Acute poisoning.pptx4567890-==-0987654332

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1. Prepare by : اية احمد عبد الرضا رغدان علاوي محسن ايلاف محمود صبري : Under supervision الدكتور كاظم موحان Acute poisoning

2. Introduction Types of acute poisoning Factors that influence toxicity Clinical features Diagnosis and differential General management Specific management Contents :

3. What is it that is not a poison ? All things are poison and nothing is without poison. It is the dose only that makes a thing not a poison." Paracelsus (1493-1541), the Renaissance "Father of Toxicology," in his Third Defense .

4. WHAT IS POISON? Refers to any substance that injected into living body by any means (oral , IV , inhalation or dermal ) Causes local or systemic effects (or even both ) Results in ill-effects/death of individual INTRODUCTION Acute poisoning is common, accounting for about 1% of hospital admissions in the UK. In developed countries, the most frequent cause is intentional drug overdose in the context of self-harm, often involving prescribed or ‘over-the-counter’ medicines. Accidental poisoning is also common, especially in children and the elderly. Toxicity also results from alcohol, or following occupational or environmental exposure.

5. Poisoning is a major cause of death in young adults, but most deaths occur before patients reach medical attention, and mortality is low (<1%) in those admitted to hospital. In developing countries, the frequency of self-harm is more difficult to estimate. Because of their widespread availability and use, household and agricultural products, such as pesticides and herbicides, are common sources of poisoning and have a much higher case fatality. In China and South-east Asia, pesticides account for about 300 000 suicides each year. Snake bite and other forms of envenomation are also important causes of morbidity and mortality

6. Types of Posing Involved

7. Types of Posing Involved

8. Factors that influence toxicity Factors related to posion : 1 . Amount taken (Dose ). 2. The physical and chemical composition of the toxicant . 3. Concentration (or dilution) b) Factors related to person : 1. Age :(Children & old age more affected ). 2. State of health (hepatic, renal, cardiac failure). 3. Stomach contents (fatty ) and Gastric secretion (ph ). 4. Route of administration : I.v . > inhalation > intraperitoneal >intramuscular > subcutaneous >intradermal >oral > topical . 5 . Frequency of exposure . 6. Metabolism of toxic agents e.g. methanol, parathion

9. 7. Tolerance . 8. Presence of other drugs(antagonism, synergism. 9-personal hypersensitivity 10-idiosyncrasy (Toxicogenetics)

10. Clinical features: Poisoning has a dynamic presentation as the patient may present at varying points in the time course of poisonin g.

11. Mechanisms of Toxicity 1. Interfere with O₂ transport or tissue utilization of oxygen (i.e: cyanide, CO) 2. Affect lungs (paraquat) 3. Affect cardiovascular system (TCA, Ca++ channel blockers) 4. Affect CNS (cocaine, sedatives) 5. Affect ANS (organophosphates) 6. Direct local damage (acids, bases) 7. Delayed effects on liver or kidneys (acetaminophen, metals)

12. Diagnosis : HISTORY 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 other substance (or substances, including drugs of misuse) been taken as well? • Obtain details from witnesses (e.g. family, friends, ambulance personnel) of the circumstances of the overdose. • Assess immediate suicide risk in those with apparent self-harm (full psychiatric evaluation when patient has recovered physically). • Assess capacity to make decisions about accepting or refusing treatment. • Establish past medical history, drug history and allergies, social and family history. • Record all information carefully.

13. B. EXAMINATION

14. Clinical signs suggestive of poisoning 1- small pupil : opioids, organ phosphorus compounds, clonidine. 2- dilated pupils : tricyclic antidepressants, cocaine, amphetamine . 3- hypotension: tricyclic antidepressant and haloperidol . 4- cocaine causes hypertension . 5- decreased respiratory rate : opioids, benzodiazepine . 6- increased respiratory rate: salicylate 7- right upper quadrant pain : paracetamol hepatotoxicity. 8- renal angle tenderness : salicylate poisoning. 9- epigastric tenderness : NSAIDS. 10- rhabdomyolysis : amphetamine. 11- hyperthermia : salicylates. 12- hypothermia : any CNS DEPRESSANTS DRUGS. 13- tackycardia : TCA, theophylline , digoxins . 14- bradycardia : b-blocker, calcium channel blocker 15- needle tracks : opioids and drugs of misuse. 16- extrapyramidal signs : phenothiazine , haloperidol

15. Specific toxicology screens may be available, but are, in general, of limited utility and seldom impact care or outcome. False- negative or false-positive results for drugs of abuse may be confusing and potentially distracting. Consider empiric testing for acetaminophen and aspirin in all potentially poisoned patients. Complementary testing includes blood glucose concentration, serum lactate/electrolytes, renal/liver function , urine HCG, and electrocardiography. C. INVESTIGATION : GENERAL MANAGMENT Gastrointestinal decontamination 'Single-dose activated charcoal may be considered if a patient has ingested a potentially toxic amount of a poison (known to be adsorbed to charcoal) up to 1 hr previously. 'Multiple-dose ' activated charcoal should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline. 'Gastric lavage' should not be employed routinely, if ever, in the management of poisoned patients. 'Whole bowel irrigation' should be considered for: poisoning with sustained-release or emetic-coated drugs patients who have ingested substantial amounts of iron ( as morbidity is high and other options are limited).

16. Substances poorly adsorbed by activated charcoal Medicine Iron Lithium Chemicals Acids Alkalis Ethanol Ethylene glycol Mercury Methanol Petroleum distillate ”Gastric lavage is contraindicated ” B . Urinary alkalinisation Urinary alkalinisation is currently recommended for patients with clinically significant salicylate poisoning when the criteria for haemodialysis are not met. It is also sometimes used for poisoning with methotrexate. Complications include alkalaemia, hypokalemia and occasionally alkaloid tetanic.

17. C . Haemodialysis and Haemoperfusion These techniques can enhance the elimination of poisons that have a small volume of distribution and a long halflife after overdose, and are appropriate when poisoning is sufficiently severe to justify invasive elimination methods. The toxin must be small enough to cross the dialysis membrane (haemodialysis) or must bind to activated charcoal (haemoperfusion). Haemodialysis may also correct acid-base and metabolic disturbances associated with poisoning Poisons effectively eliminated by haemodialysis or haemoperfusion Haemodialysis Ethylene glycol Isopropanol Methanol Salicylates Sodium valproate Lithium Haemoperfusion Theophylline Phenytoin Carbamazepine Phenobarbital Amobarbital

18. D. Lipid emulsion therapy Lipid emulsion therapy or "lipid rescue" is being used increasingly for the management of poisoning with lipid soluble agents such as local anathetics, tricyclic antidepressants, calcium channel blocker and lipid soluble beta blockers such as propranolol . It involves intravenous infusion of 20% lipid emulsion at a initial dose of 1.5ml/kg followed by infusion of 0.25ml/kg/min until there is clinical improvement . It is thought that lipid soluble toxins partition into intavenous lipid, reducing target tissue concentration. E. Supportive Care For most poisons, antidotes and methods to accelerate elimination are inappropriate, unavailable or incompletely effective . Outcome is dependent on appropriate nursing and supportive care, and on treatment of complications Patients should be monitored carefully until the effects of any toxins have dissipated

19. F. Antidotes Antidotes are available for some poisons and work by a variety of mechanisms: for example, by specific antagonism (isoprenaline for ẞ-blockers), chelation (desferrioxamine for iron) or reduction (methylene blue for dapsone).

20. Specific management Analgesics : Paracetamol Poisoning This drug is free and highly available, it is highly toxic in overdose. Risk of severe liver damage is based on the dose ingested, . Management Activated charcoal may be used in patients presenting within 1 hour . Antidotes for paracetamol should be administered to all patients with paracetamol concentrations above the 'treatment line ' provided on paracetamol poisoning nomograms . Acetylcysteine given intravenously(or orally) is highly efficacious if administered within 8 hours of the overdose . Administration should not be delayed in patients presenting after 8 hours to await a paracetamol blood concentration result .

21. The antidote can be stopped if the paracetamol concentration is shown to be below the nomogram treatment line . The most important adverse effect of acetylcysteine is related to dose-related histamine release, the 'anaphylactoid' reaction , which causes itching and urticaria, and in occasional severe cases, bronchospasm and hypotension. Most cases can be managed by temporary discontinuation of acetylcysteine and administration of an antihistamine. An alternative antidote is methionine 2.5 g orally (adult dose) every 4 hours to a total of 4 doses, but this is less effective, especially after delayed presentation. If a patient presents more than 15 hours after ingestion, liver function tests, prothrombin time (or international normalised ratio - INR), renal function tests and a venous bicarbonate should be measured, the antidote started, and a poisons information centre or local liver unit contacted for advice if results are abnormal . An arterial blood gas sample should be taken in patients with severe liver function abnormalities; metabolic acidosis indicates severe poisoning. Liver transplantation should be considered in individuals who develop life threatening liver failure due to paracetamol poisoning.

22. Opioid Poisoning Common Causes Heroin Morphine Methadone Pethidine Tramadol Clinical Features Respiration-Reduced respiration rate and ventilation CVS-Hypotension , relative bradycardia CNS-Confusion, hallucination, slurred speech , sedation , coma Muscle-Ataxia ,reduced muscle tone Temperature-Hypothermia Eyes-Miosis Abdomen-lleus Skin-Needle tracks

23. Management Airway should be cleared and if necessary,respiratory support and oxygen given . Oxygen saturation monitoring and measurement of arterial blood gas should be performed . Prompt use of specific opioid antagonist naloxone (0.4-2mg IV in adult , repeated if necessary ). Patient should be monitored at least 6 hours after last naloxone dose

24. digoxin Patient liable to toxicity :- Hypo & Hyperthyroidism Renal failure Advanced age Metabolic factor (Hypokalemia ,hypernatremia , hypercalcemia , acid-base disturbance ) • Clinical features:– •Vomiting, diarrhea •Arrhythmia •ECG :- arrhythmia ( prolong QRS ) , digitalis effect ( sagging ST segment) Management •ECG and cardiac monitoring •Urea and creatinine and electrolytes should be measured . •Hypoxia , Hypokalaemia , hypomagnesaemia and acidosis increase risk of arrhythmia •STOP digitalis •STOP diuretic •Give potassium •IV magnesium •Atropine in case of bradycardia •Digitalis Antibody if available

25. Antidepressants : Tricyclic antidepressants • Overdose with tricyclic antidepressants (TCAs) carries a high morbidity and mortality because of their sodium channel-blocking, anticholinergic and α- adrenoceptor-blocking effects. • Clinical features: • Anticholinergic effects are common : CVS (Tachycardia , hypertension ),CNS ( Delirium, hallucinations, sedation ), muscles (Myoclonus) , Fever , eye( Diplopia, mydriasis ), skin (Flushing , hot, dry) and dry mouth • Severe complications include seizures , coma and arrhythmias ( ventricular tachycardia, ventricular fibrillation)

26. Management • Activated charcoal should be administered if the patient presents within 1 hour •ECG should be taken and continuous cardiac monitoring maintained for at least 6 hours • Significant Prolongation of the QRS interval indicates severe sodium channel blockade and a high risk of arrhythmia •Arterial blood gasses should be measured in suspected severe poisoning • In patients with arrhythmias, significant QRS or QT prolongation or acidosis , intravenous sodium bicarbonate (50mL of 8.4% solution) should be administered and repeated to correct pH •Prolonged seizures should be treated initially with intravenou Benzodiazepines .

27. Iron Overdose with iron can cause severe and sometimes fatal poisoning, with toxicity of individual iron preparations related to their elemental iron content. Clinical features Early features include gastrointestinal disturbance with the passage of grey or black stools, progressing to hyperglycaemia , leucocytosis , haematemesis , rectal bleeding, drowsiness, convulsions, coma, metabolic acidosis and cardiovascular collapse in severe cases. Early symptoms may improve or resolve within 6–12 hours, but hepatocellular necrosis can develop 12–24 hours after overdose and occasionally progresses to hepatic failure. Gastrointestinal strictures are late complications

28. Management Activated charcoal is ineffective, but gastric lavage or whole bowel elimination may be considered in patients presenting soon after substantial overdose, although efcacy is unknown. Serum iron concentration should be measured at least 4 hours after overdose or earlier if there are features of toxicity. Desferrioxamine chelates iron and should be administered immediately in patients with severe features (e.g. coma, shock, metabolic acidosis, haemolysis ), without waiting for serum iron concentrations, as well as symptomatic patients with high serum iron concentrations (e.g. >5 mg/L). Desferrioxamine may cause hypotension, allergic reactions and occasionally pulmonary oedema . Otherwise, treatment is supportive and directed at complications.

29. Reference - TinTinalli's emergency medicine manual -Therapeutic Manual (Internal Medicine) -Oxford Handbook of Clinical Medicine -Davidson's Principles and Practice of medicine

30. Any Questions ?