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Toxicity, Organophosphate
Article Last Updated: May 30, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Kenneth D Katz, MD, FAAEM, ABMT, Assistant Professor, Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh Medical Center; Medical Director, Pittsburgh Poison Center
Kenneth D Katz is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, and American Medical Association
Coauthor(s):
Daniel E Brooks, MD, Assistant Professor of Medicine, University of Pittsburgh; Chief, Division of Medical Toxicology, Department of Emergency Medicine, University of Pittsburgh Medical Center; Clinical Assistant Professor, Medical Director, West Virginia Poison Center, University of West Virginia;
Marina C Furtado, MD, Staff Physician, Department of Emergency Medicine, University Medical Center, University of Arizona;
Lisa Chan, MD, FACEP, Associate Program Director, Department of Emergency Medicine, University of Arizona
Editors: Lisa Kirkland, MD, FACP, CNSP, MSHA, Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine; Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine; Michael R Pinsky, MD, CM, Professor of Critical Care Medicine, Bioengineering, Cardiovascular Diseases and Anesthesiology, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center
Author and Editor Disclosure
Synonyms and related keywords:
organophosphate toxicity, organophosphate poisoning, OP compounds, insecticides, malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, nerve gases, soman, sarin, tabun, VX, ophthalmic agents, echothiophate, isoflurophate, trichlorfon, herbicides, industrial chemicals
Background
Organophosphate (OP) compounds are a diverse group of chemicals used in both domestic and industrial settings. Examples of organophosphates include: insecticides (malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, ethion), nerve gases (soman, sarin, tabun, VX), ophthalmic agents (echothiophate, isoflurophate), and antihelmintics (trichlorfon). Herbicides (tribufos [DEF], merphos) are tricresyl phosphate–containing industrial chemicals.
Organophosphate compounds were first synthesized in the early 1800s when Lassaigne reacted alcohol with phosphoric acid. Shortly thereafter in 1854, Philip de Clermount described the synthesis of tetraethyl pyrophosphate at a meeting of the French Academy of Sciences. Eighty years later, Lange, in Berlin, and, Schrader, a chemist at Bayer AG, Germany, investigated the use of organophosphates as insecticides. However, the German military prevented the use of organophosphates as insecticides and instead developed an arsenal of chemical warfare agents (ie, tabun, sarin, soman). A fourth agent, VX, was synthesized in England a decade later. During World War II, in 1941, organophosphates were reintroduced worldwide for pesticide use, as originally intended.
Massive organophosphate intoxication from suicidal and accidental events, such as the Jamaican ginger palsy incident in 1930, led to the discovery of the mechanism of action of organophosphates. In 1995, a religious sect, Aum Shinrikyo, used sarin to poison people on a Tokyo subway. Mass poisonings still occur today; in 2005, 15 victims were poisoned after accidentally ingesting ethion-contaminated food in a social ceremony in Magrawa, India.
Nerve agents have also been used in battle, notably in Iraq in the 1980s. Additionally, chemical weapons still pose a very real concern in this age of terrorist activity.
Pathophysiology
The primary mechanism of action of organophosphate pesticides is inhibition of carboxyl ester hydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid. ACh is found in the central and peripheral nervous system, neuromuscular junctions, and red blood cells (RBCs).
Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the active site of AChE. The phosphorylation occurs by loss of an organophosphate leaving group and establishment of a covalent bond with AChE.
Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle.
Once an organophosphate binds to AChE, the enzyme can undergo 1 of the following 3 processes:
- Endogenous hydrolysis of the phosphorylated enzyme by esterases or paraoxonases
- Reactivation by a strong nucleophile such as pralidoxime (2-PAM)
- Complete binding and inactivation (aging)
Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.
Frequency
United States
The American Association of Poison Control Centers' National Incidence Report indicates that pesticide injuries number 102,754 persons annually. Nationally, 4.2% of poisonings are due to insecticides. In 2007, Sudakin et al reported an overall decline in poison center–recorded exposures from 1995 to 2004 because of the United States Environmental Protection Agency phase out of common household and agricultural OP agents (ie, diazinon, chlorpyrifos).1
International
Pesticide poisonings are among the most common modes of poisoning fatalities. In countries such as India, OPs are easily accessible and, therefore, a source of both intentional and unintentional poisonings.
Mortality/Morbidity
- Worldwide mortality studies report mortality rates from 3-25%. The compounds most frequently involved include malathion, dichlorvos, trichlorfon, and fenitrothion/malathion.
- Mortality rates depend on the type of compound used, amount ingested, general health of the patient, delay in discovery and transport, insufficient respiratory management, delay in intubation, and failure in weaning off ventilatory support.
- Complications include severe bronchorrhea, seizures, weakness, and neuropathy. Respiratory failure is the most common cause of death.
History
Signs and symptoms of organophosphate poisoning can be divided into 3 broad categories, including (1) muscarinic effects, (2) nicotinic effects, and (3) CNS effects.
- Mnemonic devices used to remember the muscarinic effects of organophosphates are SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset, emesis) and DUMBELS (diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; excess lacrimation; and salivation). Muscarinic effects by organ systems include the following:
- Cardiovascular - Bradycardia, hypotension
- Respiratory - Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distress
- Gastrointestinal - Hypersalivation, nausea and vomiting, abdominal pain, diarrhea, fecal incontinence
- Genitourinary - Incontinence
- Ocular - Blurred vision, miosis
- Glands - Increased lacrimation, diaphoresis
- Nicotinic signs and symptoms include muscle fasciculations, cramping, weakness, and diaphragmatic failure. Autonomic nicotinic effects include hypertension, tachycardia, mydriasis, and pallor.
- CNS effects include anxiety, emotional lability, restlessness, confusion, ataxia, tremors, seizures, and coma.
Physical
Note that clinical presentation may vary, depending on the specific agent, exposure route, and amount. Symptoms are due to both muscarinic and nicotinic effects. Interestingly, a 2007 retrospective review of 31 OP poisoned children performed by Levy-Khademi et al described that, in contrast to adults, the most common presentations were seizure and coma with relatively less muscarinic or nicotinic findings.2 The authors hypothesized the difference may be due to difficulty in detecting muscarinic findings in infants (eg, crying) and ingestion of contaminated produce instead of OP directly.
- Vital signs: Depressed respirations, bradycardia, and hypotension are possible symptoms. Alternatively, tachypnea, hypertension, and tachycardia are possible. Hypoxia should be monitored for with continuous pulse oximetry.
- Paralysis
- Type I: This condition is described as acute paralysis secondary to continued depolarization at the neuromuscular junction.
- Type II (intermediate syndrome): Intermediate syndrome was described in 1974 and is reported to develop 24-96 hours after resolution of acute organophosphate poisoning symptoms and manifests commonly as paralysis and respiratory distress. This syndrome involves weakness of proximal muscle groups, neck, and trunk, with relative sparing of distal muscle groups. Cranial nerve palsies can also be observed. Intermediate syndrome persists for 4-18 days, may require mechanical ventilation, and may be complicated by infections or cardiac arrhythmias. Although neuromuscular transmission defect and toxin-induced muscular instability were once thought to play a role, this syndrome may be due to suboptimal treatment.
- Type III: Organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks after exposure to large doses of certain OPs and is due to inhibition of neuropathy target esterase. Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, and proximal muscle groups characterizes OPIDP. Recovery can take up to 12 months.
- Neuropsychiatric effects: Impaired memory, confusion, irritability, lethargy, psychosis, and chronic organophosphate-induced neuropsychiatric disorders have been reported. The mechanism is not proven.
- Extrapyramidal effects: These are characterized by dystonia, cogwheel rigidity, and parkinsonian features (basal ganglia impairment after recovery from acute toxicity).
- Other neurological and/or psychological effects: Guillain-Barré–like syndrome and isolated bilateral recurrent laryngeal nerve palsy are possible.
- Ophthalmic effects: Optic neuropathy, retinal degeneration, defective vertical smooth pursuit, myopia, and miosis (due to direct ocular exposure to organophosphates) are possible.
- Ears: Ototoxicity is possible.
- Respiratory effects: Muscarinic, nicotinic, and central effects contribute to respiratory distress in acute and delayed organophosphate toxicity.
- Muscarinic effects: Bronchorrhea, bronchospasm, and laryngeal spasm, for instance, can lead to airway compromise.
- Nicotinic effects: These effects lead to weakness and paralysis of respiratory oropharyngeal muscles.
- Central effects: These effects can lead to respiratory paralysis.
- Rhythm abnormalities: Sinus tachycardia, sinus bradycardia, extrasystoles, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation (often a result of, or complicated by, severe hypoxia from respiratory distress) are possible.
- Other cardiovascular effects: Hypotension, hypertension, and noncardiogenic pulmonary edema are possible.
- GI manifestations: Nausea, vomiting, diarrhea, and abdominal pain may be some of the first symptoms to occur after organophosphate exposure.
- Genitourinary and/or endocrine effects: Urinary incontinence, hypoglycemia, or hyperglycemia are possible.
Gastroenteritis, Viral
Toxicity, Mushroom
Other Problems to be Considered
Carbamate
Nicotine
Carbachol
Methacholine
Arecoline
Bethanechol
Pilocarpine
Pyridostigmine
Neostigmine
Mushroom poisoning (Clitocybe, Inocybe)
Poison Hemlock (Conium maculatum)
Myasthenia gravis
Eaton-Lambert syndrome
Guillain-Barré syndrome
Botulism
Eclampsia
Lab Studies
- Organophosphate (OP) toxicity is a clinical diagnosis. Confirmation of organophosphate poisoning is based on the measurement of cholinesterase activity; typically, these results are not readily available. Although RBC and plasma (pseudo) cholinesterase levels can both be used, RBC cholinesterase correlates better with CNS acetylcholinesterase (AChE) and is, therefore, a more useful marker of organophosphate poisoning.
- If possible, draw blood for measurement of RBC and plasma cholinesterase levels prior to treatment with pralidoxime (2-PAM). Monitoring serial levels can be used to determine a response to therapy.
- RBC AChE represents the AChE found on RBC membranes, similar to that found in neuronal tissue. Therefore, measurement more accurately reflects nervous system OP AChE inhibition.
- Plasma cholinesterase is a liver acute-phase protein that circulates in the blood plasma. It is found in CNS white matter, the pancreas, and the heart. It can be affected by many factors, including pregnancy, infection, and medical illness. Additionally, a patient's levels can vary up to 50% with repeated testing.
- RBC cholinesterase is the more accurate of the 2 measurements, but plasma cholinesterase is easier to assay and is more readily available.
- Cholinesterase levels do not always correlate with severity of clinical illness.
- The level of cholinesterase activity is relative and is based on population estimates. Neonates and infants have baseline levels that are lower than adults. Because most patients do not know their baseline level, the diagnosis can be confirmed by observing a progressive increase in the cholinesterase value until the values plateau over time.
- Falsely depressed levels of erythrocyte cholinesterase can be found in pernicious anemia, hemoglobinopathies, use of antimalarial drugs, and oxalate blood tubes.
- Falsely depressed levels of plasma cholinesterase are observed in liver dysfunction, low-protein conditions, neoplasia, hypersensitivity reactions, use of certain drugs (succinylcholine, codeine, morphine), pregnancy, and genetic deficiencies.
- Other laboratory findings include: leukocytosis, hemoconcentration, metabolic and/or respiratory acidosis, hyperglycemia, hypokalemia, hypomagnesemia and elevated amylase and liver function studies A retrospective analysis of OP poisoned patients by Liu et al found a direct correlation between the severity of poisoning and mortality and the presence of pretreatment metabolic and respiratory acidosis.3
Imaging Studies
A chest radiograph may reveal pulmonary edema but typically adds little to the clinical management of a poisoned patient.
Other Tests
ECG findings include prolonged QTc interval, elevated ST segments, and inverted T waves. Although sinus tachycardia is the most common finding in the poisoned patient, sinus bradycardia, and PR prolongation can develop with increasing toxicity due to excessive parasympathetic activation.
Procedures
- Endotracheal intubation and mechanical ventilation may be necessary in patients with organophosphate poisoning for airway protection and management of bronchorrhea and seizures.
- Central venous access and arterial lines may be needed to treat the patient with organophosphate toxicity who requires multiple medications and blood-gas measurements.
Medical Care
Airway control and adequate oxygenation are paramount in organophosphate (OP) poisonings. Intubation may be necessary in cases of respiratory distress due to laryngospasm, bronchospasm, bronchorrhea, or seizures. Immediate aggressive use of atropine may eliminate the need for intubation. Succinylcholine should be avoided because it is degraded by acetylcholinesterase (AChE) and may result in prolonged paralysis.
- Continuous cardiac monitoring and pulse oximetry should be established; an ECG should be performed. Torsades de Pointes should be treated in the standard manner. The use of intravenous magnesium sulfate has been reported as beneficial for organophosphate toxicity. The mechanism of action may involve acetylcholine antagonism or ventricular membrane stabilization.
- Remove all clothing and gently cleanse patients suspected of organophosphate exposure with soap and water because organophosphates are hydrolyzed readily in aqueous solutions with a high pH. Consider clothing hazardous waste and discard accordingly.
- Health care providers must avoid contaminating themselves while handling patients. Use personal protective equipment, such as neoprene or nitrile gloves and gowns, when decontaminating patients because hydrocarbons can penetrate nonpolar substances such as latex and vinyl. Use charcoal cartridge masks for respiratory protection when decontaminating patients who are significantly contaminated.
- Irrigate the eyes of patients who have had ocular exposure using isotonic sodium chloride solution or lactated Ringer's solution. Morgan lenses can be used for eye irrigation.
Surgical Care
Patients with trauma or blast injury should be treated according to standard advanced trauma life support (ATLS) protocol. Patient decontamination should always be considered to prevent medical personnel poisoning.
The mainstays of medical therapy in organophosphate (OP) poisoning include atropine, pralidoxime (2-PAM), and benzodiazepines (eg, diazepam). A novel route of administration of intraosseous (bone injection gun, BIG) midazolam demonstrated rapid peak concentrations in swine compared with intravenous and intramuscular routes; the authors concluded this may play a role in quickly terminating seizures, especially in the prehospital arena.4 Initial management must focus on adequate use of atropine. Optimizing oxygenation prior to the use of atropine is recommended to minimize the potential for dysrhythmias.
In 1991, De Silva studied the treatment of organophosphate poisoning with atropine and 2-PAM and, later the same year, with atropine alone.5 He found that atropine seemed to be as effective as atropine plus 2-PAM in the treatment of acute organophosphate poisoning. The controversy continued when other authors observed more respiratory complications and higher mortality rates with use of high-dose 2-PAM. Low-dose (1-2 g slow IV) 2-PAM is the current recommendation. Studies are underway to assess the role of low-dose 2-PAM. Pawar et al demonstrated improved survival in moderately severe OP poisoned patients who received early, continuous 2-PAM infusion compared with those who received intermittent boluses.6
A meta-analysis and review of the literature performed by Peter et al (2007) emphasized good supportive care along with discriminate use of 2-PAM, especially early in the course of treatment of moderately to severely OP poisoned patients, are the hallmarks of treatment.7 More prospective data are required.
Because large amounts of atropine may be required for patients with organophosphate poisoning, reconstitution of powdered atropine is a viable option, especially in mass-casualty settings.
Intravenous diphenhydramine may provide an alternative centrally acting anticholinergic agent used to treat muscarinic toxicity if atropine is unavailable or in limited supply. Additionally, Yavuz et al demonstrated reduced myocardial injury and troponin leak in fenthion-poisoned rats treated with diphenhydramine.8
In a single-center, randomized, single-blind study by Pajoumand et al (2004) found a benefit to magnesium therapy in addition to standard oxime and atropine therapy in reducing hospitalization days and mortality rate in patients with organophosphate poisoning.9 The mechanisms appear to be inhibition of acetylcholine (ACh) and organophosphate antagonism. Larger randomized studies are needed to demonstrate magnesium efficacy in OP poisoning.
Possible future interventions include neuroprotective agents used to prevent nerve damage and bioscavengers aimed to prevent AChE inhibition by nerve agents or organophosphate.
Drug Category: Anticholinergic agents
These agents act as competitive antagonists at the muscarinic cholinergic receptors in both the central and the peripheral nervous system. These agents do not affect nicotinic effects.
| Drug Name | Atropine (Isopto, Atropair) |
|---|
| Description | Initiated in patients with OP toxicity who present with muscarinic symptoms.
Competitive inhibitor at autonomic postganglionic cholinergic receptors, including receptors found in GI and pulmonary smooth muscle, exocrine glands, heart, and eye.
The endpoint for atropinization is dried pulmonary secretions and adequate oxygenation. Tachycardia and mydriasis must not be used to limit or to stop subsequent doses of atropine. The main concern with OP toxicity is respiratory failure from excessive airway secretions. |
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| Adult Dose | 1-2 mg IV bolus, repeat q3-5min prn for desire effects (drying of pulmonary secretions and adequate oxygenation)
Consider doubling each subsequent dose for rapid control of patients in severe respiratory distress
An atropine drip titrated to the above endpoints can be initiated until the patient's condition is stabilized |
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| Pediatric Dose | 0.05 mg/kg IV, repeat q3-5min prn for control of airway secretions
Consider doubling each subsequent dose to rapidly correct patients with severe respiratory distress |
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| Contraindications | Documented hypersensitivity; narrow-angle glaucoma |
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| Interactions | Coadministration with other anticholinergics has additive effects |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Care should be taken in coronary heart disease, tachycardia, CHF, cardiac arrhythmias, and hypertension; bladder catheterization may be required because of urinary retention |
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| Drug Name | Glycopyrrolate (Robinul) |
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| Description | Indicated for use as an antimuscarinic agent to reduce salivary, tracheobronchial, and pharyngeal secretions. Does not cross the blood-brain barrier. Can be considered in patients at risk for recurrent symptoms (after initial atropinization) but who are developing central anticholinergic delirium or agitation.
Since glycopyrrolate does not penetrate the CNS, it is not expected to control central cholinergic toxicity. Bird et al suggested that atropine (rather than glycopyrrolate) was associated with lower, early OP-induced mortality
|
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| Adult Dose | 1-2 mg/kg IV prn to control peripheral cholinergic effects (eg, bronchorrhea) |
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| Pediatric Dose | 0.025 mg/kg IV prn to control peripheral cholinergic effects (eg, bronchorrhea) |
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| Contraindications | Documented hypersensitivity; narrow-angle glaucoma |
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| Interactions | Levodopa decreases effects; amantadine and cyclopropane increase glycopyrrolate toxicity |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Care should be taken in coronary heart disease, tachycardia, CHF, cardiac arrhythmias, and hypertension; bladder catheterization may be required because of urinary retention |
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Drug Category: Antidotes, OP poisoning
These agents prevent aging of AChE and reverse muscle paralysis with OP poisoning.
| Drug Name | Pralidoxime (2-PAM, Protopam) |
|---|
| Description | Nucleophilic agent that reactivates the phosphorylated AChE by binding to the OP molecule. Used as an antidote to reverse muscle paralysis resulting from OP AChE pesticide poisoning but is not effective once the OP compound has bound AChE irreversibly (aged). Current recommendation is administration within 48 h of OP poisoning. Because it does not significantly relieve depression of respiratory center or decrease muscarinic effects of AChE poisoning, administer atropine concomitantly to block these effects of OP poisoning.
Signs of atropinization might occur earlier with addition of 2-PAM to treatment regimen. 2-PAM administration is not indicated for carbamate exposure since no aging occurs. |
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| Adult Dose | 1-2 g (20-40 mg/kg) IV in 100 mL isotonic sodium chloride soln/D5W over 15-30 min; repeat in 1 h if muscle weakness is not relieved; then repeat q3-8h if signs of poisoning recur; other dosing regimens have been used, including continuous drip
Consultation with regional poison center is recommended for more specific case-based dosing recommendations |
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| Pediatric Dose | 20-40 mg/kg in 100 mL isotonic sodium chloride soln/D5W IV over 15-30 min; repeat in 1-2 h if muscle weakness not relieved; repeat q10-12h prn to relieve cholinergic symptoms
IM/SC can be used if IV not feasible; can be used with atropine |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Antagonism with neostigmine, pyridostigmine, and edrophonium |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | 2-PAM can cause brief adverse effects such as dizziness and blurred vision; hypertension may occur (increasing the infusion time to 30-40 min can help reduce this effect) |
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Drug Category: Benzodiazepines
These agents potentiate effects of gamma-aminobutyrate (GABA) and facilitate inhibitory GABA neurotransmission.
| Drug Name | Diazepam (Valium, Diastat, Diazemuls) |
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| Description | For treatment of seizures. Depresses all levels of CNS (eg, limbic and reticular formation) by increasing activity of GABA. |
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| Adult Dose | 5-15 mg IV q5-10 min prn, repeat prn; consider higher doses if needed |
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| Pediatric Dose | 0.05-0.3 mg/kg/dose IV q5-10 min prn |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs |
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| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
|
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| Precautions | Caution with other CNS depressants, low albumin levels, or hepatic disease (might increase toxicity) |
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Further Inpatient Care
- Because of risks of respiratory compromise or recurrent symptoms, hospitalizing all symptomatic patients for at least 24 hours for close observation is recommended. Patients who are asymptomatic 12 hours after organophosphate exposure can generally be discharged since symptoms usually occur within this time frame.
- Optimal recommendations are made on a case-by-case scenario. Consider discussing each case with a medical toxicologist or the regional poison center (1-800-222-1222).
- Following occupational exposure, patients should not be allowed to return to work with organophosphates until serum cholinesterase activity returns to 75% of the known baseline level.
Deterrence/Prevention
- Health care providers must avoid contaminating themselves while handling patients poisoned by organophosphates. The potential for cross-contamination is highest with patients who have had massive dermal exposure.
- Use personal protective equipment, such as neoprene or nitrile gloves and gowns, when decontaminating patients because hydrocarbons can penetrate nonpolar substances such as latex and vinyl.
- Use charcoal cartridge masks for respiratory protection when caring for patients with significant contamination.
Complications
Complications include respiratory failure, seizures, aspiration pneumonia, and neuropathy.
Patient Education
For excellent patient education resources, visit eMedicine's Poisoning - First Aid and Emergency Center and Bioterrorism and Warfare Center. Also, see eMedicine's patient education articles Poisoning, Activated Charcoal, Poison Proofing Your Home, Chemical Warfare, and Personal Protective Equipment.
Medical/Legal Pitfalls
- Initial treatment goal should consist of optimizing oxygenation and controlling excessive airway secretions.
- Tachycardia is neither a contraindication nor an endpoint for atropine administration.
- Patients exposed to organophosphate (OP) should be observed for at least 12 hours in the emergency department (ED). Toxicity after this is unlikely.
- Because of the risk of respiratory depression or recurrent symptoms after resolution of an acute cholinergic crisis, hospitalizing all symptomatic patients for at least 48 hours following resolution of symptoms is recommended.
- The symptoms of OP poisoning can mimic other toxidromes and disease processes. The patient may also have ingested or may have been exposed to another drug or toxin. The clinician must keep in mind that misdiagnosis is a potential medicolegal pitfall.
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Toxicity, Organophosphate excerpt Article Last Updated: May 30, 2008
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