Organophosphate and Carbamate Poisoning

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Organophosphate and carbamate poisoning

AUTHOR: Steven Bird, MD, FACEP
SECTION EDITOR: Andrew Stolbach, MD, MPH, FAACT, FACMT, FACEP
DEPUTY EDITOR: Michael Ganetsky, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Mar 27, 2023.
INTRODUCTION
Organophosphates and carbamates are potent cholinesterase inhibitors capable of causing

severe cholinergic toxicity following cutaneous exposure, inhalation, or ingestion. Although
structurally distinct ( figure 1), organophosphates and carbamates exhibit similar clinical
manifestations with toxicity and require similar management following overdose.
An overview of organophosphate and carbamate poisoning will be presented here. A

summary table to facilitate emergent management is provided ( table 1). A general
approach to suspected drug intoxication is discussed separately. (See "General approach to
drug poisoning in adults".)
EPIDEMIOLOGY AND SOURCES OF EXPOSURE
Organophosphates have been used as insecticides worldwide for more than 50 years. The
use of these agents has declined in the last 10 to 20 years, in part due to the development of
carbamate insecticides, which are associated with similar toxicities [1]. Medical applications
of organophosphates and carbamates include reversal of neuromuscular blockade
(neostigmine, pyridostigmine, edrophonium) and treatment of glaucoma, myasthenia gravis,
and Alzheimer disease (echothiophate, pyridostigmine, tacrine, and donepezil).
Worldwide, an estimated 3,000,000 people are exposed to organophosphate or carbamate

agents each year, with up to 300,000 fatalities [2-4]. In the United States, there were more
than 8000 reported exposures to these agents in 2008, resulting in fewer than 15 deaths [5].
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Toxicity generally results from accidental or intentional ingestion of, or exposure to,
agricultural pesticides [2,4,6]. Other potential causes of organophosphate or carbamate
toxicity include ingestion of contaminated fruit, flour, or cooking oil, and wearing
contaminated clothing [6,7].
Specific agents linked to human poisoning include both carbamate (methomyl and aldicarb)
and organophosphate (parathion, fenthion, malathion, diazinon, and dursban) insecticides.
Chlorpyrifos, the organophosphate agent of dursban, is found in some popular household
roach and ant sprays, including Raid and Black Flag ( figure 2). The United States
Environmental Protection Agency (EPA) banned many household uses of chlorpyrifos in 2001,
and has restricted its use on certain crops including tomatoes, apples, and grapes [8].
Several organophosphorus nerve agents (eg, tabun [GA], sarin [GB], soman [GD]) were
developed in Germany during the 1940s, but were not used for military purposes [9]. The
1995 sarin attack on the Tokyo subway system by the religious cult Aum Shinrikyo and
subsequent international events have heightened awareness regarding the prevention,
recognition, and treatment of casualties due to organophosphorus ("nerve") agent exposure
[10-12]. More recently, assassination attempts involving Novichok, a newer class of
organophosphorus nerve agent that also affects peripheral nerves, have been perpetrated in
Europe [13-15]. (See "Chemical terrorism: Rapid recognition and initial medical
management".)
MECHANISM OF ACTION
Organophosphorus compounds contain carbon and phosphorous acid derivatives

( figure 1). These agents are well absorbed through the skin, lungs, and gastrointestinal
tract. They bind to acetylcholinesterase (AChE), also known as red blood cell (RBC)
acetylcholinesterase, and render this enzyme non-functional. AChE is the enzyme
responsible for hydrolysis of acetylcholine to choline and acetic acid, and inhibition leads to
an overabundance of acetylcholine at the neuronal synapses and the neuromuscular
junction [16,17].
After some period of time (dependent on the chemical structure of the organophosphorus
agent), the acetylcholinesterase-organophosphorus compound undergoes a conformational
change, known as "aging," which renders the enzyme irreversibly resistant to reactivation
by an antidotal oxime ( figure 3) [18].
In addition, plasma cholinesterase (also called butylcholinesterase [BuChE] or

pseudocholinesterase) and neuropathy target esterase (NTE) are inhibited by
organophosphorus agents; however, the clinical significance of these interactions are less
certain [19,20].
Carbamate compounds are derived from carbamic acid ( figure 1). Like organophosphorus
agents, carbamates are rapidly absorbed via all routes of exposure. Unlike
organophosphates, these agents are transient cholinesterase inhibitors, which
spontaneously hydrolyze from the cholinesterase enzymatic site within 48 hours. Carbamate
toxicity tends to be of shorter duration than that caused by equivalent doses of
organophosphates, although the mortality rates associated with exposure to these chemical
classes are similar [1].
CLINICAL FEATURES
Onset and duration of AChE inhibition varies depending on the organophosphorus agent's
rate of AChE inhibition, the route of absorption, enzymatic conversion to active metabolites,
and the lipophilicity of the organophosphorus agent. For most agents, oral or respiratory
exposures generally result in signs or symptoms within three hours, while symptoms of
toxicity from dermal absorption may be delayed up to 12 hours. Lipophilic agents such as
dichlofenthion, fenthion, and malathion are associated with delayed onset of symptoms (up
to five days) and prolonged illness (greater than 30 days), which may be related to rapid
adipose fat uptake and delayed redistribution from the fat stores ( table 1). The great
variability in toxicity and treatment response among organophosphorus agents, however, is
not well understood, leading some to suggest that each agent be considered independently
in future studies [21].
Acute toxicity
Cholinergic excess — Acute toxicity from organophosphorus agents presents with

manifestations of cholinergic excess. Primary toxic effects involve the autonomic nervous
system, neuromuscular junction, and central nervous system (CNS) [22]. The
parasympathetic nervous system is particularly dependent on acetylcholine regulation, since
both the autonomic ganglia and end organs of the parasympathetic nervous system are
regulated by nicotinic and muscarinic cholinergic receptor subtypes, respectively
( figure 4).
The dominant clinical features of acute cholinergic toxicity include bradycardia, miosis,
lacrimation, salivation, bronchorrhea, bronchospasm, urination, emesis, and diarrhea.
Diaphoresis occurs because sweat glands are regulated through sympathetic activation of
postganglionic muscarinic receptors. At times, however, mydriasis and tachycardia may be
observed, as sympathetic ganglia also contain nicotinic receptors ( figure 4).
The muscarinic signs can be remembered by use of one of two mnemonics:
● SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis,

Bronchorrhea, Bronchospasm, Bradycardia
● DUMBELS – Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia,

Emesis, Lacrimation, Salivation [23]
It should be noted that these mnemonics do NOT take into account the critical CNS and
nicotinic effects of these toxins. The nicotinic effects include fasciculations, muscle weakness,
and paralysis via acetylcholine stimulation of receptors at the neuromuscular junction. This
mechanism is analogous to the depolarizing effects of succinylcholine in producing
neuromuscular blockade. Nicotinic and muscarinic receptors also have been identified in the
brain, and may contribute to central respiratory depression, lethargy, seizures, and coma
( figure 4).
Cardiac issues — Cardiac arrhythmias, including heart block and QTc prolongation, are
occasionally observed in organophosphorus agent poisoning [24]. It is unclear whether
these arrhythmias are due to direct toxicity or secondary hypoxemia.
Case reports and small case series suggest that up to one-third of patients with severe OP
poisoning manifest signs of myocardial ischemia, such as an elevated troponin or changes in
the electrocardiogram (ECG) [25,26]. Peak troponin concentrations occur at presentation in
most cases. Risk appears to be greatest in older patients and those with severe poisoning,
but low in patients with mild poisoning. (See "Electrocardiogram in the diagnosis of
myocardial ischemia and infarction".)
Respiratory issues — Fatalities from acute organophosphorus agent poisoning generally

result from respiratory failure due to a combination of depression of the CNS respiratory
center, neuromuscular weakness, excessive respiratory secretions, and bronchoconstriction.
Fatalities also occur due to cardiovascular collapse; although the mechanism of this
dysfunction is not completely understood, inappropriate vasodilation may play a role [27].
Intermediate (neurologic) syndrome — Ten to 40 percent of patients poisoned with

organophosphorus develop a distinct neurologic disorder 24 to 96 hours after exposure and
resolution of cholinergic excess. This disorder, referred to as the "intermediate syndrome,"
consists of characteristic neurological findings including neck flexion weakness, decreased
deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and
respiratory insufficiency [28-30].
Risk factors for the development of intermediate syndrome appear to include exposure to a
highly fat-soluble organophosphorus agent, and may be related to inadequate doses of
oximes [31]. The intermediate syndrome has rarely been described following carbamate
poisoning.
With adequate supportive care, including prolonged mechanical ventilation, most patients
have complete resolution of neurologic dysfunction within two to three weeks. Clinical
deterioration and improvement appear to correlate with red blood cell (RBC)
acetylcholinesterase levels. Nerve conduction studies on patients with intermediate
syndrome reveal unique postsynaptic abnormalities that differentiate this disorder from
delayed neurotoxicity (see 'Delayed and long-term neuropathology' below) [32]. (See
"Evaluation of peripheral nerve and muscle disease".)
Delayed and long-term neuropathology — Organophosphorus agent induced delayed

neuropathy (OPIDN) typically occurs one to three weeks after ingestion of one of a small
number of specific organophosphorus agents, including chlorpyrifos ( figure 5) [33-35].
Carbamates are only rarely associated with the development of OPIDN [36,37]. The
mechanism may involve inhibition of neuropathy target esterase (NTE), rather than
alterations in RBC acetylcholinesterase function (see 'Mechanism of action' above) [38]. This
enzyme, which is found in the brain, peripheral nerves, and lymphocytes, is responsible for
the metabolism of various esters within the cell.
Affected patients present with transient, painful "stocking-glove" paresthesias followed by a

symmetrical motor polyneuropathy characterized by flaccid weakness of the lower
extremities, which ascends to involve the upper extremities. Sensory disturbances are
usually mild. Delayed neurotoxicity primarily affects distal muscle groups, but in severe
neurotoxicity, proximal muscles groups may also be affected [39]. Electromyograms and
nerve conduction studies of affected patients reveal decreased firing of motor conduction
units [40]. Histopathologic sections of peripheral nerves reveal Wallerian (or "dying-back")
degeneration of large distal axons [41]. (See "Evaluation of peripheral nerve and muscle
disease".)
The risk of developing OPIDN is independent of the severity of acute cholinergic toxicity.
Some organophosphorus agents, such as parathion, are potent cholinergic agents but are
not associated with OPIDN. Others, such as triorthocresyl phosphate (TOCP), produce few
clinical signs of cholinergic excess but are frequently implicated in OPIDN ( figure 5) [42].
Most cases of mild delayed neurotoxicity improve with time; in severe cases, an upper motor
neuron syndrome with spasticity of the lower extremities usually causes permanent
disability.
Survivors of acute organophosphorus agent poisoning may have neurobehavioral deficits

such as decreased memory, abstraction, and attention, and Parkinsonism, which may be
permanent [43-45]. It is unclear if these neurocognitive effects are due to direct neurotoxicity
of organophosphorus agents themselves, or related to hypoxia and other non-specific
effects of serious illness.
Additional effects — Several case reports describe acute kidney injury (AKI) requiring renal
replacement therapy in the setting of severe organophosphate poisoning [46,47]. Causality
has not been established and it remains unclear whether the AKI is due directly to the OP or
the general effects of critical illness, but in severe OP poisoning it is prudent to monitor renal
function. Acute pancreatitis may complicate poisoning caused by either organophosphates
or carbamates [48].
DIAGNOSIS
Clinical findings — The diagnosis of organophosphate or carbamate poisoning is made on

clinical grounds. In the absence of a known ingestion or exposure, the clinical features of
cholinergic excess should indicate the possibility of organophosphate poisoning. Many
organophosphorus agents have a characteristic petroleum or garlic-like odor, which may be
helpful in establishing the diagnosis. (See "General approach to drug poisoning in adults".)
Due to significant variability in toxicity, every effort should be made to precisely identify the
agent. It is imperative to determine if a dimethyl or a diethyl poison was involved
( figure 1). The duration of toxicity and the therapeutic window during which oxime
treatment is likely to be effective are markedly different for these two classes of toxins.
Dimethyl compounds undergo rapid aging, making early initiation of oxime therapy critical;
diethyl compounds may exhibit delayed toxicity, and may require prolonged treatment [3].
If doubt exists as to whether an organophosphate or carbamate has been ingested, a trial of

1 mg atropine in adults (or 0.01 to 0.02 mg/kg in children) may be employed. The absence of
signs or symptoms of anticholinergic effects following atropine challenge strongly supports
the diagnosis of poisoning with an acetylcholinesterase inhibitor.
Laboratory abnormalities — Direct measurement of RBC acetylcholinesterase (RBC AChE)

activity provides a measure of the degree of toxicity. Sequential measurement of RBC AChE
activity (if rapidly available) may also be used to determine the effectiveness of oxime
therapy in regeneration of the enzyme. Determination of RBC AChE activity can also be
helpful in evaluating chronic or occupational exposure. However, most hospital laboratories
are unable to perform this test. An assay for plasma (or pseudo-) cholinesterase activity is
more easily performed, but does not correlate well with severity of poisoning and should not
be used to guide therapy [49].
MANAGEMENT
Initial resuscitation — Patients with markedly depressed mental status require 100 percent
oxygen and immediate endotracheal intubation. Furthermore, poisoned patients may rapidly
develop respiratory failure due to a combination of CNS respiratory center depression,

nicotinic receptor mediated diaphragmatic weakness, bronchospasm, and copious
secretions. Thus, even patients with normal mental status or normal vital signs may require
early endotracheal intubation. A summary table to facilitate emergent management is
provided ( table 1).
Clinicians should avoid the use of succinylcholine when performing rapid sequence
intubation (RSI) in patients with organophosphate (OP) poisoning. Succinylcholine is
metabolized by acetylcholinesterase (which is inhibited by OP compounds) leading to
exaggerated and prolonged neuromuscular blockade in poisoned patients. Nondepolarizing
neuromuscular blocking agents (eg, rocuronium) can be used, but may be less effective at
standard doses due to competitive inhibition at the neuromuscular junction. Therefore,
increased doses will likely be needed. (See "Rapid sequence intubation in adults for
emergency medicine and critical care".)
Bradycardia and hypotension are usually present in moderate to severe poisonings.

However, tachycardia or hypertension may transiently occur due to direct sympathetic
stimulation. Adequate volume resuscitation with isotonic crystalloid (eg, normal saline or
Lactated Ringer solution) should be performed concomitantly with other resuscitative and
diagnostic efforts. (See "Definition, classification, etiology, and pathophysiology of shock in
adults".)
Cholinergic toxicity — Patients with cholinergic toxicity due to organophosphate or

carbamate poisoning are treated with atropine and oxime therapy (typically pralidoxime) as
described below.
Atropine — Atropine competes with acetylcholine at muscarinic receptors, preventing

cholinergic activation. For moderate to severe cholinergic toxicity, atropine should be
administered beginning at a dose of 2 to 5 mg IV for adults and 0.05 mg/kg IV for children. If
no effect is noted, the dose should be doubled every three to five minutes until pulmonary
muscarinic signs and symptoms are alleviated. It is not necessary to provide oxygen prior to
initiating treatment with atropine [50].
Atropine dosing should be titrated to the therapeutic end point of the clearing of respiratory
secretions and the cessation of bronchoconstriction [51]. Tachycardia and mydriasis are not
appropriate markers for therapeutic improvement, as they may indicate continued hypoxia,
hypovolemia, or sympathetic stimulation. In patients with severe poisoning, hundreds of
milligrams of atropine by bolus and continuous infusion may be required over the course of
several days. For patients who do not respond to high doses of atropine, clinicians may add
treatment with epinephrine. (See 'Epinephrine' below.)
In patients with moderate or severe toxicity, after desired response is achieved with atropine
by bolus, we administer 10 to 20 percent of the total cumulative bolus dose as an IV
continuous infusion per hour [52-54]. We adjust the infusion rate as needed to maintain
adequate response (eg, clear lung auscultation, heart rate >80 beats/minute, systolic blood
pressure >80 mmHg, dry axilla, pupils no longer pinpoint) without causing atropine toxicity
(eg, confusion, pyrexia, absent bowel sounds, urinary retention). We adjust the infusion
according to clinical response and taper until recovery. When atropine toxicity occurs, we
hold the infusion until toxicity resolves and restart at 70 to 80 percent of the previous
infusion rate.
This individualized approach to treatment is supported by the results of an open label

randomized trial in which patients (n = 156) treated with incremental doses of atropine plus
infusion experienced lower mortality (6 versus 18 deaths) and fewer episodes of atropine
toxicity than patients treated with a standard bolus dose plus infusion [52].
In June 2003, the United States Food and Drug Administration (FDA) approved pediatric
doses of Atropen (atropine autoinjector) for children and adolescents exposed to certain
nerve agents and pesticides [55]. Atropen is designed for acute use by nonphysicians trained
in the recognition and treatment of nerve agent or insecticide intoxication. The approved
doses for mild symptoms of nerve agent poisoning vary by weight, as follows:
● 15 to 40 pounds (7 to 18 kg): 0.5 mg

● >40 to 90 pounds (>18 to 41 kg): 1.0 mg
● >90 pounds and adults (>41 kg): 2.0
Up to three times these doses may be administered to children with acute symptoms of
severe nerve agent poisoning.
Epinephrine — A relatively small percentage of patients do not respond adequately to

high-dose atropine therapy and may require treatment with epinephrine. Little evidence is
available to guide such decisions. The author would initiate an epinephrine infusion for
patients whose heart rate remains below 80 beats per minute (bpm) or who remains
hypotensive with an adequate heart rate (eg, 80 to 100 bpm) despite receiving high doses of
atropine.
In a clinical trial of 155 patients treated for organophosphate poisoning, 21 (13.6 percent) did
not mount a heart rate of at least 100 bpm despite high-dose atropine therapy and were
additionally treated with an epinephrine infusion. All patients treated with epinephrine had
an increase in heart rate, with 14 (75 percent) able to meet a prespecified goal of 100 bpm.
Most patients needed epinephrine for less than 12 hours, and all patients were successfully
weaned off epinephrine within 24 hours. Given limitations of the study design, no mortality
benefits were evident with the addition of epinephrine.
Pralidoxime — Since atropine does not bind to nicotinic receptors, it is ineffective in

treating neuromuscular dysfunction. Pralidoxime (2-PAM) and other oximes, such as HI-6 and
obidoxime, are cholinesterase reactivating agents that are effective in treating both
muscarinic and nicotinic symptoms ( figure 3) [3,17,56]. Pralidoxime should not be
administered without concurrent atropine in order to prevent worsening symptoms due to
transient oxime-induced acetylcholinesterase inhibition [57].
We suggest that oxime therapy be given to all patients with evidence of cholinergic toxicity,
patients with neuromuscular dysfunction, or patients with exposures to organophosphorus
agents known to cause delayed neurotoxicity ( figure 5). The current World Health
Organization recommendation for IV bolus therapy with pralidoxime is at least 30 mg/kg in
adults, and 25 to 50 mg/kg for children, based upon the severity of symptoms [18,58].
Although no treatments have been shown to prevent the intermediate syndrome or
organophosphorus agent-induced delayed neuropathy (OIDN), early oxime treatment may
be of benefit in this situation [59].
Pralidoxime should be administered slowly over 30 minutes, since rapid administration has
occasionally been associated with cardiac arrest, and slow administration prevents the
muscle weakness that results from the transient inhibition of acetylcholinesterase as
pralidoxime binds to the enzyme [60]. After the bolus dose, it appears that superior antidotal
effects occur with pralidoxime given as a continuous infusion of at least 8 mg/kg per hour in
adults and 10 to 20 mg/kg per hour for children [58,61].
Severe poisonings may result in prolonged redistribution of toxin; therefore, continuous IV

therapy should be adjusted based upon the patient's clinical response, and several days of
therapy may be required [62]. If rapidly available, serial red blood cell acetylcholinesterase
(RBC AChE) concentrations may be valuable in determining the efficacy of oxime-induced
acetylcholinesterase regeneration.
Evidence about the use of oximes to treat OP poisoning is inconsistent and difficult to
interpret [63]. There appears to be great variability among victims of organophosphorus
poisoning in their clinical response to pralidoxime, which is not well understood. In one
large, prospective study, patients poisoned with diethyl compounds (eg, chlorpyrifos) had
significantly lower mortality and intubation rates following treatment with pralidoxime than
those poisoned with dimethyl agents (eg, dimethoate, fenthion) [21]. Conversely, in a small,
double-blinded randomized trial, no significant benefit, and a trend towards harm, was
found in the group treated with pralidoxime compared to patients given placebo, regardless
of the type of organophosphate ingested [64]. Until this variability is better understood and
other treatments become available, we believe that all patients poisoned with
organophosphorus agents should be treated with an oxime.
Seizures — Organophosphorus agent-induced seizures should be treated with a

benzodiazepine. Prophylactic diazepam has been shown to decrease neurocognitive
dysfunction after organophosphorus agent poisoning [65,66]. This led, in part, to the United
States military development of a 10 mg autoinjector of diazepam for use in the setting of
chemical attack [67,68]. There is no evidence that phenytoin has any effect on
organophosphorus agent-induced seizures, and this agent is not recommended.
Decontamination — In cases of topical exposure with potential dermal absorption,

aggressive decontamination with complete removal of the patient's clothes and vigorous
irrigation of the affected areas should be performed. The patient's clothes and belongings
should be discarded since they absorb organophosphorus agents, and reexposure may
occur even after washing. Health care workers must take precautions to avoid accidental
exposure, including providing treatment in a well-ventilated area [11,69,70]. (See "Chemical
terrorism: Rapid recognition and initial medical management".)
We generally do not perform gastric lavage. Nevertheless, some clinicians may elect to do so
in patients who present less than one hour following ingestion of an organophosphorus
agent, AFTER performing endotracheal intubation and initiating therapy with atropine and
an oxime. Gastric lavage involves substantial risk of aspiration in patients with increased
secretions and decreased mental status, and this intervention has never been shown to
decrease morbidity or mortality [51].
Following initial resuscitation and treatment, we suggest activated charcoal (AC) be given to
patients presenting within one hour of an organophosphorus agent or carbamate ingestion.
The standard dose is 1 g/kg (maximum dose 50 g). We do not give AC to patients presenting
more than one hour following ingestion. Findings from randomized and observational trials
suggest that AC given after the first hour provides no benefit to patients with these
ingestions [71].
Forced emesis is contraindicated because of the risk of aspiration and seizures. Urinary
alkalinization has been suggested, but there is no clear evidence that this intervention
improves outcome [72]. (See "Gastrointestinal decontamination of the poisoned patient" and
"Enhanced elimination of poisons".)
Cardiac complications — Cardiac complications are typically not the major morbidity
associated with OP poisoning, and management is best focused on treating cholinergic
toxicity. Based on limited evidence, we believe it is reasonable to monitor patients with
severe poisoning for myocardial ischemia by obtaining serial electrocardiograms and serum
troponin concentrations approximately every 8 to 12 hours while the patient’s condition
remains critical. Given that many of these cases are managed in resource-limited settings,
the appropriate level of monitoring will vary.
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In the setting of OP poisoning, myocardial ischemia appears to stem from non-occlusive

disease. Treatment with aspirin is probably safe and prudent. We do not suggest other
therapies. Should arrhythmias develop, we suggest standard treatments based on the
protocols of Advanced Cardiac Life Support. Note that ventricular tachycardia in the setting
of OP poisoning may be related to QTc prolongation and treatment with magnesium is
reasonable. (See "Advanced cardiac life support (ACLS) in adults".)
PROGNOSIS
In the only prospective study to examine prognostic factors for patients acutely poisoned
with OP or carbamate (n = 1365), the authors found that a Glasgow Coma Score (GCS) of less
than 13 portends a poor prognosis, and using the GCS was as good as using the
International Program on Chemical Safety Poison Severity Score (IPCS PSS) [73]. However, the
authors point out that the OP agent involved must be taken into account, as one-half of the
fenthion-poisoned patients who died had only mild symptoms at presentation. A
retrospective study of nearly 400 OP-poisoned patients examined the performance of several
standard ICU-based clinical scoring systems [74]. This study reported that the Acute
Physiology and Chronic Health Evaluation II (APACHE-II), Simplified Acute Physiology Score II
(SAPS-II), and the Mortality Prediction Model II (MPM-II) scoring systems outperformed the
Poisoning Severity Scale in predicting death. Again, however, the performance of these
scoring systems was partly dependent upon the OP agent involved.
Until larger prospective studies can be performed, we suggest using one of the above clinical
scoring systems to help determine prognosis, but only for those specific OP-pesticides that
were included in the relevant study. Particular attention must be given to patients poisoned
with lipophilic OPs such as fenthion and parathion, as these patients may exhibit delayed
and prolonged poisoning symptoms.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are
available at all times for consultation on patients with known or suspected poisoning, and
who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-
222-1222). In addition, some hospitals have medical toxicologists available for bedside
consultation. Whenever available, these are invaluable resources to help in the diagnosis and
management of ingestions or overdoses. Contact information for poison centers around the
world is provided separately.
Further information on pesticide intoxication can be obtained in the United States from
National Pesticide Telecommunications Network at: 1-800-858-7378 or
http://npic.orst.edu/ (outside the United States: 1-806-743-3091).
Society guideline links — Links to society and government-sponsored guidelines from

selected countries and regions around the world are provided separately. (See "Society
guideline links: General measures for acute poisoning treatment" and "Society guideline
links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)
SUMMARY AND RECOMMENDATIONS
● Clinical features – Acute toxicity from organophosphorus agents presents with

manifestations of cholinergic excess. The dominant clinical features of acute cholinergic
toxicity include bradycardia, miosis, lacrimation, salivation, bronchorrhea,
bronchospasm, urination, emesis, and diarrhea. (See 'Acute toxicity' above.)
Ten to 40 percent of organophosphorus-poisoned patients develop a distinct

neurologic disorder 24 to 96 hours after exposure. This disorder consists of
characteristic neurological findings including neck flexion weakness, decreased deep
tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and
respiratory insufficiency. (See 'Intermediate (neurologic) syndrome' above.)
● Diagnosis – The diagnosis of organophosphate or carbamate poisoning is made on

clinical grounds. Organophosphate poisoning should be suspected in a patient with
clinical features of cholinergic excess in the absence of a known ingestion or exposure.
Due to significant variability in toxicity and treatment, every effort should be made to
precisely identify the agent when known. (See 'Diagnosis' above.)
Diagnosis can be confirmed by either direct measurement of RBC acetylcholinesterase

(RBC AChE) activity or plasma (or pseudo-) cholinesterase activity. Most hospital
laboratories are unable to perform the former test, while the latter is more easily
performed but does not correlate well with severity of poisoning. Determination of RBC
AChE activity can also be helpful in evaluating chronic or occupational exposure. (See
'Laboratory abnormalities' above.)
● Overview of management – All symptomatic patients should receive therapy with

oxygen, atropine, an oxime (eg, pralidoxime), and a benzodiazepine. The management
of these patients may be complex and protracted. A summary table to facilitate
emergency management is provided ( table 1). (See 'Management' above.)
• Decontamination – In cases of topical exposure with potential dermal absorption,

aggressive decontamination with complete removal of the patient's clothes and
vigorous irrigation of the affected areas should be performed. (See
'Decontamination' above.)
• Supportive care and ABCs – Patients with markedly depressed mental status or
respiratory failure require 100% oxygen and immediate tracheal intubation.
Succinylcholine should be avoided when performing rapid sequence intubation in
patients with organophosphate poisoning. Bradycardia and hypotension are usually
present in moderate to severe poisonings. Adequate volume resuscitation with
isotonic crystalloid should be performed concomitantly with other resuscitative and
diagnostic efforts. (See 'Initial resuscitation' above.)
• Atropine – We recommend atropine therapy for all patients with any degree of
possible cholinergic toxicity from organophosphate or carbamate poisoning (Grade
1A). Atropine is started at a dose of 2 to 5 mg intravenously (IV) for adults and 0.05
mg/kg IV for children. If no effect is noted, the dose is doubled every three to five
minutes until pulmonary muscarinic signs and symptoms are alleviated. (See
'Atropine' above.)
• Oxime therapy – We suggest that oxime therapy (eg, pralidoxime) be given to all
patients with evidence of cholinergic toxicity, patients with neuromuscular
dysfunction, or patients with exposures to organophosphorus agents known to
cause delayed neurotoxicity (Grade 2C). The current World Health Organization
recommendation for IV bolus therapy with pralidoxime is at least 30 mg/kg in
adults, and 25 to 50 mg/kg for children, based on severity of symptoms,
administered slowly over 30 minutes. Pralidoxime should not be administered
without concurrent atropine. (See 'Pralidoxime' above.)
• Seizure treatment – Organophosphate-induced seizures should be treated with a

benzodiazepine. Prophylactic diazepam (eg, 10 mg IV) can decrease neurocognitive
dysfunction after organophosphate agent poisoning. (See 'Seizures' above.)
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REFERENCES
1. Rotenberg M, Shefi M, Dany S, et al. Differentiation between organophosphate and

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Topic 339 Version 38.0
GRAPHICS
General structures of organophosphate (left) and carbamate (right) agents
The variable R1 and R2 groups are composed of either methyl (CH3) or ethyl (CH3CH2) moieties. The
leaving group is generally an oxime or an aromatic group. Organophosphorones are similar to
organophosphates, but they lack a sulfur atom, and are instead bound to four oxygen molecules.
Graphic 57527 Version 1.0
Organophosphate and carbamate poisoning: Rapid overview of emergency

management
To obtain emergency consultation with a medical toxicologist, in the United States, call 1-800-222-1222
for the nearest regional poison control center. Contact information for poison control centers around
the world is available at the WHO website and in the UpToDate topic on regional poison control centers
(society guideline links).
Clinical syndromes
Acute toxicity
Generally manifests in minutes to hours
Evidence of cholinergic excess
SLUDGE = Salivation, Lacrimation, Urination, Defecation, Gastric Emptying
BBB = Bradycardia, Bronchorrhea, Bronchospasm
Respiratory insufficiency can result from muscle weakness, decreased central drive, increased
secretions, and bronchospasm
Intermediate syndrome
Occurs 24-96 hours after exposure
Bulbar, respiratory, and proximal muscle weakness are prominent features
Generally resolves in 1-3 weeks
Organophosphorus Agent-Induced Delayed Peripheral Neuropathy (OPIDN)
Usually occurs several weeks after exposure
Primarily motor involvement
May resolve spontaneously, but can result in permanent neurologic dysfunction
Diagnostic evaluation of acute toxicity
Atropine challenge if diagnosis is in doubt (1 mg IV in adults, 0.01 to 0.02 mg/kg in children)
Absence of anticholinergic signs (tachycardia, mydriasis, decreased bowel sounds, dry skin)
strongly suggests poisoning with organophosphate or carbamate
Draw blood sample for measurement of RBC acetylcholinesterase activity to confirm diagnosis
Treatment of acute toxicity

Deliver 100% oxygen via facemask; early intubation often required; avoid succinylcholine
Decontamination if ingestion within 1 hour give single dose activated charcoal, adult 50 g (1 g/kg in
children) unless airway not protected or other contraindication. Aggressive dermal and ocular
irrigation as needed. Bag/discard clothing.
Atropine 2 to 5 mg IV/IM/IO bolus (0.05 mg/kg IV in children)
Escalate (double) dose every 3-5 minutes until bronchial secretions and wheezing stop
TACHYCARDIA AND MYDRIASIS ARE NOT CONTRAINDICATIONS TO ATROPINE USE
Hundreds of milligrams may be needed over several days in severe poisonings
Inhaled ipratropium 0.5 mg with parenteral atropine may be helpful for bronchospasm; may
repeat
Pralidoxime (2-PAM) 2 g (25 mg/kg in children) IV over 30 minutes; may repeat after 30 minutes or
give continuous infusion if severe
Continuous infusion at 8 mg/kg/hour in adults (10 mg/kg/hour in children)
If no IV access, give pralidoxime 600 mg IM (15 mg/kg in children <40 kg). Rapidly repeat as
needed to total of 1800 mg or 45 mg/kg in children.
Pralidoxime is given with atropine
Benzodiazepine therapy
Diazepam 10 mg IV (0.1 to 0.2 mg/kg in children), repeat as necessary if seizures occur. Do not
give phenytoin.
Chlorpyrifos structure
Mechanism of action: Organophosphate and pralidoxime
Neurologic effects of organophosphate and carbamate agents
ACH: acetylcholine; Epi: epinephrine; NE: norepinephrine; NMJ: neuromuscular junction.
Agents associated with organophosphorous induced delayed neuropathy

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21/2/24, 19:53 Organophosphate and carbamate poisoning - UpToDate

Official reprint from UpToDate®

Organophosphate and carbamate poisoning

Literature review current through: Jan 2024.

Organophosphates and carbamates are potent cholinesterase inhibitors capable of causing

An overview of organophosphate and carbamate poisoning will be presented here. A

EPIDEMIOLOGY AND SOURCES OF EXPOSURE

Worldwide, an estimated 3,000,000 people are exposed to organophosphate or carbamate

Organophosphorus compounds contain carbon and phosphorous acid derivatives

In addition, plasma cholinesterase (also called butylcholinesterase [BuChE] or

Cholinergic excess — Acute toxicity from organophosphorus agents presents with

The muscarinic signs can be remembered by use of one of two mnemonics:

● SLUDGE/BBB – Salivation, Lacrimation, Urination, Defecation, Gastric Emesis,

● DUMBELS – Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia,

Respiratory issues — Fatalities from acute organophosphorus agent poisoning generally

Intermediate (neurologic) syndrome — Ten to 40 percent of patients poisoned with

Delayed and long-term neuropathology — Organophosphorus agent induced delayed

Affected patients present with transient, painful "stocking-glove" paresthesias followed by a

Survivors of acute organophosphorus agent poisoning may have neurobehavioral deficits

Clinical findings — The diagnosis of organophosphate or carbamate poisoning is made on

If doubt exists as to whether an organophosphate or carbamate has been ingested, a trial of

Laboratory abnormalities — Direct measurement of RBC acetylcholinesterase (RBC AChE)

develop respiratory failure due to a combination of CNS respiratory center depression,

Bradycardia and hypotension are usually present in moderate to severe poisonings.

Cholinergic toxicity — Patients with cholinergic toxicity due to organophosphate or

Atropine — Atropine competes with acetylcholine at muscarinic receptors, preventing

This individualized approach to treatment is supported by the results of an open label

● 15 to 40 pounds (7 to 18 kg): 0.5 mg

Epinephrine — A relatively small percentage of patients do not respond adequately to

Pralidoxime — Since atropine does not bind to nicotinic receptors, it is ineffective in

Severe poisonings may result in prolonged redistribution of toxin; therefore, continuous IV

Seizures — Organophosphorus agent-induced seizures should be treated with a

Decontamination — In cases of topical exposure with potential dermal absorption,

In the setting of OP poisoning, myocardial ischemia appears to stem from non-occlusive

http://npic.orst.edu/ (outside the United States: 1-806-743-3091).

Society guideline links — Links to society and government-sponsored guidelines from

SUMMARY AND RECOMMENDATIONS

● Clinical features – Acute toxicity from organophosphorus agents presents with

Ten to 40 percent of organophosphorus-poisoned patients develop a distinct

● Diagnosis – The diagnosis of organophosphate or carbamate poisoning is made on

Diagnosis can be confirmed by either direct measurement of RBC acetylcholinesterase

● Overview of management – All symptomatic patients should receive therapy with

• Decontamination – In cases of topical exposure with potential dermal absorption,

• Seizure treatment – Organophosphate-induced seizures should be treated with a

Use of UpToDate is subject to the Terms of Use.

1. Rotenberg M, Shefi M, Dany S, et al. Differentiation between organophosphate and

17. Khurana D, Prabhakar S. Organophosphorus intoxication. Arch Neurol 2000; 57:600.

26. Vijayakumar S, Fareedullah M, Ashok Kumar E, Mohan Rao K. A prospective study on

39. Abou-Donia MB. Organophosphorus ester-induced chronic neurotoxicity. Arch Environ

48. Sahin I, Onbasi K, Sahin H, et al. The prevalence of pancreatitis in organophosphate

51. Eddleston M, Roberts D, Buckley N. Management of severe organophosphorus pesticide

in Bangladesh. J Med Toxicol 2012; 8:108.

64. Eddleston M, Eyer P, Worek F, et al. Pralidoxime in acute organophosphorus insecticide

General structures of organophosphate (left) and carbamate (right) agents

Graphic 57527 Version 1.0

Organophosphate and carbamate poisoning: Rapid overview of emergency

Generally manifests in minutes to hours

Evidence of cholinergic excess

SLUDGE = Salivation, Lacrimation, Urination, Defecation, Gastric Emptying