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Neurology of Acute Organophosphate Poisoning

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Neurology of Acute Organophosphate Poisoning Indian Perspective Neurology of acute organophosphate poisoning Gagandeep Singh, Dheeraj Khurana1 Departments of Neurology, Dayanand Medical College, Ludhiana, and 1Postgraduate Institute of Medical Education and Research, Chandigarh, India Abstract Acute organophosphate (OP) poisoning is one of the most common poisonings in emergency medicine and toxicological practice in some of the less-developed nations in South Asia. Traditionally, OP poisoning comes under the domain of emergency physicians, internists, intensivists, and toxicologists. However, some of the complications following OP poisoning are neurological and involve neurologists. The pathophysiological basis for the clinical manifestations of OP poisoning is inactivation of the enzyme, acetylcholinesterase at the peripheral nicotinic and muscarinic and central nervous system (CNS) nerve terminals and junctions. Nicotinic manifestations occur in severe cases and late in the course; these comprise of fasciculations and neuromuscular paralysis. There is a good correlation between the electrophysiological abnormalities and the severity of the clinical manifestations. Neurophysiological abnormalities characteristic of nicotinic junctions (mainly neuromuscular junction) dysfunction include: (1) single, supramaximal electrical-stimulus-induced repetitive response/s, (2) decrement–increment response to high frequency (30 Hz) repetitive nerve stimulation (RNS), and (3) decremental response to high frequency (30 Hz) RNS. Atropine ameliorates muscarinic manifestations. Therapeutic Address for correspondence: Dr. Gagandeep Singh, agents that can ameliorate nicotinic manifestations, mainly neuromuscular, are oximes. Department of Neurology, However, the evidence for this effect is inconclusive. This may be due to the fact that Dayanand Medical College, there are several factors that determine the therapeutic effect of oximes. These factors Ludhiana - 141 001, include: The OP compound responsible for poisoning, duration of poisoning, severity of Punjab, India. poisoning, and route of exposure. There is also a need to study the effect of oximes on E-mail: [email protected] the neurophysiological abnormalities. Key words: Atropine, neurophysiology, organophosphate poisoning, oximes, DOI: 10.4103/0028-3886.51277 pralidoxime, repetitive nerve stimulation Introduction Historical Aspects Organophosphate (OP) compounds are a large Organophosphate compounds were known to exist since group of compounds having potential to irreversibly early 1800s, when Lassaigne synthesized OP compounds. inhibit the cholinesterases, acetylcholinesterase, and However, the earliest recorded description of their neuropathy target esterase (NTE), in humans and synthesis was by de Clermont in 1854. Subsequently, animals. The OP compounds are not only used as Michaelis in Germany and Arbusov in Russia described insecticides and pesticides, but also used as chemical synthesis of a large number of OP compounds in early warfare agents, petroleum additives, and industrial 1900s.[1] However, the toxic effects of OP compounds were plasticizers. Serious human exposure leads to both not recognized until 1932, when Lange and von Kruger muscarinic (cholinergic) hyperstimulation and described the toxic effects of OP vapors. In Germany, nicotinic receptor stimulation. Few OPs also inhibit Schrader’s deep involvement in the systematic research NTE irreversibly. of OP compounds led to the development of more than Neurology India | Mar-Apr 2009 | Vol 57 | Issue 2 119 Singh and Khurana: Organophosphate poisoning 2000 OP compounds including sarin, parathion, and strata, unemployment, unstable emotional relationships, paroxon. Sadly however, given the prevailing scenario psychiatric disorders, and alcohol abuse were the risk at the time, World War II, Schrader’s work was mainly factors associated with self-intentional or suicidal pesticide oriented toward the synthesis of chemical warfare poisoning and suicidal intent accounted for almost agents.[2,3] However, after the war, the pharmacological 85% cases of pesticide poisoning.[13] properties of these agents were published leading to the realization of their potential use as insecticides and Intoxication due to OP compounds may also occur by pesticides. This eventually led to the development of accidental exposure to agricultural pesticides while many more new OP compounds and their main use as spraying, through skin and inhalational route.[14] Other insecticides and pesticides worldwide. potential modes of OPs poisoning include ingestion of adulterated fruit, ß our, or cooking oil, and wearing Contemporaneous to the development of OPs as contaminated clothing.[15] Choudary et al., reported a food- insecticides, another group of OP compounds were borne outbreak of OP compound poisoning.[16] The kitchen, developed for industrial use. These compounds are in which, food was prepared had been sprayed earlier with triaryl esters of phosphoric acid (e.g. tricresyl phosphate) malathion. Among agricultural laborers, OP compound and are now used as plasticizing agents, lead scavengers poisoning due to accidental exposure to agricultural in gasoline, and as additives to hydraulic lubricants. pesticide spraying is not uncommon in India. Tri-orthocresyl phosphate was implicated in the enormous epidemic of Jinger-Jake paralysis in people Biochemical Basis who consumed contaminated alcoholic extract of [3] Jamaican ginger in the United States in 1930s. Organophosphate compounds irreversibly inhibit the enzyme, acetylcholinesterase [Figure 1].[1] They combine Epidemiology with acetylcholinesterase to form a phopshorylated enzyme (enzyme–OP complex). This enzyme is Poisoning with OP compounds is a worldwide functionally important at muscarinic and nicotinic phenomenon. An estimated three million cases of nerve endings and also at central nervous system pesticide poisoning with 2000 deaths occur worldwide, (CNS) synapses. Acetylcholinesterase inhibition results each year.[4] According to the World Health Organization in prolonged action and excess of acetylcholine at the (WHO), one million serious unintentional poisonings autonomic, neuromuscular, and the CNS synapses. occur every year and an additional two million people The clinical manifestations of acute OP poisoning are the are hospitalized for suicide attempts with pesticides.[4] result of dysfunction in these synapses. In India, OP compounds are among the most commonly Recovery from acute OP intoxication depends upon used agents for suicidal poisoning.[5] Systematic community the reactivation of acetylcholinesterase–OP complex based data on the epidemiology of poisoning are not [Figure 1]. Although, the reactivation of the enzyme available from India. Hospital-based data suggest that occurs spontaneously, this is a very slow process. Rapid barbiturates and copper sulfate were the commonly used reactivation can be achieved by pharmacological agents agents in the years, 1972–1977; however, later they were such as oximes [Figure 1]. The latter compounds are replaced by OP compounds and aluminum phosphide.[6] In 1995, National Poison Information Center (NPIC) was established at the All India Institute of Medical Sciences, New Delhi. Data on the pattern of poisonings in North India accumulated at this center suggest that suicidal poisoning with house-hold agents is the most common modality of poisoning.[7,8] The common house-hold agents included OPs, carbamates, pyrethrinoids, rodenticides, detergents, and corrosives. Agricultural pesticides accounted for 12.8% all cases of poisonings. Likewise, OPs caused most self-poisoning deaths in South and Central India.[9-12] In a study from Andhra Pradesh, two-thirds of the patients were young adults aged less than 30 years, more than half were males, and attempted suicide was the most common intent for poisoning. Majority of deaths were due to poisoning with monocrotophos and [11] Figure 1: Biochemical basis of acute OP poisoning, its reaction with endosulfan (an organochlorine). Another study from the enzyme acetylcholinesterase, the aging reaction, and reactivation Sri Lanka showed that young age, lower socioeconomic following the administration of oximes 120 Neurology India | Mar-Apr 2009 | Vol 57 | Issue 2 Singh and Khurana: Organophosphate poisoning nucleophilic agents and act as acetylcholinesterase results in fasciculations, later followed by neuromuscular reactivators. However, the action of oximes is limited by the paralysis which may last for 2–18 days.[20,22] The paralysis aging reaction, a time-dependent process that hydrolyses usually involves the ocular, bulbar, neck, proximal limb, the enzyme–OP complex [Figure 1]. As a result of aging, and respiratory muscles in that order of severity. the enzyme is not susceptible to reactivation by oximes. As a general rule, the aging reaction occurs 48–72 hours after Central nervous system syndrome poisoning; hence at least theoretically, oximes are unlikely Central nervous system is uncommonly involved in acute to provide therapeutic beneÞ t beyond 48–72 hours after OP poisoning and occurs with OP compounds that cross poisoning. In reality, different OP compounds have different the blood–brain barrier.[22,23] The manifestations include aging half-lives. For instance, diethylphosphorylated depressed mental status and central respiratory drive. In acetylcholinesterase (a compound formed in poisoning severe poisoning, patients may have convulsive seizures. by compounds such as parathion, chlorpyrifos, diazion, and chlorfenvinphos) has
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