Anesthesia, Srishti Gupta acute poisoning.pptx

Acute exogenous poisoning

1. ACUTE EXOGENOUS POISONING SRISHTI GUPTA LDK-3-18S

2. Contents Definition Etiology General Approach Specific Management -Paracetamol Poisoning - Organophosphorous (OP)Insecticides Poisoning -Opiate Poisoning

3. Definition Acute toxicity describes the adverse effects of a substance that result either from a single exposure or from multiple exposures in a short period of time (usually less than 24 hours). To be described as acute toxicity, the adverse effects should occur within 14 days of the administration of the substance.

4. Etiology Acute poisoning is common . In developed countries, the most frequent cause is intentional drug overdose in the context of self-harm and usually involves prescribed or “over-the-counter” medicine. Toxicity may also occur as a result of alcohol or recreational substance use,or other occupational or environmental exposure. In developing countries, the frequency of self-harm is more difficult to estimate. Household and agricultural products such as pesticides and herbicides,are more freely available,and more common causes of poisoning and are associated with a much higher case fatallity .

5. General Approach ABC,clear airway Consider ventilation(if the respiratory rate is <8/min or PaO2 <8kPa when breathing 60% O2 or the airway is at risk,eg GCS<8) Treat shock If unconscious,nurse semi-prone

6. Further Management Assess the patient History from patient,friends or family is vital Features from the examination may help Investigations Glucose,U&E,FBC,LFT,INR,ABG,ECG,paracetamol and salicylate levels urine/serum toxicology,specific assays as appropriate Monitor - Temperature,pulse and respiratory rate,BP,O2 saturations,urine output,ECG Treatment -Supportive measures may need catheterization Absorption consider gastric lavage and activated charcoal Specific measures for antidotes ,consider naloxone if conscious level and pinpoint pupil,consider pabrinex and glucose if drowsy/confused

7. Taking a history in poisoning What toxins 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 from witness of the circumstances of overdose( family,friends,ambulance personnel) Ask the GP for background and details of prescribed medication Assess suicide risk (full psychiatric evaluation) Assess capacity to make decisions about accepting or refusing treatment Establish past medical history,drug history and allergies,social and family history Record all informations carefully

8. Clinical Signs of Poisoning by Pharmaceutical agents and drugs of misuse

9. General Management A. 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)

10. Substances poorly adsorbed by activated charcoal Medicine Iron Lithium Chemicals Acids* Alkalis* Ethanol Ethylene glycol Mercury Methanol Petroleum distillates* *Gastric lavage is contraindicated.

11. 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 , hypokalaemia and occasionally alkalotic tetany.

12. 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 .

13. Poisons effectively eliminated by haemodialysis or haemoperfusion Haemodialysis • Ethylene glycol • Isopropanol • Methanol • Salicylates • Sodium valproate • Lithium Haemoperfusion • Theophylline • Phenytoin • Carbamazepine • Phenobarbital • Amobarbital

14. 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.

15. 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.

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

17. Paracetamol Poisoning Paracetamol toxicity results in hepatic and renal failure. 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.

18. 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.

19. Figure;The management of a paracetamol overdose

20. 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 center or local liver unit contacted for advice if results are abnormal.

21. 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. Organophosphorous (OP)insecticides Poisoning Sequential triphasic illness follows OP intoxication Acute cholinergic phase Intermediate syndrome(IMS) Organophosphate-induced delayed polyneuropathy(OPIDN)

23. Clinical features Toxic effects usually appear within 4 hours of exposure/ingestion .Organophosphates used in agriculture are generally the most toxic. Miosis the most characteristic sign . SLUDGE syndrome(Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis), bronchospasm, bronchorrhoea , diaphoresis, bradycardia, hypotension, convulsions, ataxia, muscle spasm, respiratory paralysis and death due to respiratory failure.

24. Muscle fasciculation, cramps and weakness can progress to areflexia and paralysis. Respiratory failure may be secondary to weakness of muscle of respiration. Hypertension, tachycardia, papillary dilatation and pallor may result from ganglion stimulation. Headache, giddiness, anxiety, restlessness, drowsiness, confusion, tremors, slurred speech and generalized weakness are early signs of mild to moderate poisoning. In severe cases, delirium, psychosis, seizures, coma and cardiorespiratory depression are the predominant features.

25. Treatment Further contamination is prevented by removal from the site of exposure and of contaminated clothing and contact lenses. The airway is cleared and high flow oxygen administered. Direct mouth-to-mouth/nose resuscitation must avoided. Contaminated clothing and contact lenses should be double-bagged , the skin washed with soap and water, and the eyes are irriagated . Following ingestion, gastric lavage may be undertaken within an hour of intake, followed by activated charcoal via nasogastric tube, after establishing intravenous access and airway protection.

26. Convulsions are controlled with intravenous diazepam. Monitoring of ECGs, temperature, urea and electrolytes, amylase and glucose is mandatory. Severe cases should be managed in an ICU and may require supported ventilation. Antidote IV atropine Loading dose 1.8-3 mg(1 ampoule=0.6 mg),continue every 5 minute until the patient is fully atropinized . Maintainence dose 20%-30% of loading dose given by infusion.

27. Complete and early atropinization is essential in early management. Speed of administration is as important as use of sufficient doses. Regarding intermediate syndrome, ventilator support should be instituted before a patient develops respiratory failure. Parenteral nutrition is often required. For OPIDN, there is no specific therapeutic measures. Regular physiotherapy may reduce deformity caused by muscle wasting.

28. Opioid Poisoning Common Causes Heroin Morphine Methadone Pethidine Tramadol

29. Clinical Features Respiration-Reduced respiration rate and ventilation CVS-Hypotension, relative bradycardia CNS-Confusion, hallucination, slurred speech,s edation , coma Muscle-Ataxia, reduced muscle tone Temperature-Hypothermia Eyes- Miosis Abdomen-Ileus Skin-Needle tracks

30. 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.