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Dr.Dhaher JS Al-habbo FRCP London UK Assistant Professor in Medicine Department of Medicine
College of Medicine POISONING
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‘Grandfather of Toxicology’
Paracelsus ( ) ‘Grandfather of Toxicology’ "All things are poison and nothing is without poison, only the dose permits something not to be poisonous." “The dose makes the poison” therapeutic effect toxic increasing dose
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Recognition of poisoning Identification of agents involved
Taking a history in poisoning What toxin(s) have been taken and how much? Recognition of poisoning Identification of agents involved Assessment of severity Prediction of toxicity
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Taking a history in poisoning What toxin(s) have been taken and how much?
What time were they taken and by what route? Has alcohol or any drug of misuse been taken as well? Obtain details of the circumstances of the overdose from family, friends and ambulance personnel Ask the general practitioner for background and details of prescribed medication
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Taking a history in poisoning What toxin(s) have been taken and how much?
Assess suicide risk (full psychiatric evaluation when patient has physically recovered) Capacity to make decisions about accepting or refusing treatment? Past medical history, drug history and allergies, social and family history? Record all information carefully
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EVALUATION OF THE ENVENOMED PATIENT
Neurotoxic paralysis 'Sleepy' or drooping eyelids Difficulty swallowing, dysarthria and drooling Limb weakness Respiratory distress Excitatory neurotoxicity. Sweating, salivation, piloerection Tingling around mouth, tongue or muscle twitching Dyspnoea (pulmonary oedema)
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Assessment of type and extent of envenoming
Coagulopathy. Blood oozing from bite site and/or gums Bruising Melaena, haematemesis Local effects :Pain, sweating, blistering, bruising etc. Myolysis ; Muscle pain or weakness
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Important substances involved in poisoning
IN UK Analgesics, e.g. paracetamol and non-steroidal anti- inflammatory drugs (NSAIDs) Antidepressants, e.g. tricyclic antidepressants (TCAs), selective serotonin re-uptake inhibitors (SSRIs) and lithium Cardiovascular agents, e.g. β-blockers, calcium channel blockers and cardiac glycosides Drugs of misuse, e.g. opiates, benzodiazepines, stimulants (e.g. amphetamines, MDMA, cocaine) Carbon monoxide Alcohol
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Important substances involved in poisoning
In South and South-east Asia. Organophosphorus and carbamate insecticides(mostly fatal) Aluminium and zinc phosphide Oleander Snake venoms Antimalarial drugs, e.g. chloroquine Antidiabetic medication
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Important substances involved in poisoning
Poisoning in old age Aetiology: commonly results from accidental poisoning (e.g. due to confusion or dementia) or drug toxicity as a consequence of impaired renal or hepatic function or drug interaction. Toxic prescription medicines are more likely to be available. Psychiatric illness: self-harm is less common than in younger adults but more frequently associated with depression and other psychiatric illness, as well as chronic illness and pain. There is a higher risk of subsequent suicide. Severity of poisoning: increased morbidity and mortality result from reduced renal and hepatic function, reduced functional reserve, increased sensitivity to sedative agents and frequent comorbidity.
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Epidemiology More than 2 million toxic exposures reported in 200
Over half were children < 6 years Poisoning third leading cause of death from Incidence of toxin related deaths increase 300%. All chemicals have potential to be poisons if given a large enough dose Poisoning occurs when exposure to a substance adversely affects function of any organ system
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Examination Physiologic excitation – Physiologic depression –
anticholinergic, sympathomimetic, or central hallucinogenic agents, drug withdrawal Physiologic depression – cholinergic (parasympathomimetic), sympatholytic, opiate, or sedative-hypnotic agents, or alcohols Mixed state – polydrugs, hypoglycemic agents, tricyclic antidepressants, salicylates, cyanide
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Physical Examination Oropharynx for increase salivation or excessive dryness CV: rhythm, rate, regularity Lungs: bronchorrhea or wheezing Abd: bowel sounds, tenderness or rigidity Ext: fasiculations, tremor Neuro: CN, reflexes, muscle tone coordination, cognition, ability to ambulate
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Drug detection
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Drug levels
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General Management A (Airway) B (Breathing) C (Circulation)
D (Disability- /Glasgow Coma Scale) DEFG ( Don’t ever forget the Glucose) GET A SET OF BASIC OBSERVATIONS
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Airway Airway obstruction can cause death after poisoning
Flaccid tongue Aspiration Respiratory arrest Evaluate mental status and gag/cough reflex Airway interventions Sniffing position Jaw thrust Head-down, left-sided position Examine the oropharynx Clear secretions Airway devices: nasal trumpet, oral airway Intubation? Consider naloxone first
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Breathing Determine if respirations are adequate
Give supplemental oxygen Assist with bag-valve-mask Check oxygen saturation, ABG Auscultate lung fields Bronchospasm: Albuterol nebulizer Bronchorrhea/rales: Atropine Stridor: Determine need for immediate intubation
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Circulation IV access Obtain blood work Measure blood pressure, pulse
Hypotension treatment: Normal saline fluid challenge, 20 mL/kg Vasopressors if still hypotensive PRBC’s if bleeding or anemic Hypertension treatment: Nitroprusside, beta blocker, or nitroglycerin Continuous ECG monitoring Assess for arrhythmias, treat accordingly
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Supportive care Vital signs, mental status, and pupil size
Pulse oximetry, cardiac monitoring, ECG Protect airway Intravenous access cervical immobilization if suspect trauma Rule out hypoglycaemia Naloxone for suspected opiate poisoning
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Preventing absorption
Gastric lavage Not in unconscious patient unless intubated (risk aspiration) Flexible tube is inserted through the nose into the stomach Stomach contents are then suctioned via the tube A solution of saline is injected into the tube Recommended for up to 4hrs in Salicylate OD Induced Vomiting Ipecac - Not routinely recommended Risk of aspiration
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Preventing absorption
Activated charcoal Adsorbs toxic substances or irritants, thus inhibiting GI absorption Addition of sorbitol →laxative effect Oral: g as a single dose repetitive doses useful to enhance the elimination of certain drugs (eg, theophylline, phenobarbital, carbamazepine, aspirin, sustained- release products) not effective for cyanide, mineral acids, caustic alkalis, organic solvents, iron, ethanol, methanol poisoning, lithium
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Elimination of poisons
Renal elimination Medication to stimulate urination or defecation may be given to try to flush the excess drug out of the body faster. Forced alkaline diuresis Infusion of large amount of NS+NAHCO3 Used to eliminate acidic drug that mainly excreted by the kidney eg salicylates Serious fluid and electrolytes disturbance may occur Need expert monitoring Hemodialysis or haemoperfusion: Reserved for severe poisoning Drug should be dialyzable i.e. protein bound with low volume of distribution may also be used temporarily or as long term if the kidneys are damaged due to the overdose.
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