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It is characterized by mental status changes, muscle weakness and excessive secretory activity. Acetylcholine is the neurotransmitter at all preganglionic autonomic nerve endings (nicotinic receptors), all parasympathetic and some sympathetic postganglionic nerve endings (muscarinic receptors), the neuromuscular junction (nicotinic receptors) and at some CNS synapses. Acetylcholine undergoes continuous degradation by acetylcholine esterase. Excessive stimulation of acetylcholine receptors occurs as a result of inhibition of acetylcholine esterase or direct stimulation of acetylcholine receptors. TOXIC CAUSES Acetylcholine esterase inhibition Carbamate pesticides Neostigmine Organophosphorus pesticides Organophosphorus warfare agents Sarin Soman Tabun Physostigmine Pyridostigmine Direct stimulation of acetylcholine receptors Arecholine Betanechol Carbachol Choline Metacholine Mushrooms Boletus sp. Clitocybe sp. Inocybe sp. Pilocarpine NON-TOXIC CAUSES None CLINICAL FEATURES Clinical manifestations of excessive cholinergic activity may be divided into muscarinic, nicotinic and central effects. The relative severity of these effects differs between individual cases. Muscarinic effects are those of parasympathetic overactivity and include bradycardia, pinpoint pupils, sweating, blurred vision, excessive lacrimation, excessive bronchial secretions, wheezing, dyspnoea, coughing, vomiting, abdominal cramping, diarrhoea, and urinary and faecal incontinence. Nicotinic effects are those of sympathetic overactivity and
confusion. Atropine is the specific antidote for the muscarinic effects and should be administered as soon as the diagnosis is suspected. coma and seizures. The initial dose of 1 to 2 mg (0. It has no effect on nicotinic receptors. endotracheal or intraosseous (children) routes. In severe cases.neuromuscular dysfunction and include tachycardia. Decontamination appropriate to the offending agent and route of exposure should be performed. subcutaneous. Where intravenous access is not available. the following conditions may be considered: Bronchial asthma Gastroenteritis Myasthenic crisis Pulmonary oedema Status epilepticus of other aetiology RELEVANT INVESTIGATIONS Arterial blood gases Chest X-ray ECG Electrolytes. psychosis. maintain ventilation and oxygenation. DIFFERENTIAL DIAGNOSIS The full clinical syndrome usually presents no diagnostic dilemma. very large doses of atropine (up to 100 mg) may be required. the initial priority is to secure the airway. In moderate-to-severe cases of cholinergic syndrome due to organophosphorus pesticide or warfare agent poisoning. TREATMENT In severe cases. muscle fasciculation and muscle weakness. Either pralidoxime or obidoxime are .05mg/kg in children) intravenously should be repeated every 5 to 10 minutes until drying of respiratory secretions is achieved. Where particular manifestations of poisoning predominate. Excessive dosing of atropine will manifest itself as agitation and tachycardia. dilated pupils. atropine may be administered via the intramuscular. The patient should remain under close observation and further doses of atropine should be given as required. Central effects may include agitation. hypertension. an acetylcholine esterase reactivator should be administered (if available) following atropine. urea and creatinine Glucose Oximetry Serum and/or erythrocyte acetylcholine esterase activity. Depression of acetylcholine esterase activity is diagnostic of carbamate or organophosphorus poisoning but is not helpful in the acute management of the cholinergic syndrome. secure intravenous access and control seizures with intravenous diazepam.
doses greater than this may be necessary to achieve enzyme reactivation. Warsaw Poisons Control Centre. 03-701 Warszawa.5 mg/kg/hour until clinical recovery is observed and at least 24 hours. In severely poisoned patients. Jacobsen. They should not be discharged from hospital until they remain asymptomatic for at least 24 hours after the withdrawal of all antidote therapy. despite complete resolution of all symptoms and signs of toxicity. Szajewski. Szpital Praski. CLINICAL COURSE AND MONITORING The severity and duration of the clinical syndrome depend on the agent responsible and the dose. Birmingham 3/99: T. Patients should remain under close observation after cessation of oxime therapy. L. Alternatively. especially following ingestion. Alternatively. Weteranow 4. The term "Intermediate Syndrome" is applied to recurrent muscle weakness occurring some days after the exposure. Nantel. It is usually relatively benign and of short duration following overdose of a cholinergic drug. Those cases severe enough to require supportive care measures or antidote therapy require close monitoring and are ideally managed in an intensive care unit setting. Meredith. continued administration of obidoxime may be by intermittent intramuscular or intravenous doses of 2 mg/kg every 4 hours. A. L. . Murray. continued administration of pralidoxime may be by intermittent intravenous or intramuscular doses of 30 mg/kg every 4 hours. It may be associated with inadequate oxime therapy. Murray. Recurrence of clinical manifestations of toxicity indicates the need for further oxime therapy. Poland (February. Reviewers: Geneva 8/98. Pl. J. J Pronczuk.suitable. LONG TERM COMPLICATIONS Peripheral neuropathy Neuropsychiatric sequelae AUTHOR(S)/REVIEWERS Authors: Ryszard Feldman & Janusz Szajewski. 1998). D. The clinical features of poisoning by carbamate pesticides are usually of shorter duration and less severe than those of organophosphorus compounds. The dose of pralidoxime is 30 mg/kg intravenously followed by a continuous infusion of 8 mg/kg/hour until clinical recovery is observed and for at least 24 hours. Cholinesterase activity often remains low for weeks after the acute poisoning. More severe poisoning is usual with carbamate and organophosphorus compounds. The dose of obidoxime is 4 mg/kg intravenously followed by a continuous infusion of 0.