2004

Speed of Initial Atropinisation in Significant Organophosphorus

Pesticide Poisoning—A Systematic Comparison of
Recommended Regimens

Michael Eddleston,1,2,* Nick A. Buckley,1,3 Helaina Checketts,4

Lalith Senarathna,1 Fahim Mohamed,1 M. H. Rezvi Sheriff,1
and Andrew Dawson1,5
1
South Asian Clinical Toxicology Research Collaboration, Department of Clinical
Medicine, Faculty of Medicine, University of Colombo, Sri Lanka
2
Centre for Tropical Medicine, Nuffield Department of Clinical Medicine,
University of Oxford, UK
3
Department of Clinical Pharmacology and Toxicology,
Canberra Clinical School, ACT, Australia
4
Medical Toxicology Unit, Guy’s and St. Thomas’s Hospitals, London, UK
5
Department of Pharmacology, University of Newcastle, Australia

ABSTRACT

Objective: Early deaths from organophosphorus (OP) pesticide self-poisoning result

from respiratory failure and cardiovascular collapse. Therapy requires the urgent use
of atropine to reverse cholinergic excess, thereby improving respiratory function, heart
rate, and blood pressure. We aimed to assess variation in textbook recommendations
for early atropinisation and to see whether this variation affected time to stabilisation
using model data from 22 severely poisoned patients seen in a Sri Lankan clinical
trial. Methods: We extracted prospectively recorded data on atropine requirements for
22 OP poisoned patients who required intubation but survived to discharge. We did a
systematic search for textbook recommendations for initial atropinisation regimens.
These regimens were then applied to data from the Sri Lankan patients. Results: The
patients required a mean of 23.4 mg (standard deviation 22.0, range 1 – 75 mg)
atropine to clear the lungs, raise the pulse above 80 bpm, and restore systolic blood
pressure to more than 80 mmHg. Textbook recommendations varied markedly—
atropinisation of an average patient, requiring the mean dose of 23.4 mg, would have
taken 8 to 1380 mins; atropinisation of a very ill patient, requiring 75 mg, would have
taken 25 to 4440 mins. Atropinisation was attained most rapidly with a regimen of

*Correspondence: Michael Eddleston, South Asian Clinical Toxicology Research Collaboration, Department of Clinical Medicine,
Faculty of Medicine, University of Colombo, P.O. Box 271, 25 Kynsey Road, Colombo 08, Sri Lanka; E-mail: eddlestonm@eureka.lk.

865

DOI: 10.1081/CLT-200035223 0731-3810 (Print); 1097-9875 (Online)

Copyright D 2004 by Marcel Dekker, Inc. www.dekker.com
866 Eddleston et al.

increasing bolus doses after failure to respond to the previous bolus. Conclusions:
There is great variation in recommendations for atropinisation, with some regimens
taking hours and even days to stabilise a patient. The guidelines are very flexible—
possibly appropriate for experienced emergency physicians or clinical toxicologists,
but completely inappropriate for the inexperienced junior doctors who see most cases
worldwide. We recommend that a consensus guideline be developed by appropriate
organisations to bring order to this important part of OP therapy, while acknowledging
the paucity of data to drive the guidelines.

INTRODUCTION hospital serving 750,000 people, who had been

intubated but survived were identified from the study
Acute organophosphorus (OP) pesticide poisoning database. The ingested pesticide was identified by
is a major global clinical problem (1 – 3), with hundreds history from patient or relative, or by the bottle being
of thousands of deaths occurring every year (4,5). Early brought into the hospital; clinical features shown by
deaths result from respiratory failure—due to central patients were consistent with a diagnosis of OP
respiratory depression, neuromuscular junction weak- poisoning. The quantity of atropine given to each
ness, bronchorrhoea and bronchospasm—and from car- patient was noted from entries made in the patient’s
diovascular collapse (6). Therapy requires urgent admi- records at the time of initial management. All patients
nistration of sufficient atropine to reverse signs of were managed following a standard protocol (11);
cholinergic excess (attain ‘atropinisation’) (7 –9), as criteria used for atropinisation are given in Box 1.
well as airway and ventilatory support (10). Current We searched for textbooks of clinical toxicology
guidelines recommend the use of bolus doses to attain published between 1993 and 2003 using www.ama-
atropinisation, followed by an infusion (8). zon.com and the keywords ‘clinical toxicology,’ and
Carrying out a randomized controlled trial (RCT) ‘poisoning.’ The searches produced 2386 and 16848
of activated charcoal in acute self-poisoning in north hits, respectively. The title and accompanying descrip-
central Sri Lanka, we have managed more than 600 OP tion was reviewed for the first 450 and 800 hits for
poisoned patients over 18 months. Major issues with each search—200 past the last text found to be a
their management have been how to give the loading clinical toxicology textbook. The ‘clinical toxicology’
doses of atropine and for which criteria of atropinisa- search revealed nine texts (14 – 22), the ‘poisoning’
tion to aim (11). A review of textbooks found many search an additional fifteen (23 – 37). One text (27) was
different regimens with little consensus. an updated concise version of another (28); only the
Widely varying regimens of atropinisation have also former was therefore included.
been reported by doctors seeing OP poisoned patients in We also searched three library catalogues: Royal
different parts of the world. One group infused atropine Society of Medicine (http://www.rsm.ac.uk/librar/
0.02– 0.08 mg/kg over one hour to attain atropinisation library.htm) using the complex search option, ‘poison-
(12). Such a regimen would take four hours to administer ing’ or ‘clinical toxicology’ in the title, for 1993 –2003,
20 mg of atropine to a severely ill 70 kg patient (13). search restricted to books. 44 texts were retrieved; four
Noting this wide variation, we reviewed texts of texts were relevant, one not previously found (38).
clinical toxicology for recommendations on early British Library (http://www.bl.uk/catalogues/toppage.
atropine administration. We aimed to compare the html) using ‘all catalogues’ option, ‘poisoning’ or
regimens by calculating the time it would take for each
recommended regimen to fully atropinise two hypo-
thetical significantly ill patients—one requiring the
mean amount of atropine given to severely ill patients Box 1.
in our study and one requiring the highest amount of Target end-points for atropine therapy
atropine given to a surviving patient. . Clear chest on auscultation
. Heart rate > 80/min
. Systolic BP > 80 mmHg
. Pupils no longer pinpoint
METHODS . Dry axillae

Patients with OP self-poisoning admitted to We aimed to attain at least four end-points, including all of the
Anuradhapura General Hospital, a secondary district first three, before considering a patient atropinised.
 Table 1. Atropine recommendations in textbooks, handbooks, and online databases of clinical toxicology.

Recommended regimen
to attain atropinisation Max dose of
Source Edition/year (IV unless stated otherwise) Markers of atropinisation atropine first 24 h

Aggarwal (24) 1st/1997 2 – 4 mg, repeated every 5 – 15 min Dry secretions NG

Bryson (18) 3rd/1996 2 – 4 mg, repeat or increase Drying of secretions, skin and 1g
until atropinisation mouth, mydriasis, flushed skin,
and tachycardia
Casarett (23) 7th/2003 5 mg, repeated every 20 – 30 min No sweating or salivation, Up to 50 mg
flushed skin, mydriasis
Dreisbach (30) 13th/2001 2 mg IM, repeat every 3 – 8 min Control of ‘‘signs of NG
parasympathetic toxicity’’
Dart 1 (40)* 1st/2000 2 – 4 mg, repeated every 5 – 10 min Control of pulmonary secretions ‘‘Massive amounts’’
(or doubling the dose)
Dart 2 (15)* 3rd/2003 2 – 4 mg, repeated every 2 – 5 mins, Control of pulmonary secretions, with NG
with increasing incremental doses clear lungs and adequate oxygenation
(e.g., 4 – 8 mgs)
Fernando (49) 2nd/1998 2 – 10 mg, then 2 mg repeated Counteract muscarinic effects on pulse, > 100 mg
Speed of Initial Atropinisation in Significant OP Pesticide Poisoning

every 10 – 15 min secretions, pupil

Flanagan (19) 1st/2001 2 mg, every 5 – 10 min Dry mouth, pulse of 70 – 80 bpm, 1–2 g
reduction of bronchial secretions
Ford (17) 1st/2001 1 – 2 mg; repeated every 5 min Drying of the tracheobronchial tree 100 s of mg
doubling the dose and ability to oxygenate the patient
Goldfrank (20) 7th/2002 1 – 5 mg, repeated every 2 – 3 min Dry skin and mucous membranes, 1g
decreased or absent bowel sounds,
tachycardia, reduced secretions, no
bronchospasm and usually mydriasis
Gossel (32) 3rd/1994 2 – 4 mg, repeated every 10 – 15 min Diminish bradycardia, salivation, and 50 mg
bronchial secretions; produce signs
of atropinisation (mydriasis,
tachycardia and dry mouth)
Haddad (16) 3rd/1998 1 – 2 mg, then 2 mg repeated Flushing, drying of airway secretions, NG
every 15 – 30 min dilated pupils, increased heart rate
Henry (29) 1st/1997 2 – 4 mg, repeated every 10 min Dry mouth, plus pulse >100, pupils dilated ‘‘Large amounts’’
Hypertox (45) 3.7/2003 1 – 2 mg, repeated every 5 – 10 min No secretions NG
867
Jones (34) 1st/2001 2 mg, repeated every 10 min Flushed red skin, tachycardia, 30 mg or more
dilated pupils, dry mouth 868
Krieger (38) 2nd/2001 2 – 5 mg, repeated every 10 – 20 min Flushed skin, dry mouth, dilated pupils, 3.5 g
bronchodilation, raised heart rate
Lall (22) 1st/1998 2 – 5 mg, repeated every 5 – 10 min Control of parasympathetic manifestations, NG
or clearing of rales and drying of
pulmonary secretions
Leikin (27) 3rd/2001 2 – 5 mg, repeated every 5 – 10 min Dry pulmonary secretions > 100 mg
Poisindex (46) 2003 2 – 5 mg, repeated every 10 – 30 min Clear lungs, no secretions NG
Olson (14) 3rd/1999 1 – 5 mg, repeated every 5 – 10 min Clear chest, dry secretions, reversal of Several grams
significant bradycardia
PAPA (50) 2nd/1999 1 – 3 mg, repeated every 5 – 10 min Dry flushed skin, pupillary size at least NG
4 mm, heart rate >120/min
Proudfoot (25) 2nd/1993 2 mg, repeated every 10 – 30 min Flushed dry skin, tachycardia, dilated NG
pupils, dry mouth
Proudfoot (31) 2nd/1996 2 mg, repeated to control peripheral Control of bronchospasm and bronchorrhoea 100 mg or more
muscarinic signs
Reigart (26) 5th/1999 If GCS normal: 2 – 4 mg, repeated Control of pulmonary secretions 300 mg
every 15 min. If GCS reduced:
 4 – 8 mg, repeated every 5 – 15 min
Seyffart (10) 4th/1996 1 – 2 mg, repeated or increased in Abolition of excess bronchial secretion, NG
increments every 15 – 60 min dry mouth and skin, flushing
Toxbase (47) 2002 2 mg, repeated every 10 – 30 min Reversal of bronchospasm and bronchorrhoea ‘‘Very large doses’’
Toxinz (48) 2003 1 – 5 mg, repeated every 5 – 30 min Clear lungs, no secretions >200 mg
WHO PIM (43) 1986 1 – 2 mg, then same or increased Full atropinisation (signs include dilated ‘‘Several hundred mgs’’
dose every 15 – 30 min pupils, dry mouth, skin flushing)
WHO EHC (42) 1999 2 mg, then same or increased Full atropinisation (signs include dilated ‘‘Several hundred mgs’’
dose every 15 – 30 min pupils, dry mouth, skin flushing)
WHO OP Antidotes (9) 2002 2 mg, then same or increased Reduction in secretions, especially NG
dose every 15 – 30 min bronchial secretions
WHO Treatment guide (44) 1999 1 – 2 mg, repeated every 5 – 10 min Drying of respiratory secretions 100 mg
Viccellio (37) 2nd/1998 1 – 2 mg, then 2 mg repeated every Control of bronchial secretions 1g
5 – 10 min. Larger increments of and bronchospasm
atropine may be used.

*These texts had two and three different recommendations, respectively, for atropinisation. The recommendations given for OP poisonings are presented here.
Eddleston et al.
Speed of Initial Atropinisation in Significant OP Pesticide Poisoning 869

‘clinical toxicology’ in the title, for 1993 –2003. 144 (for example, 1.2 mg initial bolus, then 2.4 mg, then
texts were retrieved; 12 texts were relevant, one not 5 mg, etc). Criteria for atropinisation are given in Box 1.
previously found (39). National Library of Medicine All patients received pralidoxime 1 g qds for 1 –3 days.
(http://locatorplus.gov/) using advanced menu search The 22 patients required a mean of 23.4 mg of
option, ‘poisoning’ or ‘clinical toxicology’ in the title, for atropine on admission (standard deviation 22.0, range
1993 –2003, restricting the search to books in English— 1 – 75 mg; the patients requiring the lower doses had
471 texts were retrieved; 18 texts were relevant, two not previously received atropine at a peripheral hospital
previously found (40,41). One of these texts (41) could before transfer). This quantity of atropine given to attain
not be obtained because it is not yet in print. atropinisation does not include the atropine that was
Online sources were also checked: INTOX project subsequently given by infusion. Seventeen patients were
of the WHO/IPCS (four texts (9,42 – 44); Hypertox intubated on admission; the other five were intubated
(Australia) (45), Poisindex (USA) (46), Toxbase (UK) during the next few days for the intermediate syndrome.
(47), and Toxinz (New Zealand) (48). Interview of
colleagues and communication with the AACT central Recommended Atropine Regimens in
office revealed four other books (10,49 –51). Data were Textbooks of Clinical Toxicology
also extracted from WHO (52), UK (53), and Australian
(54) formularies, and from international textbooks of We obtained thirty eight recommendations for
internal medicine (55 – 57). atropinisation from clinical toxicology textbooks and
Regimens for atropine administration in acute OP electronic sources, national formularies, and interna-
poisoning were sought in each text. The following in- tional textbooks of internal medicine (Tables 1 and 2).
formation was extracted: administration rate of atropine, All (15 – 17,20) the texts commonly used by American
criteria for full atropinisation, and maximum amount of poison control centers were included (R Soloway,
atropine that might be required in a severely poisoned AAPCC, personal communication). Overall, thirty three
patient (Tables 1 and 2). Such information was not different recommendations were obtained.
given in five sources (21,33,35,36,51), which were Most sources gave a range of atropine dosages and/
therefore excluded from the analysis. or intervals between repeat doses, for example, ‘give 2 to
These atropine administration rates were then 5 mg of atropine every 5 –10 minutes.’ Using this reg-
applied to the mean dose of atropine required by the imen, the time to give 10 mg varies from 5 minutes after
Sri Lankan patients and to the highest dose of atropine the first dose (5 mg every 5 minutes) to 40 minutes
required by one patient (75 mg). after the first dose (2 mg every 10 minutes). In this way,
a range of times to atropinisation was calculated for
each recommendation.
RESULTS Applying these recommendations to a Sri Lankan
patient, intubated but surviving to discharge, and
Cohort of OP Poisoned Patients requiring the mean atropine dose of 23.4 mg, between
8 and 1380 minutes were required to give the necessary
Between 31st March and 3rd December 2002, 23.4 mg (Fig. 1). For recommendations specifying a
1000 patients with acute poisoning were reviewed on range of atropine doses, there was often marked varia-
admission to Anuradhapura Hospital. 226 had ingested tion in time to atropinisation: e.g., using the regimen
OP pesticides; a further 44 had ingested an unknown of Harrison’s textbook (0.5 – 2 mg repeated every 5– 15
pesticide that required atropine and was most likely an min) (56) atropinisation would have occurred after
OP (less commonly, carbamates). either 55 or 690 mins depending on whether the larger
Sixty one patients required intubation. Of these dose was given every 5 mins or the smaller dose given
patients, 38 died after admission while 23 required in- every 15 mins. Even when given most aggressively,
tubation but survived to hospital discharge. Data on some of the regimens took more than 100 mins to give
atropine administration and intubation timing was avail- 23.4 mg.
able in the notes made by the study team at the time of The regimen given in Ford’s textbook (17) had the
admission for all but one of these patients. least variation in time to atropinisation—15 and 20
All the patients were seen on admission by a study mins for the fastest and slowest administration regi-
doctor and 0.6 – 3 mg of atropine administered to mens, respectively.
patients with signs of cholinergic poisoning (11). If Twenty four texts indicated that large amounts of
there was no response after five minutes, this initial dose atropine might be required for a severely ill patient—
was doubled until the patient was judged to be stable specific estimates ranged from 20 mg to 3.5 g (Tables 1
 870

Table 2. Atropine recommendations in major textbooks of internal medicine and national formularies.

Recommended regimen
Source Edition/year to attain atropinisation Markers of atropinisation Max dose of atropine first 24 h

Australian Medicines 4th/2003 2 mg IV repeated as necessary until Abolish all secretions Maximum dose may
Handbook (54) patient is atropinised, then infusion be > 50 – 100 mg/hour
titrated against clinical effects
British National Formulary (53) 46th/2003 2 mg, repeated every 5 – 10 min Dry flushed skin, dilated NG
(IM or IV according to severity) pupils, tachycardia
Davidsons (55) 19th/2002 2 mg, repeated every 10 min Dry secretions, reversal of bradycardia 30 mg, rarely more
Harrisons (56) 15th/2001 0.5 – 2 mg, repeated every 5 – 15 min Dry secretions NG
Oxford Textbook of 4th/2003 2 mg, repeated every 10 – 30 min No bronchorrhoea and bronchospasm, 30 mg, occasionally much more
Medicine (57) or flushed dry skin, dry
mouth, tachycardia
WHO Model Formulary (52) 1st/2002 2 mg, repeated every 20 – 30 min Flushed dry skin and tachycardia NG
Eddleston et al.
Speed of Initial Atropinisation in Significant OP Pesticide Poisoning 871

Figure 1. Range of times to give mean (23.4 mg; pale bars) and high (75 mg; dark bars) atropine loading doses for patients with
severe OP poisoning, following instructions from each text. Doses were based on 22 Sri Lankan patients. A range was not given for
three regimens (18,31,54) and they are not included in this figure. The times are curtailed at 18 hrs; eleven regimens took more than
18 hrs.

and 2). However, using the fastest regimen suggested by hospitals see 500 –1000 patients every year with case
each source, it would take between 25 and 740 minutes fatality over 20%. Since OPs are responsible for around
(12 h 20 min) to atropinise the Sri Lankan patient who two thirds of deaths in most case series of pesti-
required 75 mg (Fig. 1). With three regimens, it would cide poisoned patients (3), there are likely to be at
have taken more than 37 hours to give 75 mg using the least 200,000 deaths every year with these com-
slower of their recommended dosage rates. Some of pounds (4,5).
the regimens required as many as 70 bolus injections Full and early atropinisation is an essential and
of atropine. simple part of early management. Delayed atropinisa-
There was also marked variation in the criteria for tion can result in death from central respiratory
atropinisation. Fourteen sources used reversal of depression, bronchospasm, bronchorrhoea, severe bra-
bronchorrhoea and bronchospasm as their main criteria. dycardia and hypotension (6). Animal work suggests
Some used pupil size, flushed skin, or heart rate, in the that these early deaths may be primarily due to central
latter case often setting a lower limit of 120 bpm. cholinergic stimulation (58,59). Adoption of a regimen
that results in rapid atropinisation to block such
stimulation will likely save significant numbers of
DISCUSSION lives across the developing world where junior doctors
manage patients without advice from clinical toxicol-
Severe OP pesticide self-poisoning is a major ogists. Recommended regimens must be simple and
clinical problem in the Asia Pacific region—some easily used by such doctors.
872 Eddleston et al.

Our systematic search of clinical toxicology text- until pupils were dilated and pulse more than 120 –
books revealed multiple guidelines based on little 140/min. Since patients die from respiratory failure
evidence and varying from one source to another. For and/or cardiogenic shock, we think it more important
example, five texts stated that 2 –4 mg of atropine to reverse bronchospasm and bronchorrhoea, and
should be given ‘every 5 –10 min,’ ‘every 5– 15 min,’ improve systolic blood pressure and heart rate, than
‘every 10 min,’ ‘every 10– 15 min,’ or ‘every 15 min’ to dilate pupils or produce a tachycardia. Furthermore,
(Tables 1 and 2). It is tempting to wonder whether each both dilated pupils and tachycardia can result from
new recommendation is simply a tweaked old recom- stimulation of nicotinic ACh receptors, and tachycardia
mendation, made to look different from its predecessors. result from low total peripheral resistance with a
Most importantly, in inexperienced hands, the re- partially compensatory high cardiac output (61).
gimens could result in atropinisation not being reached There is currently little clear evidence for selecting
for many hours—over 11 hours to give 23.4 mg in atropine endpoints. Giving atropine to reverse signs
three cases and 23 hours in one case (Fig. 1)—leaving attributable to specific muscarinic (M) receptor sub-
patients in a dangerously unstable state. types may not reverse OP effects at other receptors. In
Many texts state that very large amounts of particular, since current endpoints do not include a
atropine might be required to stabilise a patient but CNS endpoint, it is possible that atropinisation is not
still recommend regimens that take hours to give these reversing the CNS cholinergic syndrome, which may
amounts. Taking the Sri Lankan patient who required have significant consequences for preventing early
the greatest amount of atropine (75 mg, well below the death from OP poisoning (58,59).
maximum amount stated in most texts—see Tables 1 Excess atropine can be dangerous. Endpoints such as
and 2), time to atropinisation varied from 25 min to pulse rates > 120/min and dilated pupils suggest that the
740 min (greater than 12 hrs) using the most aggressive patients are being given too much atropine. Atropine
regimens in each text. Time to atropinisation using toxicity causes confusion, agitation, and hyperthermia
some of the less aggressive regimens would have (7). Such effects are major problems in the hot, non-air
required more than 1.5 days. Note that the mean dose conditioned wards of the tropical developing world
of 23.4 mg and maximum dose of 75 mg are con- where most patients present. Agitated patients in ambient
servative estimates since many patients received some temperatures greater than 35C, not sweating because of
atropine at peripheral hospitals, prior to their admission atropine, can become very hot. The situation is
to the study hospital. exacerbated by alcohol or alcohol-withdrawal induced
There was also variation in the recommended in- agitation and may result in atropine-induced hyper-
terval between bolus injections—from 5 min to 30 min thermia and cardiac arrest (Eddleston, unpublished).
(Tables 1 and 2). Since blood levels peak quickly af- A further problem with fast heart rates is ischae-
ter IV injection and time to peak effect is within three mic heart disease in elderly patients. We have noted
minutes (60), waiting just five minutes for a response patients with fairly mild poisoning who died in ICU
before deciding whether to give another dose is prob- from myocardial infarctions after being given atropine
ably sufficient. to keep their heart rate at 120– 140 bpm. We therefore
The regimen that performed best was that of Ford’s prefer criteria for atropinisation to concentrate on
textbook (17). An initial bolus of 1 –2 mg is recom- clearing lungs, raising systolic blood pressure, and in-
mended with subsequent doses doubled every 5 minutes creasing the heart rate to just 80 –100 bpm.
until atropinisation is achieved. This regimen requires no
more than 20 minutes to administer 25 mg of atropine. It
also works well for the rare patient who requires very CONCLUSIONS
large amounts of atropine, permitting administration of
75 mg in 25– 30 minutes, and for patients requiring small This review of the clinical toxicology reference
doses since the initial bolus can be as little as 1 mg. sources reveals a variety of recommendations for
Importantly, it permits little variation in time to atropinisation, many of which would delay its attain-
atropinisation in the hands of an inexperienced junior ment for hours. In addition, some sources used criteria
doctor. Eight other regimens (9,10,15,18,37,40,42,43) for atropinisation that would cause atropine toxicity
suggested the use of larger bolus doses after the first dose rather than resolution of the poisoning. Evidence for
but did not specify increasing the amount given with each the recommendations is weak—there has been only one
subsequent dose administered. comparative study of different atropine regimens and
Criteria for atropinisation varied widely among this used historical rather than parallel group controls
sources—some texts recommended giving atropine (62). This situation is not unique to OPs—rather it
Speed of Initial Atropinisation in Significant OP Pesticide Poisoning 873

appears to be true for all forms of pesticide poisoning, 7. Heath AJW, Meredith T. Atropine in the manage-
if not all of clinical toxicology (63). ment of anticholinesterase poisoning. In: Clinical
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worldwide, we call upon clinical toxicology associa- and Carbamates. Oxford: Butterworth Heinemann,
tions to work with the WHO to review the evidence for 1992:543– 554.
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a simple guideline that will be useful for junior doctors Heath AJW, Ligtenstein DA, Marrs TC, Szinicz L,
faced by this severe form of poisoning across the world. Vale JA, Haines JA. Evaluation of antidotes for
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We thank the members of the Ox-Col Collabora- Intoxication. 4th ed. Miami, FL: PABST, 1996.
tion Poisoning Team for their superb work on the RCT, 11. Eddleston M, Dawson AH, Karalliedde L,
the medical and nursing staff of the study hospitals Dissanayake W, Hittarage A, Azher S, Buckley
for their support, and Nida Besbelli, Lewis Nelson, NA. Early management after self-poisoning with
Ladislaus Szinicz, Peter Eyer, and the journal referees an organophosphorus or carbamate pesticide. Crit
for their critique. ME is a Wellcome Trust Career Care 2004. In press.
Development Fellow, funded by grant GR063560MA 12. Sungur M, Guven M. Intensive care management
from the Tropical Interest Group. The South Asian of organophosphate insecticide poisoning. Crit
Clinical Toxicology Research Collaboration is funded Care 2001; 5:211 –215.
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