Description
This comprehensive lecture on acute poisoning, authored by Dr. CK Mwandama from the Haematology Unit, Department of Internal Medicine at the University Teaching Hospital (UTH) in Lusaka, Zambia, provides a systematic overview of common toxicological emergencies. The presentation covers the general clinical features and toxic syndromes associated with various poisons, followed by detailed sections on specific agents: organophosphates, paracetamol (acetaminophen), salicylates, warfarin, and digoxin. For each toxin, the lecture explains the core pathophysiology, such as acetylcholinesterase inhibition by organophosphates and NAPQI-mediated hepatotoxicity from paracetamol. It delineates the characteristic clinical presentations, including the muscarinic, nicotinic, and CNS effects of organophosphate poisoning and the four-stage progression of paracetamol toxicity. The management strategies are thoroughly outlined, encompassing general supportive care, decontamination methods like activated charcoal, and specific antidotal therapies such as atropine and pralidoxime for organophosphates, N-acetylcysteine for paracetamol, and vitamin K for warfarin. The lecture also includes a valuable reference table summarizing key antidotes for various poisons. This resource is essential for medical students, postgraduate trainees in internal medicine, emergency medicine, and critical care, as well as practicing clinicians seeking to reinforce their knowledge of the diagnosis, pathophysiology, and evidence-based management of acute poisonings commonly encountered in clinical practice. It serves as a crucial study and revision guide for both examinations and emergency department rotations. Review this detailed presentation to enhance your clinical decision-making in toxicological emergencies.
What's inside
Acute Poisoning Dr CK Mwandama Haematology Unit, Department of Internal Medicine, UTH, Lusaka, Zambia 30/08/2021 Learning Objectives At the end of this session, learners should be able to do the following: • List general and common clinical features of Poisoning. • Understand the pathogenesis, clinical features and management of specific poisoning listed below: o Organophosphate oParacetamol o Salicylate o Warfarin o Digoxin • Know common antidotes for specific poisoning Introduction • In developed countries, poisoning causes approximately 10% of acute hospital medical presentations. • Statistics are not readily available for the developing countries including Zambia. • Most cases of poisoning are usually by self-administration of prescribed and over-the-counter medicines, or illicit drug. • Common cases of poisoning seen in emergency departments include the following: o Organophosphate o Paracetamol o Salicylate o Warfarin o Digoxin Common clinical features of Poisoning Clinical features Likely Poisoning Constricted pupils (miosis) Opioids, organophosphorus insecticides, nerve agents Dilated pupils ( mydriasis ) Tricyclic antidepressants, amphetamines, cocaine, antimuscarinic drugs Divergent strabismus Tricyclic antidepressants Nystagmus Carbamazepine, phenytoin Loss of vision Methanol, quinine Papilloedema Carbon monoxide, methanol Convulsions Tricyclic antidepressants, theophylline, opioids, mefenamic acid, isoniazid, amphetamines Dystonic reactions Metoclopramide, phenothiazines Delirium and hallucinations Amphetamines, antimuscarinic drugs, cannabis, recovery from tricyclic antidepressant poisoning Hypertonia and hyper- reflexia Tricyclic antidepressants, antimuscarinic drugs Tinnitus and deafness Salicylates, quinine Hyperventilation Salicylates, phenoxyacetate herbicides, theophylline Hyperthermia Ecstasy (MDMA), salicylates Blisters Usually occur in comatose patients Organophosphate poisoning(OPP) Introduction • Organophosphates (OP) are used as insecticides in agricultural and domestic settings throughout the world. • As nerve agents, they have also been used in warfare terrorist attacks. Mechanism of action • Mechanism of action is through the inhibition of the enzyme acetylcholinesterase, leading to the accumulation of acetylcholine at cholinergic synapses. • Excess acetylcholine causes constant acetylcholine receptor triggering, resulting in malfunction of the autonomic, somatic and central nervous systems Normal neuromuscular junction physiology • Acetylcholine (ACh) is synthesized from choline and acetyl-CoA through the action catalysed by choline acetyl-transferase in Cholinergic neurons. • An action potential in presynaptic neuron triggers influx of Ca²⁺ • Ca²⁺ stimulate exocytosis of presynaptic vesicles containing ACh, which is t released into the synaptic cleft. • ACh binds to ACh receptors (muscarinic and nicotinic receptors ) on the post- synaptic membrane resulting in nerve transmission. • Acetylcholinesterase ( AchE ), located on the post-synaptic membrane, terminates the signal transmission by hydrolyzing Ach. Pathophysiology of OPP • Organophosphates acts as AchE inhibitor . • ACh accumulates throughout the nervous system, resulting in overstimulation of cholinergic junctions (muscarinic effects), and at autonomic ganglia (nicotinic effects). Signs and symptoms of organophosphate poisoning can be divided into three broad categories: o Muscarinic effects o Nicotinic effects o Central nervous system effects Muscarinic • Diarrhoea • Urinary incontinence • Miosis • Bradycardia • Bronchospasms • Bronchorrhoea • Bronchoconstriction • Rhinorrhea • Nausea Clinical manifestations of acute organophosphate poisoning • Vomiting • Hypersalivation • Lacrimation • Emesis • Hypotension • Cardiac arrhythmias • Diaphoresis • Fecal incontinence Nicotinic • Muscle fasciculations • Tremors • Muscle weakness • Hypertension • Tachycardia • Sweating • Mydriasis • Muscle cramps • Diaphragmatic and respiratory failure • Anxiety • Emotional lability • Restlessness • Confusion • Ataxia • Tremors • Seizures • Coma • Impaired memory • Confusion • Irritability • Lethargy • Psychosis CNS and Neuropsychiatric Effects Treatment General Treatment • Airway control • Adequate oxygenation • Intubation may be an indication in patients severe respiratory distress due to: o Laryngospasm o Bronchospasm o Bronchorrhea o Seizures. • Gastric lavage should be done for decontamination in patients presenting early. Specific treatment This involves administration of specific drags including the following o Atropine o Pralidoxime o Magnesium sulphate o Diazepam Atropine • Anticholinergic & parasympatholytic • Competitive muscarinic antagonist of OP • Blocks OP binding to muscarinic receptor thus preventing or reducing the mucarinic response to acetylcholine. • Full atropinization is achieved when there is: o Mydriasis o Pulmonary secretions are dry o Adequate oxygenation. o Tachycardia
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