Approach to Poisoned Patient

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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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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Hot as a hare

Dry as a bone

Red as a beet

Mad as a hatter

Blind as a bat


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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





seizure Ephedrine


Tachycardia

Tachypnea


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seizure Ephedrine


Tachycardia

Tachypnea



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seizure Ephedrine


Tachycardia

Tachypnea



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Common toxidromes


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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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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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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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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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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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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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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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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


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


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


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


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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O h h i i


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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

Approach to Poisoned Patient

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