Supportive management of poisoning in ICU

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. 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 Phases of Poisoning & Treatment priorities

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. Respiratory Cardio vascular CNS: Respiratory depression Pulmonary edema, Intubation, Aspiration pneumonia Cardiac arrhythmias, hypotension AV block (2 or 3rd 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 Indications for admission in ICU

6. 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 Indications-Contd

7. Enhancement of Poison Elimination • Multiple-dose activated charcoal • Forced diuresisand Alteration of urine PhDiuresis 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. 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 Specific Antidotes

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

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