Organophosphate Toxicity


Article Author:
Erika Robb


Article Editor:
Mari Baker


Editors In Chief:
Ron Feller
Grant Goold
Kyle Cohen


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
3/2/2019 8:17:54 AM

Introduction

Most patients exposed to organophosphates come into contact with insecticides. The first organophosphate insecticide was created in the mid-1800s but was not widely used until after World War II. Organophosphates are used as medications, insecticides, and nerve agents as a weapon. Symptoms include increased saliva and tear production, diarrhea, nausea, vomiting, small pupils, sweating, muscle tremors, and confusion. The onset of symptoms is often within minutes, and it can take weeks to disappear.[1][2][3][4][5]

Etiology

Organophosphate pesticide exposure may occur through inhalation, ingestion, or dermal contact. Crops that farm workers come into contact with that also may include organophosphates such as apples, celery, bell peppers, peaches, strawberries, nectarines, grapes, spinach, lettuce, cucumbers, domestic blueberries, and potatoes.

Epidemiology

An estimated 3 million or more people worldwide are exposed to organophosphates each year, accounting for about 300,000 deaths. In the United States, there are around 8000 exposures per year with very few deaths. While most often the exposure occurs from an agricultural pesticide, there are household items, such as ant and roach spray, that also contain organophosphate compounds.

Toxicokinetics

Organophosphate molecules can be absorbed via the skin, inhalation, or in the gastrointestinal tract. Once absorbed, the molecule binds to an acetylcholinesterase molecule in red blood cells thus making the enzyme inactive. This leads to an overabundance of acetylcholine within synapses and neuromuscular junctions. Overstimulation of nicotinic receptors found at neuromuscular junctions can lead to fasciculations and myoclonic jerks. This eventually leads to flaccid paralysis because of the depolarizing block. Nicotinic receptors also are found in the adrenal glands which may cause hypertension, sweating, tachycardia, and a leukocytosis with left shift. [6][7][8][9]

Organophosphate poisoning also produces symptoms based on its action at muscarinic receptors. These effects are usually slower than the nicotinic receptors because the effects occur via a G-protein-coupled receptor mechanism. Muscarinic receptors are found in the parasympathetic and sympathetic nervous system. Sweat glands within the sympathetic nervous system get overstimulated and cause large amounts of sweating. The parasympathetic effects of organophosphate poisoning can be seen in multiple systems including the heart, exocrine glands, and at smooth muscles. At some point, which is different for each specific compound, the acetylcholinesterase-organophosphate compound undergoes a process called aging. This is a conformational change that renders the enzyme resistant to reactivation, making some treatment options useless.

History and Physical

Organophosphates stimulate both the sympathetic and parasympathetic nervous systems. A typical clinical scenario will involve symptoms of overstimulation of the parasympathetic system. An exception is in children, as they typically have a predominance of symptoms mediated by nicotinic receptors.

There are a couple of mnemonics that are helpful to remember the symptoms of organophosphate poisonings and the receptor that is responsible. 

For nicotinic signs of acetylcholinesterase inhibitor toxicity, think of the days of the week:

  • Monday = Mydriasis
  • Tuesday = Tachycardia
  • Wednesday = Weakness
  • Thursday = Hypertension
  • Friday = Fasciculations.

The more common mnemonic that captures the muscarinic effects of organophosphate poisonings is DUMBELS:

  • D = Defecation/diaphoresis
  • U = Urination
  • M = Miosis
  • B = Bronchospasm/bronchorrhea
  • E = Emesis
  • L = Lacrimation
  • S = Salivation.

Additional symptoms can include anxiety, confusion, drowsiness, emotional lability, seizures, hallucinations, headaches, insomnia, memory loss and circulatory or respiratory depression. When death occurs, the most common reason is respiratory failure stemming from bronchoconstriction, bronchorrhea, central respiratory depression or weakness/paralysis of the respiratory muscles. If the patient survives the acute poisoning, there are other long-term complications. 

Intermediate neurologic symptoms typically occur 24 to 96 hours after exposure. Symptoms include neck flexions, weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and respiratory insufficiency. With supportive care, these patients can have a complete return to normal neurologic function within 2 to 3 weeks. Another later complication is neuropathy. This is linked to very specific organophosphate compounds that contain chlorpyrifos. Most commonly this starts as a stocking-glove paresthesia and progresses to symmetric polyneuropathy with flaccid weakness that starts in the lower extremities and progresses to include the upper extremities.

Evaluation

Diagnosis of acute or chronic organophosphate poisoning is strictly clinical. You must have a high clinical suspicion for organophosphate poisoning when no history of exposure or ingestion is known. Some organophosphates have a distinct garlic or petroleum odor that may help in diagnosis. If organophosphate poisoning is on the differential but not confirmed, a trial of atropine may be employed. If symptoms resolve after atropine, this increases the likelihood of an acetylcholinesterase inhibitor poisoning. Some labs can directly measure red blood cell acetylcholinesterase activity, but these are often sent out to labs that are not available in a timely enough fashion to guide therapy.

Treatment / Management

The first step in the management of patients with organophosphate poisoning is putting on personal protective equipment. These patients may still have the compound on them, and you must protect yourself from exposure. Secondly, you must decontaminate the patient. This means removing and destroying all clothing because it may be contaminated even after washing. The patient’s skin needs to be flushed with water. Dry agents such as flour, sand, or bentonite also can be used to decontaminate the skin. In the case of ingestion, vomiting and diarrhea may limit the amount of substance absorbed but should never be induced. Activated charcoal can be given if the patient presents within 1 hour of ingestion, but studies have not shown a benefit.

The definitive treatment for organophosphate poisoning is atropine, which competes with acetylcholine at the muscarinic receptors. The initial dose for adults is 2 to 5 mg IV or 0.05 mg/kg IV for children until reaching the adult dose. If the patient does not respond to the treatment, double the dose every 3 to 5 minutes until respiratory secretions have cleared and there is no bronchoconstriction. In patients with severe poisoning, it may take hundreds of milligrams of atropine given in bolus or continuous infusion over several days before the patient improves.

Pralidoxime (2-PAM) also should be given to affect the nicotinic receptors since atropine only works on muscarinic receptors. Atropine must be given before 2-PAM to avoid worsening of muscarinic-mediated symptoms. A bolus of at least 30 mg/kg in adults or 20 to 50 mg/kg for children should be given over 30 minutes. Rapid administration can cause cardiac arrest. After the bolus, a continuous infusion of at least 8 mg/kg/hr for adults and 10 to 20 mg/kg/hr for children should be started and may be needed for several days.[10][11]

Enhancing Healthcare Team Outcomes

The diagnosis and management of organophosphate poisoning is done with a multidisciplinary team that consists of an emergency department physician, poison control, nurse practitioner, anesthesiologist, intensivist and other specialists depending on organ system involvement. The key is to prevent further absorption via the skin, eyes, or lungs. The treatment should follow the trauma protocol with the first emphasis on the airways. Symptomatic patients need to be monitored in the ICU. Both atropine and pralidoxime can be used in symptomatic patients but close monitoring is necessary. The outlook for most patients is excellent.[12] (Level V)


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Organophosphate Toxicity - Questions

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What is the drug of choice for organophosphate insecticide poisoning?



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A farm worker presents to the ER with findings of pinpoint pupils, sweating, bronchoconstriction, diarrhea, and muscle fasciculations. What is the best treatment?



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What is the initial antidote for organophosphate insecticide poisoning?



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A patient has been exposed to excessive organophosphate insecticide. What is the best agent to treat this patient?



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A man working on the farm presents with increased diarrhea, miosis, difficulty breathing, excessive salivation, and tearing. To what was he most likely exposed?



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Which is the definitive treatment for organophosphate insecticide poisoning?



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Which of the following is NOT one of the potential treatment modalities for patients poisoned by organophosphates (OPs)?



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Pralidoxime is used to treat ototoxicity caused by which of the following?



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A patient has been poisoned with an organophosphate insecticide. What is the drug that can reactivate the affected enzyme?



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A patient was admitted to the emergency room with symptoms of blurred vision, diarrhea, excess salivation, and tremor. Which of the following is the most likely cause?



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A patient presents to the emergency department with symptoms of vomiting, diarrhea, abdominal cramping, bronchospasm, miosis, bradycardia, excessive salivation, and sweating. He also exhibits muscle fasciculations and weakness and has difficulty breathing. He is treated with multiple doses of atropine and pralidoxime. This patient was most likely poisoned with which of the following?



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An 11-year-old boy with attention deficit hyperactivity disorder presents with anxiety, diaphoresis, palpitations, and tachycardia. On examination, the patient has warm, dry skin and tremors. What is the most likely cause of his symptoms?



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A 13-year-old child with ADHD that lives on a farm is brought in with palpitation and tachycardia. On examination he has warm dry skin and buccal mucosa and fasciculations. What is the most likely cause of his symptoms?



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An individual who flies crop dusters presents to the emergency department with excessive lacrimation, sweating, diarrhea, and pupil miosis. What is the likely diagnosis?



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Symptoms of an organophosphate poisoning include all of the following EXCEPT:



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Organophosphate toxicity may be treated with:



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Why is atropine used to treat organophosphate poisoning?



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A 67-year-old farmer presents with a chief complaint of altered mental status. His family notes when came in from working on the crops tonight he was acting funny, he seemed really anxious and was sweating a lot, coughing up a lot of watery looking sputum, and vomiting. He can tell you today he was spraying the crops for bugs and the bottle he was using was leaking next to where he was working. What is the next step in management?



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A 47-year-old male presented to the emergency department 36 hours ago after a farming accident where the container of pesticide broke and the chemical swept his legs out from under him and he landed in a puddle of the pesticide. He was decontaminated and given atropine which seemed to control his symptoms until now. He is having trouble lifting his head off the pillow. His reflexes are trace/4 when yesterday they were normal. He has some difficulty lifting his legs up off the bed. The patient wants to know what you think his prognosis will be. What do you tell him?



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A patient was sprayed today by a bottle of roach killer. He comes in complaining of coughing up watery sputum, vomiting, having diarrhea, and he feels like he is crying constantly. After he was sprayed he took a shower but still feels poorly and thinks some of it may have gotten into this mouth. What is the treatment for this patient?



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Organophosphate Toxicity - References

References

Verheyen J,Stoks R, Current and future daily temperature fluctuations make a pesticide more toxic: Contrasting effects on life history and physiology. Environmental pollution (Barking, Essex : 1987). 2019 Feb 11;     [PubMed]
Aroniadou-Anderjaska V,Figueiredo TH,Apland JP,Braga MF, Targeting the glutamatergic system to counteract organophosphate poisoning: A novel therapeutic strategy. Neurobiology of disease. 2019 Feb 21;     [PubMed]
Dagg K,Irish S,Wiegand RE,Shililu J,Yewhalaw D,Messenger LA, Evaluation of toxicity of clothianidin (neonicotinoid) and chlorfenapyr (pyrrole) insecticides and cross-resistance to other public health insecticides in Anopheles arabiensis from Ethiopia. Malaria journal. 2019 Feb 22;     [PubMed]
Mendes PA,Pereira TC,Pina R,Santos R, Chlorpyrifos-Induced Delayed Neurotoxicity with A Rare Presentation of Flaccid Quadriplegia: A Diagnostic Challenge. European journal of case reports in internal medicine. 2018;     [PubMed]
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Dardiotis E,Aloizou AM,Siokas V,Tsouris Z,Rikos D,Marogianni C,Aschner M,Kovatsi L,Bogdanos DP,Tsatsakis A, Paraoxonase-1 genetic polymorphisms in organophosphate metabolism. Toxicology. 2019 Jan 1;     [PubMed]
Jokanović M, Neurotoxic effects of organophosphorus pesticides and possible association with neurodegenerative diseases in man: A review. Toxicology. 2018 Dec 1;     [PubMed]
Naughton SX,Terry AV Jr, Neurotoxicity in acute and repeated organophosphate exposure. Toxicology. 2018 Sep 1;     [PubMed]
Walton EL, Pralidoxime and pesticide poisoning: A question of severity? Biomedical journal. 2016 Dec;     [PubMed]
Myhrer T,Aas P, Choice of approaches in developing novel medical countermeasures for nerve agent poisoning. Neurotoxicology. 2014 Sep;     [PubMed]
Yu S,Yu S,Zhang L,Gao Y,Walline J,Lu X,Ma Y,Zhu H,Yu X,Li Y, Efficacy and outcomes of lipid resuscitation on organophosphate poisoning patients: A systematic review and meta-analysis. The American journal of emergency medicine. 2018 Nov 17;     [PubMed]

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