1. REVISITING ACUTE SELF POISONING Arosha Dissanayake

2. Mortality rates DSH - East vs West Mortality of acute poisoning East vs West 20% vs 0.5%

3. Reason - Self poisoning in SL Pesticides / Herbicides Plant poisons Corrosives Medicinal drugs Everyday household chemical compounds

4. Management principles GI decontamination Antidotes

5. GI decontamination 1. Induced emesis 2. Gastric lavage (GL) 3. Activated charcoal (AC)

6. 1. Induced emesis Syrup of Ipecac / Traditionally, Coconut milk, Salt water and Soap water Evidence 1) Activated Charcoal (AC) alone is as effective as induced emesis or a combination of AC + Induced emesis (Kulig et al 1985) 2) Poor Risk vs Benefit profile - Aspiration pneumonia, bronchospasm, Mallory Weiss tears, Bradycardia and Baro trauma to mediastinum

7. Induced emesis AACT / EAPCCT Position statement “No evidence that Ipecac improves the outcome of poisoned patients and its routine use in the ED should be abandoned” Ipecac use - 14.99% (1985) to 0.02% (2009) (Bronstein et al 2009)

8. Summary – Place of Induced Emesis NO place (Though National Guidelines still mention) Home? – We do not know the effect

9. 2. Gastric Lavage (GL) Traditionally used for self poisoned patients with impaired consciousness AACT / EAPCCT Position statement Only for potentially life threatening ingestion Only if within 60 minutes Not for routine use in poisoning as clinical benefit is uncertain Risks Perforation of oesophagus and stomach Pulmonary aspiration and aspiration pneumonia

10. Recommended GL Come within first 2 hours of poisoning (National Guidelines) Patient has to be fully conscious If consciousness is not full only with cuffed ET tube Pass size 18 NG tube / Ryles tube Doctor has to do this Aspirate stomach contents 200 – 400 ml of water or normal saline, given via tube and aspirated Maximum of three cycles

11. GL in the hospital setting Observational study of 14 consecutive GLs performed in 4 hospitals in Sri Lanka Given irrespective of giving consent or time elapsed Given for those taking non lethal ingestions Airway rarely protected in patients with impaired consciousness Large volumes upto 1000 ml given 5 Aspirations and 2 major cardiac events (Eddleston et al 2007)

12. Summary - Place of GL in poisoning Rarely indicated Clinical benefit doubtful Impossible in many hospital settings

13. 3. Activated Charcoal (AC) Egyptians 1500 BC Tovery 1831, French Academy of Med Sci. Carbon material grounded, superheated and injected (activated) with steam to produce a highly adsorbent powder with an immense surface area Adsorpent action + gut dialysis

14. Activated Charcoal AACT / EAPCCT Position statement “Clinical benefit greatest within 1hr after ingestion.” Risks Generally well tolerated Nausea and vomiting Pulmonary aspiration and aspiration pneumonia is infrequent

15. Recommendations - AC Within 2 hours of admission (Upto 4 hours with Yellow Oleander and some slow release medications) (National Guidelines) Drinking this is much more comfortable for the patient than giving it via an NG tube Dose 1 g / kg. Dissolve 50 g of activated charcoal in 200 ml of water and get patient to drink (If unconscious, after securing airway with cuffed ET tube, can give via NG tube)

16. Multi Dose Activated Charcoal (MDAC) “Multiple dose activated charcoal is effective in reducing deaths and life threatening cardiac arrythmias after yellow oleander poisoning” De Silva HA et al (2003) “Mortality did not differ in the three groups (Control / AC / MDAC) with pesticide and yellow oleander poisoning” Eddleston et al (2008)

17. Summary - Place of Activated Charcoal Probably the only useful and practical gastric decontamination method for most hospital settings Not useful for acids and alkali

18. 1. GI decontamination 1. Induced emesis - NO 2. Gastric lavage (GL) – Very limited place 3. Activated charcoal (AC) - Yes

19. Rarely used methods of poison elimination 1. Whole bowel irrigation – Slow release medicines, drug packet elimination (Polyethylene glycol electrolyte solution PO, 15ml/kg till effluent is clear) 2. Forced alkaline diuresis – Salicylates, Phenobarbitone (NaHCO3 in 5% Dextrose) 3. Haemodialysis – Lithium, anti epileptics

20. 2. Antidotes PoisonAntidote Organophosphat es Atropine, Pralidoxime ParacetamolNAC, Methionine Yellow OleanderAnti Digoxin Fab

21. Antidotes – Organophosphates Five features to monitor Lung crackles and wheezes Hypotension (SBP <80) Bradycardia (HR<80) Small pupils Excess sweating Antidotes 1) Atropine 2) Pralidoxime

22. 1) Atropine 3 – 5 vials (0.6 X 5 = 3 g) as a bolus Double the vials in boluses 4 vials, 8 vials, 16 vials, every five minutes till lungs are clear, HR is >80 and SBP is > 80 mmHg Once this is achieved, do not stop atropine. Start infusion using 20% (1/5ths) of what was given as boluses every hour Keep reducing rate every ½ hour depending on three vital parameters, lungs clear, HR and BP are alright Can transfer to tertiary care centre at this stage if needed

23. 2) Pralidoxime IV loading dose (1 g over 20 minutes) and infusion in addition to Atropine Continue for at least 24 hours after stopping atropine May need up to 7 days Transfer to tertiary care hospital after patient is on stable dose Atropine infusion and Pralidoxime infusion is in place Clinical Benefit – Uncertain (De Silva HJ et al 1992)

24. Antidotes – Paracetamol Toxic dose > 20 tablets Oral methionine – effective in the early hours, in the peripheral hospital setting 2.5 g stat and 2.5 g every four hours, three more doses (No AC) NAC 1) Coming more than 8 hours after ingestion 2) Severe vomiting

25. Cardiac glycoside poisoning (Cardenolides) Yellow oleander (Thevitia peruviana) Eddleston 2002 – Anti Digoxin Fab effective in resolving arrythmias, increasing heart rates and reducing potassium levels Too expensive (USD 10,000 per life saved) Diya Kaduru (Cerbera manghas) – Sea Mango Mostly in Eastern province

26. Management of Cardenolide (cardiac glycoside) poisoning Anti Digoxin Fab Cardiac pacing Insulin Dextrose for hyperkalaemia

27. ‘Kaduru’ Diya kaduru (Cardiac glycosides) Goda Kaduru (Strychnine) Divi Kaduru (Hallucinogenic substance)

32. ‘Prinso’ Poisoning “Emerging epidemic of fatal human self poisoning with a washing powder in Southern Sri Lanka” Gawarammana IB et al. (2009) “Pus Kudu” - Two packets – KMnO4 (small packet) and Oxalic acid (White, larger packet) Case Fatality Rate – 9.8 to 25.4 %

33. “Prinso” poisoning Deaths often occur before reaching hospital Most likely cause – severe hypocalcaemia causing cardiac arrhythmias IV 10 % Calcium gluconate, 10 ml over 10 min Calcium lactate, crush 35 tablets and drink stat Post Mortem – Severe mucosal ulceration Initial survivors – Cardio vascular instability and renal failure

34. Prevention of acute poisoning 1. Restriction of access – Safe storage (Pearson et al 2011) 2. Regulatory Control 1) Banning of WHO Class 1 poisons, Monocrotophos and Methamidophos (1995) and Class 11 poison Endosulfan (1998) (Eddleston et al 2011) 2) Changing formulation of Paraquat and subsequent restriction of access (Wilks et al 2011) 3. Effect on Glyphosate poisoning ??

35. Paradigm Shift 1. Shift focus from GI decontamination to early use of antidote 2. Wider use of Methionine for Paracetamol 3. Measuring Paracetamol levels (Shihana et al 2010) 4. Affordable anti toxins (Anti digoxin anti toxin) (Eddleston et al 2003) 5. Capacity building in doctors manning peripheral hospitals

36. Paradigm Shift 5. Restriction of access – Safe storage (Pearson et al 2011) 6. Regulatory Control 1) Banning of WHO Class 1 poisons, Monocrotophos and Methamidophos (1995) and Class 11 poison Endosulfan (1998) (Eddleston et al 2011) 2) Changing formulation of Paraquat and subsequent restriction of access (Wilks et al 2011) 7. Capacity building in doctors manning peripheral hospitals