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Toxicology Case Presentation

Toxicology Case Presentation. Ng Fu A&E, QMH. History. F/30, Indonesian Maid Found collapse at home by employer With an insecticide spray beside her Good past health, no history of suicide Good relation with present family. Physical Examination. GCS E4V2M4 10/15; confused

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Toxicology Case Presentation

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  1. Toxicology Case Presentation Ng Fu A&E, QMH

  2. History • F/30, Indonesian Maid • Found collapse at home by employer • With an insecticide spray beside her • Good past health, no history of suicide • Good relation with present family

  3. Physical Examination • GCS E4V2M4 10/15; confused • BP 148/89; P 123/min; T 36oC; SpO2 90% • Flaccid 4 limbs • Smell of insecticide • Bronchorrhea noted; air entry good • Pin point pupils both sides • No external wounds

  4. Progress in A&E • GCS decreased to E4M1V1 6/15 • Atropine 0.6mg iv x 1 → P 147 • Patient intubated after given Dormicum 3mg iv followed by Suxamethonium 25mg iv • Pralidoxime 1g in100ml NS over 15min • Another dose of Dormicum 2mg iv • P122/min → another dose of atropine 0.6mg iv • Medical ICU consulted • Ryles tube, Foley inserted

  5. Investigation in A&E • ECG : Sinus tachycardia 147/min • Hb 14; H’stix 14.3; urine x PT neg • Istat before intubation : Na 139; K 2.9; pH 7.235; pCO2 6.87 pO2 11.9; HCO3 22 • CXR : ET tube in position, no active lung consolidation

  6. Types of Insecticide • Pyrethrins e.g.Mosquito coils; Raid Roach & Ant Killer 2. Chlorinated hydrocarbon insecticides e.g. DDT analogue (Raid Moth Proofer) 3. Thiocyanate Insecticides 4. Organophosphate Insecticides e.g. chlorpyrifos (Baygon Roach Bait); Fenitrothion (Zoro Zoro Cockroach Bait) 5. Carbamate Insecticides e.g. Propoxur (No Frills, Baygon Insect Spray)

  7. Common Insecticides in HK Supermarket

  8. Progress in Ward • Admitted medical ICU • Developed aspiration pneumonia with WCC 24.9 and neutrophil 22.2 • Plasma Cholinesterase 2175 (4650 – 10440) • CK elevated temporarily (483) then in downward trend later • Amylase increased to 499 then decreased. • Toxicology screen : no paracetamol, no salicylate and no ethanol • Further Hx confirmed carbamate poisoning resulting in muscle paralysis.

  9. Progress in ward • Discharge to general ward on Day 4 • Psychiatrist consulted : admitted that she had an argument with her father and boyfriend in Indonesia for her plan at the end of current contract one month later. She wanted to stay in HK but her family disagreed. She then drank the insecticide at home • Finally discharged on Day 7

  10. Carbamate Poisoning c.f. Organophosphate insecticide • Widespread agricultural and home use • Rapid hydrolysis into harmless cpds with little long-term accumulation in the environment. • Propoxur (Baygon); Aldicarb (Temik)

  11. Pathophysiology

  12. Carbamate Poisoning Reversibly binds to cholinesterase The carbamate-cholinesterase bond reverses spontaneously in 4-8 h, yielding a normal cholinesterase. Organophosphate Permanently bind to cholinesterase Pralidoxime reverses the organophosphate-cholinesterase bond if it is given within 24 to 36 h of acute exposure.

  13. Clinical Features • Due to cholinergic excess causing : • Muscarinic overstimulation (hyperactivity of parasympathetic system) - SLUDGE • Overstimulation of nicotinic receptors in sympathetic system - tachycardia, HT, stimulation of adrenal medulla • Overstimulation of nicotinic receptors in NM junction - muscle faciculation, cramping, weakness • Cholinergic excess in CNS - delirium, confusion, coma, seizure

  14. Classification of s/s of acute carbamate poisoning according to Receptor Site and Type Muscarinic • Miosis** • Blurred vision • Nausea & Vomiting • Diarrhoea • Salivation • Lacrimation • Bradycardia • abdominal pain • Diaphoresis • Wheezing • Urinary incontinence • Fecal incontinence • Nicotinic • - Muscle fasciculations** • (striated muscle) • Paralysis • Muscle weakness • Hypertension • Tachycardia • Pallor • Mydriasis (rare) • Central • Unconsciousness • Confusion • Toxic psychosis • Seizures • Fatigue • Respiratory depression • Dysarthria • Ataxia • anxiety

  15. Clinical Features Usual cause of DEATH is Respiratory failure due to : • CNS resp. centre depression • Resp. muscle weakness • Increased bronchial secretions

  16. Investigations • Non-diagnostic • ↑sugar; ↓K; ↑WBC; ↑amylase • Glycosuria; proteinuria • ECG changes • CXR usu unremarkable but may show pulmonary edema in severe cases • Serum cholinesterase vs RBC cholinesterase activities – diagnostic aids only, no specific value in the Mx

  17. Management If asymptomatic →observe 6-8 h For seriously poisoned patients, • Vigorous decontamination • Respiratory support • Use of specific antidotes

  18. Management • Rescuers’ safety • Establishment of Airway and adequate ventilation • Use of atropine • Decontamination • Gastric larvage / activated charcoal • Use of Pralidoxime

  19. Atropine • Acts as a physiologic antidote by competitively blocking the action of Ach at muscarinic (but not nicotinic) receptors. • No effect on the nicotinic receptors at skeletal myoneural junctions or within the sympathetic ganglia. • May be therapeutic for CNS symptoms esp. in children • 2 mg iv every 5 to 15min until signs of atropinization (mydriasis, tachycardia, flushing, xerostomia, anhydrosis,etc) • Difficult to use pupils size as a guide • Should be given aggressively esp. in case of organophosphate poisoning (atropine refractoriness)

  20. Should Atropine be used more liberally in this patient ? • Tachycardia is usu due to hypoxia or ganglionic stimulation • Tachycardia >140 – ?contraindication to atropine use

  21. Pralidoxime • A biochemical antidote for organophospate poisoning but probably not for pure carbamate poisoning. • Little toxicity • 3 beneficial effects : 1. Reactivate the cholinesterase that has been phosporylated by an organophosphate if given in 24 to 36h 2. Reverses the cholinergic nicotinic effects not affected by the use of atropine alone (i.e. muscle fasciculation, weakness and stimulation of sympathetic ganglia. 3. Direct reaction and detoxification of unbounded organophosphate molecules.

  22. Pralidoxime • 1 g iv over 15-30 min, repeated 1 to 2 h after the initial dose, then every 10 to 12 h as needed. (Paed. 20-50mg/kg) • OR continuous iv infusion 0.5g/h in adult or 10-20mg/kg/h in children • Reversal of muscle weakness and fasciculation usu begins in 10-40min • Rx is usu continued for 24-48h

  23. FOR Not harmful Severe s/s with impending resp failure Prominent muscle weakness May be mixture of organophosphate and carbamate poisoning AGAINST The carbamate-cholinesterase bond reverses spont. in 4-8 hrs Not without side effects Atropine not fully given Use is controversial Should Pralidoxime be used in this patient ?

  24. Use of Pralidoxime in Carbamate Poisoning • Its use is still controversial After aequate atropinization, pralidoxime may be indicated in (Consensus, 1986) • life-threatening symptoms with severe muscle weakness, fasciculations, paralysis, or decreased resp effort • Continued excessive requirement of atropine • Concomitant organophosphate and carbamate exposure

  25. Learning Points • Atopine should be used aggressively in organophosphate and carbamate poisoning. The therapeutic end-point should be clearing up of bronchial secretions. Tachycardia alone should not be a contra-indication to adequate atropinization. • Pralidoxime can be given in carbamate poisoning when severe toxicity occurs, as in this case.

  26. Learning Points • Succinylcholine should be used with caution or avoided because: • Hydrolysis of Sch by plasma cholinesterase is delayed • Increased levels of Ach at neuromuscular junction may aggravate the neuromuscular blocking effect

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