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OP POISONING-case presentation.pptx
- 1. Case Presentation G KalaiAmuthan Gurusamy MD
- 2. History ◈ 36 yearsold female brought into RZ at 10pm ◈ Presentation � NKMI � Found unconscious at home � Noted frothy saliva around the mouth � Family unsure what happened � Ambulance called for ? Fitting – IV valium 5mg given in ambulance � What other relevant history to ask??
- 3. Differential diagnosis ◈ Vascular– Stroke, MI ◈ Infection – Meningoencephalitis, Sepsis ◈ Neoplasm – Brain tumor, Advanced malignancy ◈ Drugs – Overdose/Poisoning ◈ Inflammation – Hypoxia ◈ Congenital – AVM ◈ Autoimmune –SLE, vasculitis ◈ Trauma - ICB ◈ Endocrine – DKA/Thyroid storm/Hypoglycemia ◈ Degenerative – Dementia
- 4. Further history fromfamily ◈ Not depressed/low mood or any acute psychological stressor ◈ Was seen by family member on the same evening – no altered behavior noted ◈ No history of fitting ◈ Unsure if feverish
- 5. ◈ Upon arrivalto ED : � No jerky epileptic movements � Foam from nose and mouth – yellowish secretion � No OP/hydrocarbon smell � Diaphoretic � Gasping, Pin point pupils, GCS 3 ◈ BP 161/50mmHg ◈ PR 102 ◈ RR 32 ◈ SPO2 100 HFO � Lungs : crepitation � Abd :soft active bowel sound ◈ Intubated for airway protection � Post intubation – hypotensive and bradycardic
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- 7. ◈ UPT –negative ◈ REFLO 11.3 ◈ UFEME ketone 2+
- 10. Further history ◈ Patientfamily found a bottle of insecticide in the rubbish bin at home ◈ Noted patient had changed her attire at home prior, soaked with sweat
- 11. Insecticides Chemical Group Activeingredients Organophosphate (Industrial grade) Chlorpyrifos Malathion Carbamate Carbofuran Pyrethin/Pyrethroids (Household pesticides) Cyfluthrin Cypermetrin Cyphenothrin Permetrin Pyrethrin Tetrametrin Others Abamectin Boric acid Fipronil
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- 14. Overview of Organophosphatepoisoning ◈ Organophosphate compounds are used as commercial insecticides ◈ Similar mechanism as nerve agent (tabun, sarin, VX) ◈ Entry : ingestion, inhalation, skin/eye contact ◈ Potent inhibitor of acetylcholinesterase ◈ Excessive accumulation of Ach in CNS + PNS ◈ results in cholinergic crisis � SLUDGE + Killer B’s (Bronchorrea, Bradycardia, Bronchospasm, Bradypnea)
- 15. Risk Factors ◈ insecticides/fertilisers ◈surface and room sprays ◈ baits for cockroaches ◈ shampoos against head lice ◈ pet preparations ◈ crop protection and livestock dipping ◈ fumigation ◈ nerve agents (sarin)
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- 17. Mechanism of OPpoisoning Inhibit AChE Excess Ach Muscarinic + Nicotinic ACHe-OP complex undergo aging with time New ACHe need to be synthesized despite antidote
- 18. Pharmacokinetics ◈ Well absorbedvia GI, Resp tract, mucous membrane, skin ◈ Some OP activated into more toxic ‘oxone’ in body � Parathion � Paraoxon � Malathion � Malaoxon ◈ Onset : min to hours (depends on agent/route/extend of exposure) ◈ Most OP metabolized in liver to INACTIVE compounds
- 19. Organophophate Toxidromes MUSCARINIC NICOTINIC S– Salivation M – Muscle cramps L – Lacrimation T – Tachycardia U – Urination W – Weakness muscle D – Defecation H – Hypertension G - GI Cramp F – Fasciculation E – Emesis S – Sugar (hyperglycemia) Killer B’s – Bronchorrea, Bradypnea, Bronchospasm, Bradycardia
- 20. Other clinical features ◈CVS � No cardiogenic pulmonary edema � Hypotension � Arythmias (Prolong QtC, PVC, VT/VF) ◈ CNS � Irritablity � Restless � Agitation � Confusion ◈ GI � Acute panceratitis
- 21. OP vs Carbamate OPCarbamate Binding at NMJ Irreversible Reversible Action at active site on AChE molecule Phosphorylation Carbamoylation Half Life 10 days 1 day CNS action Yes No Treatment Atropine + Pralidoxime Atropine
- 22. Investigations ◈ Treatment shouldbe started based of CLINICAL FEATURES! ◈ Diagnostic test only for suspected cases ◈ Specific insecticide and metabolite level not available in most centres 1. Serum Plasma Cholinesterases 2. RBC Cholinesterase level
- 23. Plasma Serum cholinesterase ◈Low level ~ Toxicity ◈ Metabolizes various compounds ie suxamethonium/codeine ◈ Less specific as indication for exposure to OP ◈ More reflective of ACUTE poisoning (decline and regenerate faster than RBC cholinesterase) ◈ Can be low in various conditions � Hereditery, malnutrition, chronic debilitating illness
- 24. RBC Cholinesterase ◈ Notavailable most centers ◈ More specific ◈ Regenerates slower – use as historical marker of exposure ◈ Can be used as monitoring in occupational exposure ◈ Low levels can be found in � Pernicious anemia, hemoglobinopathy, on antimalarial tx
- 25. Principle of Management ◈Early decontamination ◈ Supportive care ◈ Appropriate use of antidote ◈ Treat the complication ◈ Police report
- 26. Early decontamination ◈ Staffprotection � Prevention of secondary poisoning from vomitus, lavage fluid, surface contaminant � Universal precaution ◈ Dermal decontamination with copious soap and water ◈ Remove clothing ◈ Gastric lavage � Substantial amount of OP ingested - <1H
- 27. Supportive care ◈ Airwaysupport – intubation and frequent suctioning � Non depolarizing agent used as muscle relaxant as depolarizing agent(suxa) may have prolonged action in the face of depleted ACHe ◈ Seizure – benzodiazepines ◈ Fluids - Give 500 –1000 ml (10–20 ml/kg) of normal saline over 10–20 min
- 28. Antidote (ATROPINE) ◈ Toreverse muscarinic effect (no nicotinic effect) ◈ Dose � IV 0.8 to 1.2mg ( paeds 0.01mg/kg, not less than 0.1mg to prevent paradoxical brady) � Double the dose every 5 minutes if no improvement (up to 1000mg/day) � Infusion can follow after initial dose at 10-20% of total initial bolus per hour ◈ AIM � Clear chest � HR > 80 � SBP > 80 � Dry Axillae � Pupil not pinpoint ◈ Confusion, pyrexia + absent bowel sound/urinary retention � atropine toxicity
- 30. Modified Atropine Chart® Time Signs of atropinization Signs of atropine toxicity Drugs and doses HR>80 Clear Lung Pupil size dilated Dry Axilla SBP>80 Bowel sound absent Confused Fever (>37.5) Atropine infusion (mg/H) Bolus (mg) 0000H 0005H 0010H
- 31. Antidote (Oximes-Pralidoxime) ◈ MOA �Reactivates the phosphorylated AChE by binding to the OP molecule � Does not work if aging has occur (<48H) ◈ Synergistic effect with atropine ◈ No definite evidence to prove/disprove efficacy of oxime ◈ Reasonable to start in severe poisoning with 24H-36H ◈ DOSE � 1-2g in 100mls NaCl over 30 mins (do not give bolus—fatal) � Followed by infusion 8-20mg/kg/H � Child : 25-50mg/kg 15-30min (rpt 1-2H) ◈ Continue until OP toxicity subside
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- 34. Intermediate syndrome (IMS) ◈Occur after cholinergic symptom resolves ◈ Occur up to 20-50% cases ◈ Early sign : weakness of neck flexion ◈ Respiratory paralysis, muscle weakness, motor cranial nerve palsy, no sensory deficit ◈ Recover 1-3 weeks ◈ Treatment supportive
- 35. Organophosphate induced delayed peripheralneuropathies (OPIND) ◈ Days to weeks to occur ◈ Occur through inhibition of neuropathiy target esterase (NTE) Delayed Neuropsychiatric sequalae ◈ Chronic neurological sequalae after stop OP exposure ◈ Cognitive defect – memory, concentration, problem solving ◈ Depression and anxiety
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- 37. Paraquat ◈ Banned on2002 – but lifted after few years ◈ Swallowing 20-24% paraquat � > 10ml of � significant illness � > 30ml (mouthful) � Lethal ◈ Rapidly-acting, effective, nonselective and relatively inexpensive widespread ◈ Used in much of the developing countries
- 38. Mechanism of Toxicity Transported to pneumocytes Paraquat� PQ+ (monocation radical) PQ+ + O2 (excess in lungs) � superoxide radical + Paraquat ® Superoxide radicals � free radical � cell damage
- 39. Clinical Features ◈ Corrosive– GI tract ◈ Early death � cardiac toxicity + shock ◈ Late death � pulmonary fibrosis / Respiratory failure ◈ Multi-organ failure
- 40. Investigation ◈ Urine paraquat �To confirm exposure � Remain positive 6H-few days ◈ Serum Paraquat
- 41. Management ◈ Precaution ◈ Resuscitation– avoid O2 therapy unless significant hypoxia ◈ GI Decontamination (<2H) � Recommended to limit systemic exposure (grade 2C) � Activated charcoal (1g/kg in water, max 50g) � Fullers earth (2g/kg in water, max 150g) ◈ Gastric lavage and forced emesis are contraindicated due to paraquat-induced caustic injury ◈ Definitive tx � NONE
- 42. Specific treatment &antidotal treatment • Treatment with hemoperfusion for four hours • if it can be initiated within four hours of ingestion (grade 2c) Extracorporeal therapies • Glucocorticoid with cyclophosphamide for paraquat induced lung fibrosis – may be beneficial Anti-inflammatory and Immunosuppressant • Acetylcysteine – under study Anti-oxidant therapy
- 43. Glyphosate (Roundup®) ◈ Nonselective herbicide ◈ Kills any green plant with little environmental persistence
- 44. Clinical features ◈ Mosttoxicity is a believed to be due to the surfactant component ◈ Most common surfactant polyoxyethyleamine (POEA), concentration up to 50% ◈ GI : NVD, corrosive injury to GI tract (>85ml) ◈ Respiratory : Bronchospasm, Laryngeal corrosive injury, ARDS ◈ CVS + CNS : hypotension, cardiogenic shock, AMS, cerebral edema
- 45. Treatment ◈ Supportive ◈ GIDecontamination
- 46. Reference ◈ Shirley Ooi ◈UptoDate ® ◈ Clinical Toxicology Coursebook 2017