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8/21/2019 Approach to Poisoned Patient
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An approach to a poisonedpatient
Dr. J V Peter, MD, DNB (Med), FRACPChristian Medical College & Hospital, Vellore
Second CME and workshop on Critical care
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Introduction
What is a poison?
In common usage - poisons arechemicals or chemical products thatare distinctly harmful to human
More precisely - a poison is a
foreign chemical (xenobiotic) that iscapable of producing a harmfuleffect on a biologic system
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Other terminology
What is a toxin?
It originally referred to apoison of animal or plantorigin
Toxicant is the currentlypreferred scientific term forall poisons.
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Other terminology
What is a toxidrome?
It is the association of several clinicallyrecognizable features, signs, symptoms,phenomena or characteristics which oftenoccur together, so that the presence of one
feature alerts the physician to the presenceof the others.
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Common toxidromes
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The cholinergic toxidrome
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The cholinergic toxidrome
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The cholinergic toxidrome
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What toxidrome?
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The anticholinergic toxidrome
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
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The anticholinergic toxidrome
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
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The anticholinergic toxidrome
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
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What toxidrome?
disorientation Amphetamine
hallucinations Cocaine
Hallucinogenic hyperactive bowel Pseudoephedrine
panic Phencyclidine Benzodiazepenes
seizure Ephedrine
Toxidrome Hypertension
Tachycardia
Tachypnea
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HallucinogenicSympathomimetic toxidrome
disorientation Amphetamine
hallucinations Cocaine
Hallucinogenic hyperactive bowel Pseudoephedrine
panic Phencyclidine Benzodiazepenes
seizure Ephedrine
Toxidrome Hypertension
Tachycardia
Tachypnea
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disorientation Amphetamine
hallucinations Cocaine
Hallucinogenic hyperactive bowel Pseudoephedrine
panic Phencyclidine Benzodiazepenes
seizure Ephedrine
Toxidrome Hypertension
Tachycardia
Tachypnea
HallucinogenicSympathomimetic toxidrome
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disorientation Amphetamine
hallucinations Cocaine
Hallucinogenic hyperactive bowel Pseudoephedrine
panic Phencyclidine Benzodiazepenes
seizure Ephedrine
Toxidrome Hypertension
Tachycardia
Tachypnea
HallucinogenicSympathomimetic toxidrome
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Common toxidromes
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Sedative/hypnotic toxidrome
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Sedative/hypnotic toxidrome
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Sedative/hypnotic toxidrome
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Common toxidromes
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Opiate toxidrome
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Opiate toxidrome
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Opiate toxidrome
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Common toxidromes
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Serotonergic syndrome
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Serotonergic syndrome
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Serotonergic syndrome
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Recognition of poisoning
May be difficult because of non-specific symptoms
High index of suspicion - especially occult
poisoning history may be unreliable
look for corroborative history - missing pills, emptycontainer
Course that a poison runs (toxidromes) ! - mayhelp
Toxicology screening - helpful only in a few
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Clinical manifestations
Very diverse and varied - depends on thepoison
Clinical examination should be focused onthe possible manifestations of common
poisons in the geographical area
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Clinical manifestations
Skin and mucosal damage
Neurotoxic manifestations
Cardiovascular manifestations
Metabolic consequences
Eye manifestations
Hepatic dysfunction
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When do you consider ICU?
Respiratory
Airway protection
Respiratory failure
Cardiovascular
Hypotension despite fluid challenge
Heart block, arrhythmias, QTc prolongation as in TCA
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When do you consider ICU?
Neurologic GCS < 8
Seizures
Metabolic Hypoglycaemia
Significant electrolyte abnormalities
metabolic acidosis
Hepatic failure
Coagulopathy with bleeding
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Assessment & management
ASSESSMENT & THERAPY shouldproceed in parallel
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Clinical assessment
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Clinical assessment
Airway - ensure clear airway, clear secretions,check for cough/gag
Breathing - check oxygenation, supplementalO2, breathing pattern & adequacy
Circulation - heart rate, rhythm, blood pressure
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Clinical assessment
Neurologic - GCS, seizures, agitation, spasms,pupils, autonomic dysfunction
Miscellaneous - odour, temperature, pallor,cyanosis, jaundice
Abdomen - rigidity, bleeding, urine output
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Laboratory assessment
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Laboratory assessment
Of limited value
Paracetamol levels, salicylate levels, alcohol,
Red cell/pseudocholinesterase, anti-epilepticdrug levels
Urinary drug screen - opiates, barbiturates,
benzodiazepines, amphetamines, cocaine
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Laboratory assessment
Anion gap & Osmolal gap
Increased anion gap (Normal 12 4 mEq/L)
Ethylene glycol Methanol
Salicylate poisoning
Increased osmolal gap (Normal 5 7 m osmol/kg) Ethylene glycol
Methanol
Acetone, ethanol, isopropyl alcohol, propylene glycol
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Laboratory assessment
Electrolytes
Hypokalemia
Oduvanthalai poisoning (Clistanthis collinis)
Diuretics, Methyl xanthine, Toluene Hyperkalemia
Digoxin
Beta-blocker
Liver function tests Acetaminophen, Ethanol, Carbon tetrachloride
Renal function tests Ethylene glycol, NSAIDS
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Laboratory assessment
ECG
Digoxin toxicity
TCA overdose - sinus tachycardia, QT prolongation,increased QRS
Beta-blockers - conduction abnormalities
Imaging
Limited value
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Goals of treatment
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Goals of treatment
Reduce absorption of the toxin (xenobiotic)
Enhance elimination
Neutralise toxin
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Reduce absorption of the toxin
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Reduce absorption
Removal from surface skin & eye
Emesis induction
Gastric lavage Activated charcoal administration & cathartics
Dilution - milk/other drinks for corrosives
Whole bowel irrigation
Endoscopic or surgical removal of ingested chemical
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Reduce absorption
Skin decontamination
Important aspectnot to be neglected
Remove contaminated clothing
Wash with soap and water (soapscontaining 30% ethanol advocated)
However, no evidence for benefit even inOP poisoning
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Decontamination
Gastric decontamination
Forced emesis if patient is awake
Gastric lavageActivated charcoal 25 gm 2 hourly
Sorbitol as cathartic
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Reduce absorption
Gastric lavage
Gastric lavage decreases absorption by 42% if done20 min and by 16% if performed at 60 min
Performed by first aspirating the stomach and thenrepetitively instilling & aspirating fluid
Left lateral position better - delays spont. absorption
No evidence that larger tube better Simplest, quickest & least expensive way - funnel
Choice of fluid is tap water - 5-10 ml/kg
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Reduce absorption
Gastric lavage
Preferrably done on awake patients
Presence of an ET tube does not precludeaspiration, though preferred if GCS is low
No human studies in OP poisoning showingbenefit of gastric lavage
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Enhance elimination
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Enhance elimination
Increased elimination is possible only if
the drug is distributed predominantly in the ECF
has a low protein binding the induced rate of elimination is faster than the
normal rate
hazards of having a longer time of exposure to thedrug are potentially fatal
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Enhance elimination
Methods
Keep a good urine output 150-200 ml/hr
Alkalinisation of urine - clinical efficacy acceptedfor salicylate & phenobarbital poisoning
Extracorporeal removal
Hemodialysis - Barbiturates, Salicylates,Acetaminophen, Valproate, Alcohols, Glycols
Hemoperfusion - theophylline, digitalis, lipidsoluble drugs
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Neutralise toxin
Neutralise toxin-specific
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Neutralise toxin-specificantidotes
Acetaminophen N-acetyl cysteine
Anti-cholinergics Physostigmine
Benzodiazepenes Flumazenil
Ca channel blockers Glucagon, Insulin + dextrose, Calcium
Carbamate Atropine
Cyanide Thiosulphate, nitrateDigoxin Digoxin antibodies
INAH Pyridoxine
Methanol Ethanol, Fomepizole
Glycol Ethanol, Fomepizole
Opioid Naloxone
Oral hypoglycaemics Glucose
Organophosphate Atropine,? P2AM
Warfarin Vitamin K
Neutralise toxin-specific
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Neutralise toxin specificantidotes
Iron Desferroxamine
Copper Penicillamine, Dimercaprol, CaEDTA
Lead CaEDTA, Dimercaprol (BAL)
Mercury DMPS, DMSA, BAL
Arsenic BAL & derivatives
Antimony BAL & derivatives
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Summary
Poisoning a common problem in our country
A high index of suspicion required to diagnose
Know common toxidrome
Dont panic and follow a plan of action
Decreasing absorption Enhancing elimination
Neutralising toxins
Avoid potentially harmful Rxs - risk vs benefit
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Thank you
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Organophosphate poisoningClinical features
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Clinical manifestations
Muscarinic Nicotinic Central receptors
CardiovascularBradycardia
Hypotension
RespiratoryRhinorrhea
Bronchorrhea/spasm
Cough
GastrointestinalIncreased salivation
Nausea/vomiting
Abdominal pain
Diarrhoea
Fecal incontinence
GenitourinaryUrinary incontinence
OcularBlurred vision/miosis
Increased lacrimation
CardiovascularTachycardia
Hypertension
MusculoskeletalWeakness
Fasciculations
Cramps
Paralysis
Anxiety
Restlessness
Ataxia
Convulsions
Insomnia
DysarthriaTremors
Coma
Absent reflexes
CS respiration
Resp. depression
Circulatory collapse
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Neurological manifestations
Neuromuscular weakness/paralysis Type I, Type II and Type III paralysis (OPIDP)
Neuropsychiatric manifestations -COPIND
Extrapyramidal manifestations Dystonia, resting tremor, rigidity, chorea
Neuro-ophthalmic manifestations Optic neuropathy, retinal degeneration
Rarer manifestations GBS, Ototoxicity, Sphincter involvement
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Therapy of organophosphatepoisoning
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Management
Step I: Identify the nature of the poison
OrganophosphateCarbamate
Chloride
Pyrethroid
Neonicotinoids
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Management
Step II: Decontamination
Skin decontamination
Important aspectnot to be neglected
Remove contaminated clothing
Wash with soap and water (soapscontaining 30% ethanol advocated)
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Management
Step II: Decontamination
Care to be taken by health personnel to
avoid contamination
Reports of occupational illness in 3 staff caringfor OP poisoned patients
Another report 7 of 10 staff who cared for apatient developed chest tightness or discomfort
Geller RJ, Singleton KL, Tarantino ML, Drenzek CL, Toomey KE.Nosocomial poisoning associated
with emergency department treatment of organophosphate toxicityGeorgia 2000. J Toxicol Clin Toxicol
2001; 39: 109-11.
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Management
Step II: Decontamination
Skin decontaminationis thereevidence for benefit?
Skin decontamination (15 minutes post-VX on the ear) arrested the developmentof clinical signs and prevented furthercholinesterase inhibition and death in
experimental animals.
Hamilton MG, Hill I, Conley J, Sawyer TW, Caneva DC, Lundy PM. Clinical aspects of percutaneous
poisoning by the chemical warfare agent VX: effects of application site and decontamination. Mil Med 2004;
169: 856-62.
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Management
Step II: Decontamination
Skin decontaminationis there
evidence for benefit?
Cholinesterase sponges on surfaces havebeen usedcalled OP scavengers
Others have developed lotions
No human evidence for benefit of skincontamination
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Management
Step II: Decontamination
Gastric decontamination
Forced emesis if patient is awake Gastric lavage
Activated charcoal 25 gm 2 hourly
Sorbitol as cathartic
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Reduce absorption
Gastric lavage
Gastric lavage decreases absorption by 42% ifdone 20 min and by 16% if performed at 60 min
Performed by first aspirating the stomach andthen repetitively instilling & aspirating fluid
Left lateral position better - delays spont.Absorption
No evidence that larger tube better
Simplest, quickest & least expensive way -funnel
Choice of fluid is tap water - 5-10 ml/kg
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Reduce absorption
Gastric lavage
Preferrably done on awake patients
Presence of an ET tube does not precludeaspiration, though preferred if GCS is low
No human studies in OP poisoning showingbenefit of gastric lavage
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Management
Step III: Airways and Respiration Maintain airway
Ensure adequate oxygenation
Watch for intermediate syndrome (diplopia,
extra-ocular muscle weakness/neck muscleweakness)
Monitor respiratory rate/tidal volume/vitalcapacity
Blood gas analysis
Step IV: Cardiac monitoring Hemodynamic and monitor for arrhythmias
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Management
Step V: Specific therapy
Atropine
Initiate as soon as diagnosis is suspected
Adults 2 mg IV bolus - repeat dose very5-15 minutes till atropinised
children - 0.05 mg/kg initially then 0.02-0.05 mg/kg
Atropinisation
Heart rate about 100/mt Pupils mid position
Bowel sounds just heard
Clear lung fields
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RememberSteps I to V occur simultaneously
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Role of oximes
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Organophosphate poisoning
Are oximes beneficial in human OPpoisoning?
Subject of much debate & literature
Systematic review & meta-analysis
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Organophosphate poisoning
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Organophosphate poisoning
O h h i i
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Organophosphate poisoning
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OP - why no benefit with PAM
May be a true effect - it is not effective!!
Type of compound
Poison load & dose
Time of administration
Ageing of the compound
Toxicity of the antidote
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Conclusions
The key to successful management in apoisoning is early recognition and appropriatemanagement
Remember common toxidromes
OP poisoning very common in our part of theworld
Role of oximes still not established
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THANK YOU
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Is there a role?- nature of OP
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Is there a role?- nature of OPcompound
Human poisoning by OP bearing twomethoxy groupseg. malathion,paraoxon-methyl, dimethoate andoxydemeton-methyl is generally
considered to be rather resistant tooxime therapy.
Failure attributed to megadose
intoxications and to prolonged timeintervals between poison uptake andoxime administration
Dimethylphosphoryl-inhibited human cholinesterases:
inhibition, reactivation, and aging kinetics. Arch. Toxicol
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Is there a role?- dose related?
Invitro studies (isolated rat diaphragm)and in vivo studies (cats). minimum-effective plasma level for oxime therapy 4
mg/l.. higher doses may be required insevere cases of OP poisoning
Case reports where even with high dose -
course is prolonged
MK Johnson et al. Evaluation of antidotes for poisoning byorganophosphorus pesticides.Emergency Medicine (2000)
12:22-37.
Is there a role? time of
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Is there a role?- time ofadministration
Electrophysiologicalimprovements(present) whenobidoxime administered within 12hours of poisoning. Minimal or no
improvement if treatment delayedmore than 26 hours.
Efficacy of obidoxime in human organophosphorus
poisoning: determination by neuromusculartransmission studies. Besser R et al. Muscle Nerve1995; 18:15-22
Vellore - in vitro study - re-activation
of AChe is poor if P2 AM is
Is there a role? time of
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Is there a role?- time ofadministration
Obidoxime was quite ineffective inoxydemetonmethyl poisoning whenthe time elapsed between ingestionand oxime therapy was longer than 1
day..when obidoxime wasadministered shortly after ingestion (1h) reactivation was nearly complete
Cholinesterase status, pharmacokinetics and laboratoryfindings during obidoxime therapy in organophosphatepoisoned patients. Thiermann H et al (Germany). Hum ExpToxicol 1997; 16:473-80
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Is there a role?- ageing of OP
..believed that 1 day afterintoxication with a dimethyl OPinsecticide, virtually all the AChe willbe in the aged inhibited form, so that
oxime therapy will be useless after thistime.
Ageing characteristics different for di-
methyl (half life 3.7 hours) and di-ethyl(half life 33 hours) - therapeuticwindow five times the half life
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Is there a role?- toxicity
Formation of stable phosphoryl oximes(POXs) with high anticholinesteraseactivity
Obidoxime and other pyridinium-4-aldoximes form these POXs
The phosphoryl oxime-destroying activity of humanplasma. Arch. Toxicol 2000; 74:27-32
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Toxicity of oximes - II
Pralidoxime in a volunteer study -dizziness & blurring
Rapid administration of PAM - slow &shallow resps
Cardiac arrhythmias - AF, VT, VFib, AV
block
Liver function abnormalities withbid i