what are organophosphates.docx

7/29/2019 What are organophosphates.docx

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What are organophosphates?

Organophosphates are chemicals used in domestic and industrial settings, most commonly as

insecticides. Historically, organophosphates have been used in toxic nerve agents by the military in

war, or for terrorist activities. Organophosphates can be ingested or inhaled, or absorbed through

the skin. The severity and onset of symptoms is dependent on the degree of exposure.

How do organophosphates work?

Organophosphates work by inactivating acetylcholinesterase. Acetylcholinesterase is an enzyme

present in human nervous system. Its job is to break down acetylcholine, which is a chemical that

carries signals between the nerves and muscle. . Once acetylcholinesterase has been inactivated,

acetylcholine builds up in the nerves, and the nerves become over-active. Organophosphatepoisoning can occur rapidly or build up over a number of days.

Signs & Symptoms

People affected can display the following signs and symptoms:

Mild Moderate Severe

Increased saliva production

Nausea & vomiting

Abdominal pain

Increased sweating

Rhinorrhoea (runny nose)

Able to walk and talk

Headache

Dizziness

Confusion, Anxiety

Restlessness

Slow heart rate

(bradycardia)

Blurred vision, small pupils

Unable to walk

Cramps

Diarrhea

Muscle twitching

Seizures

Low blood pressure (hypotensio

Narrowing of the airways

(bronchospasm)

Increased bronchial secretions

Respiratory failure

General Treatment Options

The patient with organophosphate poisoning requires decontamination, and those in contact with the

patient must use personal protective equipment (PPE) to avoid absorption of the chemical. This

decontamination consists of thoroughly washing the patient, including hair. Clothing must be washed

and any leather article discarded (chemical cannot be removed from leather).
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Specific treatment will depend upon how the patient became poisoned and their level of symptoms.

If the patient has swallowed the poison recently they will receive activated charcoal by mouth to

absorb the residual poison.

What Happens in Intensive Care?Once the patient has been admitted to ICU their care will be focussed on monitoring their level of

cholinesterase and the residual effects of the poisoning on the patient. Treament will be supportive.

Once in ICU the patient will be cared for in a single room with special ventilation and any staff caring

for the patient will continue to wear protective clothing for a number of days. The patient will be

placed on a cardiac monitor to monitor their heart rate and rhythm and blood will be taken to check

the level of acetyl cholinesterase in their blood. This will need to be done a number of times until the

medical staff are satisfied with the recovery of the patient. The medication Atropine will be given atfrequent intervals to treat the excessive saliva, bronchial secretions and slow heart rate. Respiratory

support using an oxygen mask may be required.Occasionally the patient will experience severe

respiratory failure and will require breathing tube(endotracheal tube)is inserted, and the patient is

helped with their breathing using a breathing machine(ventilator).

How long will the patient remain in Intensive Care?

The patient will stay in ICU until the signs of respiratory failure have subsided. The degree ofexposure to the chemicals, and the symptoms experienced, will determine how long the patient

stays in hospital.

Weblinks Health Surveillance Guideline

Poisons Information CentresAcross Australia - 131126

Bayer Product Information

The information contained in this sheet is general in nature and therefore cannot reflect individual

patient variation. It is meant as a back up to specific information which will be discussed with you by

the Doctors and Nurses caring for your loved one. ICCMU attests to the accuracy of the informationcontained here BUT takes no responsibility for how it may apply to an individual patient. Please refer

to theDisclaimer.

http://intensivecare.hsnet.nsw.gov.au/organophosphate-poisoning

Organophosphate (OP) compounds are a diverse group of chemicals used in both domestic andindustrial settings. Examples of organophosphates include insecticides (malathion, parathion, diazinon,fenthion, dichlorvos, chlorpyrifos, ethion), nerve gases (soman,sarin, tabun, VX), ophthalmic agents
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(echothiophate, isoflurophate), and antihelmintics (trichlorfon). Herbicides (tribufos [DEF], merphos) aretricresyl phosphatecontaining industrial chemicals.

Organophosphate compounds were first synthesized in the early 1800s when Lassaigne reacted alcoholwith phosphoric acid. Shortly thereafter in 1854, Philip de Clermount described the synthesis of tetraethylpyrophosphate 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 insteaddeveloped an arsenal of chemical warfare agents (ie, tabun, sarin, soman). A fourth agent, VX, wassynthesized in England a decade later. During World War II, in 1941, organophosphates werereintroduced worldwide for pesticide use, as originally intended.

Massive organophosphate intoxication from suicidal and accidental events, such as the Jamaican gingerpalsy incident in 1930, led to the discovery of the mechanism of action of organophosphates. In 1995, areligious sect, Aum Shinrikyo, used sarin to poison people on a Tokyo subway. Mass poisonings stilloccur today; in 2005, 15 victims were poisoned after accidentally ingesting ethion-contaminated food in asocial ceremony in Magrawa, India.

Nerve agents have also been used in battle, notably in Iraq in the 1980s. Additionally, chemical weaponsstill pose a very real concern in this age of terrorist activity.

Exposure to organophosphates (OPs) is also possible via intentional or unintentional contamination offood sources. Although no clinical effects of chronic, low-level organophosphates (OPs) exposure from afood source have been shown, advancements in risk assessment and preparedness are ongoing.

PathophysiologyThe primary mechanism of action of organophosphate pesticides is inhibition of carboxyl esterhydrolases, particularly acetylcholinesterase (AChE). AChE is an enzyme that degrades theneurotransmitter acetylcholine (ACh) into choline and acetic acid. ACh is found in the central andperipheral nervous system, neuromuscular junctions, and red blood cells (RBCs).

Organophosphates inactivate AChE by phosphorylating the serine hydroxyl group located at the activesite of AChE. The phosphorylation occurs by loss of an organophosphate leaving group andestablishment of a covalent bond with AChE.

Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting inoverstimulation of muscarinic and nicotinic receptors. Clinical effects are manifested via activation of theautonomic and central nervous systems and at nicotinic receptors on skeletal muscle.

Once an organophosphate binds to AChE, the enzyme can undergo one of the following:

Endogenous hydrolysis of the phosphorylated enzyme by esterases or paraoxonases

Reactivation by a strong nucleophile such as pralidoxime (2-PAM)

Irreversible binding and permanent enzyme inactivation (aging)Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected. Although most patientsrapidly become symptomatic, the onset and severity of symptoms depend on the specific compound,amount, route of exposure, and rate of metabolic degradation.[3]

HistorySigns 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; andsalivation). Muscarinic effects by organ systems include the following:


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o Cardiovascular - Bradycardia, hypotensiono Respiratory - Rhinorrhea, bronchorrhea, bronchospasm, cough, severe respiratory distresso Gastrointestinal - Hypersalivation, nausea and vomiting, abdominalpain, diarrhea, fecal incontinenceo Genitourinary - Incontinenceo Ocular - Blurred vision, miosiso Glands - Increased lacrimation, diaphoresis

Nicotinic signs and symptoms include muscle fasciculations, cramping, weakness, and diaphragmaticfailure. Autonomic nicotinic effects include hypertension, tachycardia, mydriasis, and pallor.

CNS effects include anxiety, emotional lability, restlessness, confusion, ataxia, tremors, seizures, andcoma.

PhysicalNote 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 review of 31 children withorganophosphate (OP) poisoning described that, in contrast to adults, the most common presentationswere seizure and coma with relatively less muscarinic or nicotinic findings.[8] The authors hypothesized thedifference may be due to difficulty in detecting muscarinic findings in infants (eg, crying) and ingestion ofcontaminated produce instead of organophosphate (OP) directly.

Vital signs: Depressed respirations, bradycardia, and hypotension are possible symptoms. Alternatively,

tachypnea, hypertension, and tachycardia are possible. Hypoxia should be monitored for withcontinuous pulse oximetry.

Paralysiso Type I: This condition is described as acute paralysis secondary to continued depolarization at the

neuromuscular junction.o 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 manifestscommonly as paralysis and respiratory distress. This syndrome involves weakness of proximal musclegroups, neck, and trunk, with relative sparing of distal muscle groups. Cranial nerve palsies can alsobe observed. Intermediate syndrome persists for 4-18 days, may require mechanical ventilation, andmay be complicated by infections or cardiac arrhythmias. Although neuromuscular transmission defectand toxin-induced muscular instability were once thought to play a role, this syndrome may be due tosuboptimal treatment.

o Type III: Organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks afterexposure to large doses of certain organophosphates (OPs) and is due to inhibition of neuropathytarget esterase. Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, andproximal muscle groups characterizes OPIDP. Recovery can take up to 12 months .[9, 10]

Neuropsychiatric effects: Impaired memory, confusion, irritability, lethargy, psychosis, and chronicorganophosphate-induced neuropsychiatric disorders have been reported. The mechanism is notproven.

Extrapyramidal effects: These are characterized by dystonia, cogwheel rigidity,andparkinsonianfeatures (basal ganglia impairment after recovery from acute toxicity).

Other neurological and/or psychological effects: Guillain-Barrlike syndrome and isolated bilateralrecurrent 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 airwaycompromise.Respiratory failureis the most life-threatening effect and requires immediate intervention.

Nicotinic effects: These effects lead to weakness and paralysis of respiratory oropharyngeal muscles.

Central effects: These effects can lead to respiratory paralysis.
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Rhythm abnormalities: Sinus tachycardia, sinus bradycardia, extrasystoles, atrial fibrillation, ventriculartachycardia, and ventricular fibrillation (often a result of, or complicated by, severe hypoxia fromrespiratory distress) are possible.

Other cardiovascular effects: Hypotension, hypertension, and noncardiogenic pulmonary edema arepossible.

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 is

possible.

Medical CareAirway control and adequate oxygenation are paramount in organophosphate (OP) poisonings. Intubationmay be necessary in cases of respiratory distress due to laryngospasm, bronchospasm, bronchorrhea, orseizures. Immediate aggressive use of atropine may eliminate the need for intubation. Succinylcholineshould be avoided because it is degraded by acetylcholinesterase (AChE) and may result in prolongedparalysis.

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 magnesiumsulfate 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. Considerclothing as hazardous waste and discard accordingly.

Health care providers must avoid contaminating themselves while handling patients. Use personalprotective equipment, such as neoprene gloves and gowns, when decontaminating patients becausehydrocarbons can penetrate nonpolar substances such as latex and vinyl. Use charcoal cartridge masksfor respiratory protection when decontaminating patients who are significantly contaminated.

Irrigate the eyes of patients who have had ocular exposure using isotonic sodium chloride solution orlactated Ringer's solution. Morgan lenses can be used for eye irrigation.

Deterrence/Prevention Health care providers must avoid contaminating themselves while handling patients poisoned by

organophosphates. The potential for cross-contamination is highest in treating patients after massivedermal exposure.

Use personal protective equipment, such as neoprene or nitrile gloves and gowns, whendecontaminating patients because hydrocarbons can penetrate nonpolar substances such as latex andvinyl.

Use charcoal cartridge masks for respiratory protection when caring for patients with significantcontamination.

ComplicationsComplications include respiratory failure, seizures, aspiration pneumonia, delayed neuropathy, and death.

http://emedicine.medscape.com

Poisoning OverviewIf you or someone you know has swallowed or breathed in a poison, and you or they have serious

signs or symptoms (nausea, vomiting, pain, trouble breathing,seizure, confusion, or abnormal

skin color), then you must either call an ambulance for transport to a hospital emergency

department or call a poison control center for guidance. The National Poison Control Center

phone number in the U.S. is 1-800-222-1222.
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If the person has no symptoms but has taken a potentially dangerous poison, you should also call a

poison control center or go to the nearest emergency department for an evaluation.

Poison is anything that kills or injures through its chemical actions. Most poisons are swallowed

(ingested). The word poison comes from the Latin word - potare- meaning to drink. But poisons can also

enter the body in other ways:

By breathing

Through the skin

By IV injection

From exposure to radiation

Venom from asnake bite

Poisoning CausesPoisons include highly toxic chemicals not meant for human ingestion or contact, such a scyanide, paint

thinners, or household cleaning products.

Many poisons, however, are substances meant for humans to eat, including foods and medicines.

Foods

Some mushrooms are poisonous

Drinking water contaminated by agricultural or industrial chemicals

Food that has not been properly prepared or handled

When to Seek Medical Care

Call the U.S. National Poison Control Center at 1-800-222-1222 if you have questions about possible

poisoning. You can also go directly to your hospital's emergency department.

Don't assumeover-the-countermedications are safe even if taken in excess. Call the poison control

center for advice.

With many pills, it may take several hours or longer for symptoms to develop. Do not wait for

symptoms to develop, call the poison control center for advice.

Go to your hospital's emergency department if any of the following occurs:

If someone looks ill after a poisoning or possible poisoning.

Aninfantortoddlerwho may have ingested a poison, even if the child looks and feels fine.
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Anyone who has taken something in an attempt to harm himself or herself, even if the substance used

is not known to be harmful.

When you go to the hospital's emergency department, take all the medicine bottles, containers

(household cleaners, paint cans, vitamin bottles), or samples of the substance (such as a plant leaf)

with you.

Self-Care at Home

If you or someone you know has swallowed or breathed a poison and you or they have signs or

symptoms, such as nausea, vomiting, pain, trouble breathing, seizure, confusion, or abnormal

skin color, then you must call either an ambulance or the U.S. National Poison Control Center at 1-

800-222-1222 for guidance. This number is routed to the poison control center that serves your area.

Post the telephone number (along with police, fire, and 911 or equivalent) near your home phones.

Do not induce vomiting or give syrup of Ipecac.

o Ipecac was previously used to induce vomiting in poisoned patients where there was a chance to

get the toxin out of the body. Several advisory bodies such as the American Association of Poison

Control Centers and the American Academy of Pediatrics have recommended that Ipecac NOT be

used and that it should not even be kept in the household. For more information on this subject go

to:http://www.poison.org/prepared/ipecac.asp

Do not giveactivated charcoalat home.Allow medical personnel to decide if this treatment is

appropriate.

The poison control center will instruct you what to do or if an antidote is readily available.

Medical Treatment

Elimination: Get rid of the unabsorbed poison before it can do any harm.

If the person is unconscious, the doctor will put a flexible, soft, plastic tube into thewindpipeto protect

the person from suffocating in his or her own vomit and to provide artificial breathing (intubation).

Once the poison has moved past the stomach, other methods are needed.

o Activated charcoalacts as a "super" absorber of many poisons. Once the poison is stuck to

thecharcoalin theintestine, the poison cannot get absorbed into the bloodstream. Activated

charcoal has no taste, but the gritty texture sometimes causes the person to vomit. To be effective,activated charcoal needs to be given as soon as possible after the poisoning. It does not work with

alcohol, caustics, lithium (Lithobid), or petroleum products.

o Wholebowelirrigation requires drinking a large quantity of a fluid called Golytely. This flushes the

entiregastrointestinal tractbefore the poison gets absorbed.

Antidotes: Some poisons have specific antidotes. Antidotes either prevent the poison from working or

reverse the effects of the poison.
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Atropineis an antidote for certainnervegases and insecticides. During Operation Desert Storm, all

military personnel were issued atropine injectors when it was feared that the enemy would use nerve

gas.

A common antidote is N-acetylcysteine (Mucomyst), which is used to neutralizeacetaminophen

(Tylenol) overdoses. Acetaminophen, in normal doses, is one of the safest medications known, but

after a massive overdose, the liver is damaged, and hepatitis and liver failure develop. Mucomyst

works as an antidote by bolstering the body's natural detoxification abilities when they are

overwhelmed.

It may also be possible to reverse the harmful effect of a drug even if no antidote exists.

o If a person withdiabetestakes too much insulin, a dangerouslylow blood sugar(hypoglycemia) will

cause weakness, unconsciousness, and eventually death. Sugar given by mouth or IV is an

effective treatment until the insulin wears off.

o When the poison is a heavy metal, such as lead, special medicines (chelators) bind the poison in

the bloodstream and cause it to be eliminated in the urine.

o Another "binder" issodium polystyrene sulfonate(Kayexalate), which can absorbpotassiumand

otherelectrolytesfrom the bloodstream.

General supportive measures: When there are no specific treatments, the physician will treat signs and

symptoms as needed.

If the person is agitated or hallucinating, a sedative can be given to calm the person until the drug

wears off.

Aventilatorcan be used to breathe for anyone who has stopped breathing from a poisoning.

Antiseizure medicines can be used to treat or prevent seizures.
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