PREVENTION: Prevention efforts include banning every toxic\ntypes of OP. Among those who work with pesticides the use of protective\nclothing and showering before going home is also useful. <\/p>\n\n\n\n

General measures such\nas oxygen and intravenous fluids are also recommended.\nAttempts to decontaminate the stomach, with activated charcoal or\nother means, has not been shown to be useful. While there is a theoretical\nrisk of health care workers taking care of a poisoned person becoming poisoned\nthemselves, the degree of risk appears to be very small. <\/p>\n\n\n\n

TREATMENT: Treatment begins with decontamination. Airway\ncontrol and oxygenation are paramount. The mainstays of pharmacological therapy\ninclude atropine, pralidoxime, and benzodiazepines (eg, diazepam). Initial\nmanagement must focus on adequate use of atropine. Optimizing oxygenation prior\nto the use of atropine is recommended to minimize the potential for\ndysrhythmias.<\/p>\n\n\n\n

SIGNS AND SYMPTOMS: Signs and symptoms of OP poisoning can be divided into three broad categories: (1) Muscarinic effects, (2) Nicotinic effects, and (3) Central Nervous System (CNS) effects. Symptoms of exposure which typically appear within 30 to 90 minutes after exposures are due to the continuous stimulation of the muscarinic and nicotinic receptors.\u00a0 <\/p>\n\n\n\n

Muscarinic symptoms include excessive secretion from mucus\nmembranes, increased pulmonary and oropharnygeal secretions, pupillary\nconstriction manifesting as diarrhoea, excessive urination, miosis, bronchorrhea,\nbradycardia, emesis, lacrimation and salivation, commonly tagged with the\nmnemonic \u2018DUMBBELS\u2019. Adrenal medulla activity manifest as increased sweating\nand garlic smell because of vicarious excretion, bradycardia, abdominal\ncramping and intestinal hypermotility. <\/p>\n\n\n\n

Nicotinic activity results in autonomic nervous system\nstimulation manifesting as tachycardia, hypertension, sweating and rarely\ndilated pupil. Nicotinic overstimulation at the neuromuscular junction causes\nmuscle weakness, fasciculation, fatigue and paralysis <\/p>\n\n\n\n

OP toxicity is a clinical diagnosis. Diagnosis is typically\nbased on the symptoms and can be confirmed by measuring butyrylcholinesterase\nactivity in the blood; but typically, these results are not readily available. <\/p>\n\n\n\n

PATHOPHYSIOLOGY: The underlying mechanism involves the inhibition of acetylcholinesterase (ACHE), leading to the buildup of acetylcholine (ACh) in the body. 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). <\/p>\n\n\n\n

OP can be absorbed cutaneously, ingested, inhaled, or\ninjected. Although most patients rapidly become symptomatic, the onset and\nseverity of symptoms depend on the specific compound, amount, route of\nexposure, and rate of metabolic degradation.<\/p>\n\n\n\n

 MANAGEMENT OF OP POISONING DECONTAMINATION: <\/strong>The\nfirst step in the management of patients with organophosphate poisoning is\nputting on personal protective equipment. These patients may still have the\ncompound on them, and you must protect yourself from exposure. Health care\nproviders must avoid contaminating themselves while handling patients. Use\npersonal protective equipment, such as neoprene gloves and gowns, when decontaminating\npatients because hydrocarbons can penetrate nonpolar substances such as latex\nand vinyl. Use charcoal cartridge masks for respiratory protection when\ndecontaminating patients who are significantly contaminated. <\/p>\n\n\n\n

Secondly, you must decontaminate the patient. This means\nremoving and destroying all clothing because it may be contaminated even\nafter washing. Gently cleanse patients suspected of organophosphate exposure\nwith soap and water because organophosphates are hydrolyzed readily in aqueous\nsolutions with a high pH. <\/p>\n\n\n\n

Irrigate the eyes of patients who have had ocular exposure\nusing isotonic sodium chloride solution or lactated Ringer’s solution. <\/p>\n\n\n\n

In the case of ingestion, vomiting and diarrhea may limit\nthe amount of substance absorbed but should never be induced. Activated\ncharcoal can be given if the patient presents within 1 hour of ingestion, but\nstudies have not shown a benefit.  <\/p>\n\n\n\n

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 plasma cholinesterase and may result in prolonged paralysis. In addition to atropine, pralidoxime and benzodiazepines (e.g. diazepam) are mainstays of medical therapy . \u00a0 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\u00a0reaching the adult dose.\u00a0If 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. <\/p>\n\n\n\n

Pralidoxime also should be given to affect the\nnicotinic receptors since atropine only works on muscarinic receptors. Atropine\nmust be given before pralidoxime to avoid worsening of muscarinic-mediated\nsymptoms. A bolus of at least 30 mg\/kg in adults or 20 to 50 mg\/kg for children\nshould be given over 30 minutes. Rapid administration can cause cardiac arrest.\nAfter the bolus, a continuous infusion of at least 8 mg\/kg\/hr for adults and 10\nto 20 mg\/kg\/hr for children should be started and may be needed for several\ndays. Central venous access and arterial lines may be needed to treat the\npatient with organophosphate toxicity who requires multiple medications and\nblood-gas measurements.   Continuous cardiac monitoring and pulse oximetry\nshould be established; an electrocardiogram (ECG) should be performed. Torsades\nde pointes should be treated in the standard manner. The use of intravenous\nmagnesium sulfate has been reported as beneficial for organophosphate toxicity.\nThe mechanism of action may involve acetylcholine antagonism or ventricular\nmembrane stabilization. <\/p>\n\n\n\n

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. <\/p>\n\n\n\n

INPATIENT CARE: Because of risks of respiratory compromise or recurrent symptoms, hospitalizing all symptomatic patients for at least 48 hours in a high acuity setting is recommended. Patients who are asymptomatic 12 hours after organophosphate exposure can be discharged since symptom onset should usually occur within this time frame. \u00a0 Optimal recommendations are made on a case-by-case scenario. \u00a0 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. Also, establishing baseline cholinesterase levels for workers with known organophosphate exposure is recommended <\/p>\n\n\n\n

It is vital that health care providers working at primary and secondary level facilities should be informed of the hazards, clinical presentation of accidental organophosphate poisoning in children, and the key steps in its management.<\/p>\n\n\n\n

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REFERENCE<\/p>\n\n\n\n