1. Alimohammad Alimohammadi Clinical Toxicologist & Forensic Medicine
Approach to the Poisoned Patient اصول كلي مسموميت‌ها و چگونگي برخورد با آن
Alimohammad
Alimohammadi
Clinical Toxicologist & Forensic Medicine

2. Definitions of terms Poisoned patient : to injure or kill with poison
Poison : a substance that through its chemical
action usually kills , injures , or
impairs a organism
Poisoning :exposure to poison is accidental
Overdose : exposure to poison is intentional

3. Definitions of terms Accidental poisonings(children-elderly)
Over dose( Nonsuicidal Patient)
secondary to drug abuse
Occupational
Environmental
Attempt poisonings (adults)
Over dose(suicidal Patient)
Over dose(Homiside)

4. Any Pt who comes with abrupt alteration In consciousness level
in overall a clinical toxicologist should brings in mind following points if he has suspicion of overdose in comatose Pt :
Any Pt who comes with abrupt alteration In consciousness level
Any young Pt with arrhythmia
Any Pt with suicidal and psychic records .
Any Pt with drug abuse record.
Any Pt who bring in ED with multi system failure of unknown etiology should be suspected of poisoning until proved otherwise
Any Pt who had recent familial or social problem especially in young`s.
Any Pt who has metabolic acidosis without clear base .
Any Pt who was rescued from fire accident
Any Pt who was found unconscious in work environment

5. How to diagnose a poisoned patient
It may be : 1) To easy to ascertain like a child poisoning with his/her mothers iron tablets ingestion. or an elderly Pt who misreads label , or misuse a drink. 2) To difficult like a youth who was found unconscious in deserted place with unclear history.

6. IMPORTANT OR SERIOUS AFFAIR
suddenly
acute
Chronic
dealy

7. IMPORTANT OR SERIOUS AFFAIR

8. The initial approach to the poisoned patient
(1) resuscitation and stabilization;
(2) history and physical examination, including evaluation for a specific toxidrome;
(3) appropriate decontamination of the gastrointestinal tract, skin, and eyes;
(4) judicious use of laboratory tests, electrocardiograms, and radiographic studies;
(5) administration of specific antidotes, if indicated
(6) utilization of enhanced elimination techniques for selected toxins.

9. RESUSCITATION AND STABILIZATION
the same as with all patients.
The patency of the airway must be ensured,
followed by assistance of breathing and
support of circulation.
Cardiac monitoring,
pulse oximetry, and
intravenous access should be established as indicated by the patient’s clinical condition.

10. should focus on correcting:
Airway management
should focus on correcting:
hypoxia
respiratory acidosis
avoiding pulmonary aspiration. Acid, opium, hydrocarbon

11. Acidemia due to respiratory depression can exacerbate the toxicity of drugs, such as cyclic antidepressants and salicylates.
severe upper airway injury that occurs following a caustic ingestion may preclude routine endotracheal intubation, necessitating surgical management of the airway.
The use of succinylcholine for rapid-sequence intubation can result in prolonged paralysis in patients with organophosphate toxicity.

12. Standard ACLS doses of atropine are inadequate for organophosphate-induced cholinergic symptoms.
The use of procainamide is contraindicated for ventricular dysrhythmias caused by cyclic antidepressants and other myocardial sodium channel–blocking agents.
Intravenous calcium can be lifesaving in a patient poisoned with hydrofluoric acid, a calcium channel–blocking agent, or magnesium.
Sodium bicarbonate may be lifesaving in resuscitation of the patient poisoned with cyclic antidepressants or salicylates

13. In patients with altered mental status, administration of naloxone, dextrose, and thiamine should be considered,
flumazenil should be administered cautiously in cases of benzodiazepine overdose with significant respiratory depression

14. The indications generally fall into the following categories
•    Failure to maintain reasonable gas exchange    •    Failure to maintain a patent airway    •    Failure to adequately protect the airway against aspiration (which may be especially problematic in the toxicologic patient prone to vomiting)    •    To provide a route for pulmonary toilette    •    To facilitate patient and symptom control

15. history accidental poisonings Over dose Nonsuicidal Patient

16. history
Accurate identification of ingestants is particularly important in the patient exposed to agents that have delayed onset of toxic effects, such as acetonitrile, which is metabolized to cyanide, or monoamine oxidase inhibitors

17. Focused Physical Examination/Toxidromes
VITAL SIGNS
NEUROLOGIC MANIFESTATIONS OF TOXINS
DERMATOLOGIC MANIFESTATIONS OF TOXINS
GASTROINTESTINAL MANIFESTATIONS OF TOXINS

18. Focused Physical Examination/Toxidromes
Examples include the respiratory depression of barbiturate or opioid poisoning and the tachycardia and hypertension of poisoning with sympathomimetic agents. Characteristic “toxidromes” indicate the presence of agents with cholinergic, anticholinergic, sympathomimetic, and opioid effects. Less specific findings, such as nystagmus, myoclonus, asterixis, and tremor, also suggest various toxins. Characteristic odors suggest the presence of toxins, such as cyanide (almond odor) or ethchlorvynol (vinyl odor).

19. DECONTAMINATION
Dermal decontamination is best accomplished with copious amounts of water.
However, the use of water on skin contaminated with metallic sodium, metallic potassium, or phosphorus (white, yellow) may result in further skin injury owing to heat generation and explosive injury.
Irrigation of phenol burns with low molecular weight polyethylene glycol is effective.
Other therapies, such as topical calcium salts for hydrofluoric acid burns, may be indicated following initial water decontamination.
Ocular decontamination can be accomplished with water or normal saline irrigation

20. Gastrointestinal Decontamination
SYRUP OF IPECAC
GASTRIC LAVAGE
ACTIVATED CHARCOAL ALONE
CATHARTICS
OBSERVATION ALONE
WHOLE BOWEL IRRIGATION
THE BODY PACKER/BODY STUFFER PATIENT

21. activated charcoal
primary method of gastrointestinal decontamination, and it should be administered within 1 hour of toxin ingestion whenever possible. Multiple doses of activated charcoal may be beneficial in patients ingesting life-threatening amounts of carbamazepine, dapsone, phenobarbital, quinine, theophylline
bezoar

22. Laboratory Testing in Emergency Toxicology
TOXICOLOGY SCREENS (3,000,000 toxin)
SERUM QUANTITATION OF OVERDOSED DRUGS
Electrocardiograms
Radiology

23. DIAGNOSTIC TESTING
Many toxic agents are not detected on routine screening, while false-positive results are commonly reported.
Other tests, such as serum electrolytes, calculated anion gap, glucose, arterial blood gases, serum creatinine, and liver function tests, can assist in the indirect evaluation of the end-organ effects of a toxin.
Electrocardiograms should be obtained in patients ingesting toxins known to produce cardiac dysrhythmias or conduction delays, or in significantly poisoned patients as an aid to the diagnosis of an unknown toxin.

24. Radiographs
Routine radiographs may be indicated to evaluate potential adverse effects of toxins, such as pulmonary injury due to inhalation of chlorine gas or aspiration of a hydrocarbon.
Routine abdominal radiographs may be unreliable for evaluation of toxins thought to be radiopaque
MRI, CT, brain damage,

25. ANTIDOTES Antidote Indication for Use Antivenom (equine)
 Crotalid (Crotalidae polyvalent antivenin)
Crotalids: Rattlesnakes (Crotalus spp. and Sistrurus spp.), cottonmouth (Agkistrodon spp.), copperhead (Agkistrodon spp.)
 Elapid
Eastern (Micrurus fulvius fulvius) and Texas (Micrurus fulvius tenere) coral snakes
Antivenom (Fab) *
Crotalids
Antivenom, latrodectus (equine)
Black widow spider (Latrodectus spp.)
Antivenom, loxosceles (rabbit)
Brown recluse spider (Loxosceles reclusa)
Antivenom, scorpion (goat)
Scorpions (Centruroides spp.)
Botulinum antitoxin (equine)
Clostridium botulinum
Calcium
Calcium channel antagonists
Hydrofluoric acid
Hyperkalemia (except cardiac glycosides)
Hypermagnesemia
Hypocalcemia (e.g., ethylene glycol)
Calcium disodium edetate
Lead
Cyanide antidote kit:
Cyanide
 Amyl nitrite
 Sodium nitrite
 Thiosulfate
Deferoxamine
Iron
Dextrose
Ackee fruit (hypoglycin)
Insulin
Sulfonylureas
Other (e.g., salicylates, pentamidine)
Digoxin-specific antibody fragments (Fab)
Digoxin
Digitalis
Other cardiac glycosides, e.g., bufodienalides (Bufo toads)
Oleander
Dimercaprol
Arsenic
Mercury
Ethanol
Diethylene glycol
Ethylene glycol
Methanol
Experimental: sodium monofluoroacetate
Flumazenil
Benzodiazepines
Venlafaxine
Folic acid/tetrahydrofolic acid (leucovorin)
Methotrexate
Fomepizole
Glucagon
Beta-adrenergic receptor antagonists
Hyberbaric oxygen
Carbon monoxide
Experimental: carbon tetrachloride
Cyanide, hydrogen sulfide
Methylene blue
Methemoglobin-producing agents
N-Acetylcysteine
Acetaminophen
Experimental: carbon tetrachloride, chloroform, pennyroyal oil
Naloxone, nalmefene, naltrexone
Opioids
Physostigmine
Anticholinergic agents, e.g., diphenhydramine, Jimsonweed (Datura spp.), scopalamine
Pralidoxime
Organophosphates
Protamine
Heparin
Pyridoxine
Ethylene glycol (theoretical efficacy)
Isoniazid
Monomethylhydrazine mushrooms (Gyrometra esculenta)
Sodium bicarbonate
Myocardial sodium channel blockers, e.g., cyclic antidepressants, cocaine, norpropoxyphene, class Ia and Ic antidysrhythmics, piperidine phenothiazines (thioridazine, mesoridazine)
Altered tissue distribution/enhanced elimination: chlorophenoxy herbicides, chlorpropamide, formic acid (methanol), methotrexate, phenobarbital, salicylates
Neutralization: inhaled chlorine gas, hydrogen chloride, phosgene
Succimer
Vitamin K
Anticoagulants, e.g., warfarin, long-acting anticoagulant rodenticides

26. Extracorporeal Removal of Drugs and Toxins
Hemodialysis
charcoal hemoperfusion
Plasmapheresis
exchange transfusion
continuous ultrafiltration

27. DRUGS AND TOXINS COMMONLY REMOVED BY EXTRACORPOREAL THERAPY
Barbiturates - hemoperfusion or hemodialysis
Ethylene Glycol - hemodialysis
Lithium - hemodialysis
Methanol - hemodialysis
Salicylates - dialysis, at toxic levels
Theophylline - Hemoperfusion

28. COMPLICATIONS AND LIMITATIONS OF EXTRACORPOREAL REMOVAL OF TOXINS
Vascular Access
Hypotension
Bleeding

29. Advanced Life Support in the Poisoned Patient (TOX ACLS)
BASIC LIFE SUPPORT
ADVANCED LIFE SUPPORT
BRAIN DEATH AND ORGAN DONATION CRITERIA

30. Adult Basic Life Support
Immediate recognition of sudden cardiac arrest (SCA)
Activation of the emergency response system
Early cardiopulmonary resuscitation (CPR)
Rapid defibrillation With an automated external defibrillator (AED)
Initial recognition and response to heart attack and stroke are also considered part of BLS.

31. Advanced Life Support in the Poisoned Patient (TOX ACLS)
Standard supportive care for critically ill patients often follows the advanced cardiac life support (ACLS) algorithms published by the American Heart Association (AHA).
Evidence suggests that standard supportive care may not be adequate for critically ill poisoned patients
Synthetic or semisynthetic opioid poisoning may be more resistant to opioid antagonistsAs much as 10 mg of naloxone has been required for adequate reversal in rare cases

32. BASIC LIFE SUPPORT (poisoned patient)
Prolonged Resuscitation
good neurologic outcome has been reported in cases of severe poisoning requiring prolonged CPR that extended to periods of up to 3 to 5 hours

33. Adult Advanced Cardiovascular Life Support
Continuous quantitative waveform capnography is recommended for confirmation and monitoring of endotracheal tube placement.
Cardiac arrest algorithms are simplified and redesigned to emphasize the importance of high-quality CPR (including chest compressions of adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in chest compressions and avoiding excessive ventilation).

34. Adult Advanced Cardiovascular Life Support
Atropine is no longer recommended for routine use in the management of pulseless electrical activity (PEA)/asystole.
There is an increased emphasis on physiologic monitoring to optimize CPR quality and detect ROSC.
Chronotropic drug infusions are recommended as an alternative to pacing in symptomatic and unstable bradycardia.
Adenosine is recommended as a safe and potentially effective therapy in the initial management of stable undifferentiated regular monomorphic wide-complex tachycardia .

35. ADVANCED LIFE SUPPORT ( poisoned patient )
Hyperadrenergic States (Tachycardia and Hypertension)
Bradycardias
Ventricular Dysrhythmias (Tachycardia and Fibrillation)
Pacing
Hypertonic Saline and Systemic Alkalinization
Potassium

36. Hyper adrenergic States (Tachycardia and Hypertension)
physostigmine (Antilirium) is indicated for hemodynamically significant tachycardia associated with pure anticholinergic poisoning.
Benzodiazepines such as diazepam or lorazepam are generally safe and effective for chest pain, hypertension, or tachycardia associated with drug-induced hyperadrenergic states.
nitroglycerin and phentolamine have been shown to reverse cocaine-induced vasoconstriction, whereas labetalol had no effect and propranolol worsened it.

37. Bradycardias
In the ACLS bradycardia algorithm, atropine, pacing, dopamine, epinephrine, and isoproterenol are recommended in sequence for hemodynamically significant or “symptomatic” bradycardia.
In bradycardias due to severe poisoning by digoxin, calcium channel antagonists, or β-adrenergic receptor antagonists, atropine may be ineffective even in high doses
In drug-induced, symptomatic bradycardia, many authors have cautioned that isoproterenol (a nonselective β-adrenergic receptor agonist) may induce or aggravate hypotension (β2 effect) and ventricular dysrhythmias (β1 effect
In massive β-adrenergic receptor antagonist poisonings, very high-dose isoproterenol therapy has been effective
]Drug-induced, symptomatic bradycardia refractory to atropine is an indication for cardiac pacing (electrical).

38. Bradycardias
In a case of severe insecticide poisoning (organophosphate or carbamate), approximately 20 g of atropine over 24 h was required
Atropine cannot reverse the severe nicotinic effects seen with organophosphate insecticides (i.e., muscle paralysis and fasciculations), and pralidoxime will be required.
Digoxin-specific Fab antibody fragments have been shown to be extremely effective therapy for severe digoxin and cardiac glycoside poisoning.

39. Ventricular Dysrhythmias (Tachycardia and Fibrillation)
Magnesium has been recommended for polymorphic ventricular tachycardia, even when magnesium levels in the blood are normal
polymorphic ventricular tachycardia and monomorphic ventricular tachycardia respond to lidocaine
Hypokalemia is a risk factor for ventricular dysrhythmias and even with normal potassium levels, potassium supplementation has been recommended in torsades de pointes

40. Shock Vasopressor Agents
Usual Starting Dose
Amrinone
0.75–2.0 mg/kg SIVP
Calcium
1–3 g SIVP
Glucagon
5–10 mg IVP
Insulin Pump or Glucose-Insulin-Potassium (GIK)
 Glucose (D50W)
1 g/kg
 Insulin (regular)
1.5 U/kg
 Potassium chloride
10 mEq
Isoproterenol
2–20 μg/min
SIVP, slow intravenous push.

41. BRAIN DEATH AND ORGAN DONATION CRITERIA
Electroencephalograms and neurologic examinations do not provide valid criteria for proof of brain death during acute toxic encephalopathy and can be applied only when drug levels are no longer toxic. In the presence of toxic drug levels, the only valid criterion for ascertaining brain death is the absence of cerebral blood flow

42. SUMMARY
Utilization of standard AHA ACLS protocols for critically poisoned patients may not result in optimal outcomes. a more toxicology-oriented type of ACLS (TOX ACLS) may be effective. Elements of TOX ACLS not usually included in standard ACLS protocols include higher doses of standard drugs, nonstandard drugs (amrinone , calcium, esmolol , glucagon, glucose-insulin-potassium (GIK), metoprolol , phenylephrine , physostigmine , and sodium bicarbonate) and nonstandard techniques such as prolonged CPR and circulatory assist devices. Proper application of TOX ACLS techniques requires basic understanding of the pathophysiology of acute poisonings. Care of critically poisoned patients can be enhanced through consultation with a medical toxicologist or a regional poison information center

43. Thanks a lot