1. Supportive management of poisoning in ICU

2. Goals of Treatment Support of vital signs Prevention of further poison absorption Enhancement of poison elimination Administration of specific antidotes Prevention of reexposure

3. Phases of Poisoning & Treatment priorities Pre toxic-Prior to the onset of poisoning Toxic- Time between onset and it’s peak effect Resolution Decontamination, Sampling, Observation Resuscitation and stabilization, Enhance poison elimination Supportive, monitoring, Watch toxic effect of metabolite, redistribution of poison

4. Supportive care-Goals To maintain physiologic homeostasis until detoxification is accomplished To prevent and treat secondary complications such as aspiration, pneumonia bedsores cerebral and pulmonary edema rhabdomyolysis, renal failure thromboembolic disease, coagulopathy Sepsis & generalized organ dysfunction due to hypoxia or shock.

5. Indications for admission in ICU Respiratory Cardio vascular CNS: Respiratory depression Pulmonary edema, Intubation, Aspiration pneumonia Cardiac arrhythmias, hypotension AV block (2 or 3 rd degree ) TCA or Phenothiazine over dosage showing QTc>0.5sec or QRS >0.12 sec Unresponsiveness to verbal stimuli Seizures Drug over dosage with CNS depression Cerebral edema

6. Indications-Contd Metabolic Extra corporeal management Others Hyperkalemia, Hypo or Hyperthermia and NMS Severe metabolic acidosis Emergent dialysis or hemoperfusion, AV hemofiltration, Need for extracorporeal membrane oxygenation, Exchange transfusion Administration of drugs- Fab fragments, naloxone as infusion Anti snake venom administration

7. Enhancement of Poison Elimination Multiple-dose activated charcoal Forced diuresis and Alteration of urine Ph Diuresis and ion trapping via alteration of urine pH may prevent the renal absorption of poisons that undergo excretion by glomerular filtration and active tubular secretion. Extracorporeal removal –Peritoneal dialysis, hemodialysis, charcoal or resin hemoperfusion, hemofiltration, plasmapheresis, and exchange transfusion are capable of removing any toxin from the bloodstream.

8. Forced diuresis Saline diuresis -Enhance the renal excretion of alcohols, bromide, calcium, chromium, fluoride, isoniazid, lithium, meprobamate, potassium, and thallium. Alkaline diuresis (producing a urine pH 7.5 and a urine output of 3 to 6 mL/kg body weight per hour by adding sodium bicarbonate to an intravenous solution) enhances the excretion of chlorpropamide, fluoride, ethotrexate, phenobarbital, sulfonamides, and salicylates.

9. Limitations Contraindicated in congestive heart failure, renal failure, and cerebral edema. Acid-base, fluid, and electrolyte imbalance can occur which should be monitored carefully.

10. EXTRACORPOREAL REMOVAL Dialysis is effective in –acetone, atenolol, barbiturates, bromide, chloral hydrate, ethanol, ethylene glycol, isopropyl alcohol, lithium, methanol, procainamide, theophylline,salicylates, sotalol, and possibly heavy metals. Hemoperfusion –poisoning due to caffeine, carbamazepine, carbon tetrachloride, chloramphenicol, dapsone, disopyramide, hypnotic-sedatives,methotrexate, Mushrooms, paraquat, phenytoin, procainamide, theophylline, and valproate.

11. Limitations Both techniques require central venous access and systemic anticoagulation and often result in transient hypotension. Hemoperfusion cause hemolysis, hypocalcemia, and thrombocytopenia. Peritoneal dialysis and exchange transfusion when other procedures are either not available, contraindicated, or technically difficult

12. General Supportive Care Airway protection Oxygenation/ventilation Hemodynamic support Treatment of seizures Correction of temperature abnormalities Correction of metabolic derangements Treatment of arrhythmias

13. Respiratory care Endotracheal intubation: For protection against the aspiration, done prophylactically when unable to drink or speak Mechanical ventilation: For respiratory depression or hypoxia, therapeutic sedation or paralysis in neuromuscular hyperactivity. Drug-induced pulmonary edema is usually noncardiac rather than cardiac. – e.g- inhalation of poisonous gases, increased bronchial secretions in ChEase inhibitors poisoning, Overdosage of opiates

14. Respiratory care Extracorporeal measures for severe but reversible respiratory failure –membrane oxygenation, – venoarterial perfusion, –Cardiopulmonary by pass, – partial liquid(perfluorocarbon) ventilation –hyperbaric oxygen therapy

15. Cardio vascular System Hypotension- Shock: I or Vasovagal- by nitrites, anesthetic II – Severe poisoning, corrosives, depressant drugs Treatment: volume expansion –norepinephrine, epinephrine, or high-dose dopamine - Intraaortic balloon pump counter pulsation,Venoarterial or cardiopulmonary perfusion techniques should be considered for severe but reversible cardiac failure. –Correction of metabolic abnormalities, replacement of blood

16. Specific Therapy Hypotension & Brady arrhythmia: Beta blocker and calcium channel blocker poisoning: Glucagon, calcium, and high-dose insulin with dextrose. –cardiac glycoside poisoning- Antibody therapy

17. Specific Therapy Supra ventricular tachycardia with hypertension Mild to moderate- Observation, Benzodiazepines Severe with sympathetic hyperactivity- combined alpha and beta blocker (labetalol), a calcium channel blocker (verapamil or diltiazem), or a combination of a beta blocker and a vasodilator (esmolol and nitroprusside) is preferred. –Anticholinergic poisoning- physostigmine Supraventricular tachycardia without hypertension: –secondary to vasodilatation or hypovolemia -responds to fluid administration.

18. Tachyarrhythmia Of any etiology: Lidocaine and phenytoin. TCA or other membrane active agents :NaHCO3 Torsades de pointes and QT prolongation: Magnesium sulfate and overdrive pacing. Severe cardiac glycoside poisoning: Magnesium and anti-digoxin antibodies. If the patient is hemo dynamically stable: Observation Correction of underlying acid-base, electrolyte, oxygenation, and temperature derangements

19. Congestive Cardiac Failure Poisons producing myocardial damage causes CCF Digitalis doesn’t have any role Other measures for CCF helps viz., preload and afterload reduction, diuretics, O2 therapy

20. Cardiac Arrest Causes: Inhalation of GA agents CO poisoning and asphyxiation LA injections Over dosage of cardiac drugs Idiosyncrasy to drugs Management : As per ACLS protocol

21. CENTRAL NERVOUS SYSTEM Seizures: Major cause of morbidity and mortality as it results in anoxia, coma, aspiration, and serious metabolic derangement. Management: Quiet, darkened environment, ABC, Temperature control, Drugs

22. Drug treatment Thiamine, Dextrose, Naloxone Anticonvulsants-Benzodiazepines, Barbiturates( Phenytoin is CI) Specific antidotes whenever Appropriate Management of secondary complications

23. Specific Antidotes By excessive stimulation of catecholamine receptors –( e.g., sympathomimetic or hallucinogen poisoning and drug withdrawal) Isoniazid, Strychnine Isoniazid, Beta blocker, TCA OPC,OC Benzodiazepines, Barbiturates Pyridoxine (GABA enhancer) P2AM,Atropine

24. For poisons with central dopaminergic effects- phencyclidine (psychotic behavior) Treatment of seizures secondary to cerebral ischemia or edema or to metabolic abnormalities Haloperidol-dopamine antagonist Correction of the underlying cause

25. Delirium or Psychosis Causes: Fever, metabolic derangement, anticholinergic and antihistamines, neurological medications, recreational abuse of drugs, alcohol and other withdrawal syndromes, oral hypoglycemics, thiamine deficiency Management –Prevent injury –Place in quiet, dark room –Reassure –Monitoring of vitals –Treatment of complications like hyperthermia –Benzodiazepines

26. Hypoglycemia Situations Alcohol / Anesthesia following starvation Plant poisoning like mushroom Acetyl cholinesterase inhibitors like OPC Edetates chelating zinc from slow release formulations of insulin Salicylate over dosage Management: –Recognition of the problem and treatment in standard lines

27. Acute Renal Failure Causes: Direct toxicity: Amino glycosides, NSAIDs, Mushroom, Cyclosporin,CCl4, heavy metals, arsenicals, sulfonamides, ethylene glycol Hemolytic substrates: Castor beans, abrus, Naphthalene, Benzene Myoglobinuria: Stimulants, convulsants, hyperthermic agents Prolonged hypovolemia, hypotension Multifactorial as in snakebite Treatment: Treatment of shock, specific antidote for the poison, FAD for rhabdomyolysis, Dialysis along with general measures for treatment of ARF

28. Metabolic Abnormalities As the result of vomiting, diarrhea, kidney damage and other procedures If renal function and thirst is normal can be replaced orally or IV Acidosis Respiratory depression, methanol, ethylene glycol, paraldehyde poisoning, lactic acidosis Treatment: Elimination of the cause, Alkali administration as temporary measure- To alkalinize the urine (salicylate poisoning), to raise the overall pH to prevent arrhythmia (TCA Poisoning)

29. Hyperthermia Leads to Increased O2 requirement and metabolism Causes: Side effect/Drug interaction: MAO+SSRI ( Serotonin syndrome) Seizures or rigidity:TCA, Amphetamine, Cocaine, Disrupted thermo regulation: Anticholinergic agents, Malignant Hyperthermia,NMS, Increased metabolic rate: Thyroxin over dosage, Treatment: General measures, Neuro muscular paralysis, Dantroline sodium, Bromocryptine in specific situations

30. Hypothermia Though decreases the metabolic rate, circulation is impaired, detoxification and elimination of poisons are slowed Causes: Vasodilatation by alcohol and calcium channel blockers, barbiturates, oral hypoglycemic agents Treatment: Slow warming, warm blankets, extracorporeal circulation, peritoneal and gastric lavage with warm liquids

31. Liver Damage Direct cell injury-Acetyl salicylic acid, amanita phylloids,CCl4,Chloroform Delayed cell injury-Alcohol Hemolytic anemia overwhelming hepatic capacity-Castor bean, Primaquin Hepatic vein thrombosis-bush tea (Pyrazolidine alkaloids) Cholestasis and portal inflammation

32. Investigations Cell injury- Raised bilirubin, ALT, AST, LDH, A:G reversal, Low plasma prothrombin level after 24 hrs of Vit k Obstruction: Increased Sr bilirubin and Alk.Po4ase,Sr. Cholesterol, Decreased urine and fecal urobilinogen

33. Treatment D/C drugs Prevent further damage Avoid Anesthetic/ Surgical provocation Vit K Supportive treatment

34. Methaemoglobinemia Formed by oxidation of ferrous to ferric ion in Hb by chemicals which is a poor carrier of O2 Agents: Phenazopyridine, Phenacetin Anesthetic agents: Benzocaine, Lidocaine Antibiotics:Primaquin, sulfones, trimethoprim Organic nitrates & nitrites, aniline, bromate, chlorate

35. Clinical Features Level of MethHb –15% –30-40% –60% and more Symptoms cyanosis, asymptomatic Dizziness, Headache, Weakness,Dyspnea, Chocolate cyanosis Stupor, Respiratory distress

36. Investigations& Treatment Pulse oxy metry- Unreliable Spectrophotometer Analysis: For level ABG- Normal PO2& Normal Saturation Management: 100% O2 by mask Removal of poison by lavage, emesis Methylene blue-1% solution 0.1-0.2ml/kg IV over 10 mts Ascorbic acid 1g IV if methylene blue NA Exchange transfusion

37. Thank You