Approach to poisoned patient by mikeholy

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									Second CME and workshop on Critical care




       An approach to a poisoned
                patient


      Dr. J V Peter, MD, DNB (Med), FRACP
     Christian Medical College & Hospital, Vellore
                             Introduction

   What is a poison?

          In common usage - poisons are
           chemicals or chemical products that
           are distinctly harmful to human

          More precisely - a poison is a
           foreign chemical (xenobiotic) that is
           capable of producing a harmful
           effect on a biologic system
                     Other terminology

   What is a toxin?

          It originally referred to a
           poison of animal or plant
           origin

          Toxicant is the currently
           preferred scientific term for
           all poisons.
              Other terminology


   What is a toxidrome?

        It is the association of several clinically
         recognizable features, signs, symptoms,
         phenomena or characteristics which often
         occur together, so that the presence of one
         feature alerts the physician to the presence
         of the others.
Common toxidromes
The cholinergic toxidrome
The cholinergic toxidrome
The cholinergic toxidrome
What toxidrome?
           The anticholinergic toxidrome

Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
           The anticholinergic toxidrome

Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
           The anticholinergic toxidrome
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter
Blind as a bat
                 What toxidrome?

                  disorientation      Amphetamine
                  hallucinations      Cocaine
Hallucinogenic    hyperactive bowel   Pseudoephedrine
                  panic               Phencyclidine     Benzodiazepenes
                  seizure             Ephedrine
Toxidrome         Hypertension
                  Tachycardia
                  Tachypnea
                 Hallucinogenic
            Sympathomimetic toxidrome

                 disorientation      Amphetamine
                 hallucinations      Cocaine
Hallucinogenic   hyperactive bowel   Pseudoephedrine
                 panic               Phencyclidine     Benzodiazepenes
                 seizure             Ephedrine
Toxidrome        Hypertension
                 Tachycardia
                 Tachypnea
                 Hallucinogenic
            Sympathomimetic toxidrome

                 disorientation      Amphetamine
                 hallucinations      Cocaine
Hallucinogenic   hyperactive bowel   Pseudoephedrine
                 panic               Phencyclidine     Benzodiazepenes
                 seizure             Ephedrine
Toxidrome        Hypertension
                 Tachycardia
                 Tachypnea
                 Hallucinogenic
            Sympathomimetic toxidrome

                 disorientation      Amphetamine
                 hallucinations      Cocaine
Hallucinogenic   hyperactive bowel   Pseudoephedrine
                 panic               Phencyclidine     Benzodiazepenes
                 seizure             Ephedrine
Toxidrome        Hypertension
                 Tachycardia
                 Tachypnea
Common toxidromes
Sedative/hypnotic toxidrome
Sedative/hypnotic toxidrome
Sedative/hypnotic toxidrome
Common toxidromes
Opiate toxidrome
Opiate toxidrome
Opiate toxidrome
Common toxidromes
Serotonergic syndrome
Serotonergic syndrome
Serotonergic syndrome
           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, empty
           container


   Course that a poison runs (toxidromes) ! - may
    help

   Toxicology screening - helpful only in a few
          Clinical manifestations

   Very diverse and varied - depends on the
    poison

   Clinical examination should be focused on
    the possible manifestations of common
    poisons in the geographical area
     Clinical manifestations

   Skin and mucosal damage

   Neurotoxic manifestations

   Cardiovascular manifestations

   Metabolic consequences

   Eye manifestations

   Hepatic dysfunction
      When do you consider ICU?

   Respiratory

          Airway protection

          Respiratory failure


   Cardiovascular

          Hypotension despite fluid challenge

          Heart block, arrhythmias, QTc prolongation as in TCA
     When do you consider ICU?

   Neurologic
          GCS < 8
          Seizures


   Metabolic
          Hypoglycaemia
          Significant electrolyte abnormalities
          metabolic acidosis
          Hepatic failure
          Coagulopathy with bleeding
Assessment & management



ASSESSMENT & THERAPY should
      proceed in parallel
Clinical assessment
            Clinical assessment
   Airway - ensure clear airway, clear secretions,
    check for cough/gag



   Breathing - check oxygenation, supplemental
    O2, breathing pattern & adequacy



   Circulation - heart rate, rhythm, blood pressure
            Clinical assessment
   Neurologic - GCS, seizures, agitation, spasms,
    pupils, autonomic dysfunction



   Miscellaneous - odour, temperature, pallor,
    cyanosis, jaundice



   Abdomen - rigidity, bleeding, urine output
Laboratory assessment
         Laboratory assessment
   Of limited value

   Paracetamol levels, salicylate levels, alcohol,
    Red cell/pseudocholinesterase, anti-epileptic
    drug levels

   Urinary drug screen - opiates, barbiturates,
    benzodiazepines, amphetamines, cocaine
             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
            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
            Laboratory assessment
   ECG

          Digoxin toxicity

          TCA overdose - sinus tachycardia, QT prolongation,
           increased QRS

          Beta-blockers - conduction abnormalities


   Imaging

          Limited value
Goals of treatment
            Goals of treatment

   Reduce absorption of the toxin (xenobiotic)

   Enhance elimination

   Neutralise toxin
Reduce absorption of the toxin
                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
      Reduce absorption

   Skin decontamination

          Important aspect – not to be neglected

          Remove contaminated clothing

          Wash with soap and water (soaps
           containing 30% ethanol advocated)

          However, no evidence for benefit even in
           OP poisoning
            Decontamination

   Gastric decontamination
           Forced emesis if patient is awake
           Gastric lavage
           Activated charcoal 25 gm 2 hourly
           Sorbitol as cathartic
                   Reduce absorption

   Gastric lavage

          Gastric lavage decreases absorption by 42% if done
           20 min and by 16% if performed at 60 min

          Performed by first aspirating the stomach and then
           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
                 Reduce absorption

   Gastric lavage

          Preferrably done on awake patients
          Presence of an ET tube does not preclude
           aspiration, though preferred if GCS is low

          No human studies in OP poisoning showing
           benefit of gastric lavage
Enhance elimination
              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 the
           drug are potentially fatal
              Enhance elimination
   Methods

          Keep a good urine output 150-200 ml/hr
          Alkalinisation of urine - clinical efficacy accepted
           for salicylate & phenobarbital poisoning
          Extracorporeal removal
              Hemodialysis - Barbiturates, Salicylates,
               Acetaminophen, Valproate, Alcohols, Glycols
              Hemoperfusion - theophylline, digitalis, lipid
               soluble drugs
Neutralise toxin
Neutralise toxin-specific
       antidotes
Neutralise toxin-specific
       antidotes
                          Summary
   Poisoning a common problem in our country

   A high index of suspicion required to diagnose

   Know common toxidrome

   Don’t panic and follow a plan of action
          Decreasing absorption
          Enhancing elimination
          Neutralising toxins


   Avoid potentially harmful Rxs - risk vs benefit
Thank you
Organophosphate poisoning
     Clinical features
Clinical manifestations
         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
Therapy of organophosphate
         poisoning
                      Management

   Step I: Identify the nature of the poison

        Organophosphate
        Carbamate
        Chloride
        Pyrethroid
        Neonicotinoids
               Management
   Step II: Decontamination

       Skin   decontamination

            Important aspect – not to be neglected

            Remove contaminated clothing

            Wash with soap and water (soaps
             containing 30% ethanol advocated)
                                     Management
     Step II: Decontamination

               Care  to be taken by health personnel to
                 avoid contamination

                       Reports of occupational illness in 3 staff caring
                        for OP poisoned patients

                       Another report 7 of 10 staff who cared for a
                        patient developed chest tightness or discomfort
Geller RJ, Singleton KL, Tarantino ML, Drenzek CL, Toomey KE. Nosocomial poisoning associated
with emergency department treatment of organophosphate toxicity – Georgia 2000. J Toxicol Clin Toxicol
2001; 39: 109-11.
                                      Management
                Step II: Decontamination
                          Skin  decontamination – is there
                            evidence for benefit?

                                  Skin decontamination (15 minutes post-
                                   VX on the ear) arrested the development
                                   of clinical signs and prevented further
                                   cholinesterase 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.
               Management
   Step II: Decontamination

       Skindecontamination – is there
       evidence for benefit?

           Cholinesterase sponges on surfaces have
            been used – called OP scavengers

           Others have developed lotions

           No human evidence for benefit of skin
            contamination
             Management
   Step II: Decontamination

       Gastric   decontamination
           Forced emesis if patient is awake
           Gastric lavage
           Activated charcoal 25 gm 2 hourly
           Sorbitol as cathartic
                 Reduce absorption

   Gastric lavage

          Gastric lavage decreases absorption by 42% if
           done 20 min and by 16% if performed at 60 min

          Performed by first aspirating the stomach and
           then 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
                 Reduce absorption

   Gastric lavage

          Preferrably done on awake patients
          Presence of an ET tube does not preclude
           aspiration, though preferred if GCS is low

          No human studies in OP poisoning showing
           benefit of gastric lavage
                Management
   Step III: Airways and Respiration
          Maintain airway
          Ensure adequate oxygenation
          Watch for intermediate syndrome (diplopia,
           extra-ocular muscle weakness/neck muscle
           weakness)
          Monitor respiratory rate/tidal volume/vital
           capacity
          Blood gas analysis


   Step IV: Cardiac monitoring
          Hemodynamic and monitor for arrhythmias
                Management
   Step V: Specific therapy
          Atropine
             Initiate as soon as diagnosis is suspected
             Adults 2 mg IV bolus - repeat dose very
              5-15 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
            Remember
Steps I to V occur simultaneously
Role of oximes
      Organophosphate poisoning

   Are oximes beneficial in human OP
    poisoning?

   Subject of much debate & literature

   Systematic review & meta-analysis
Organophosphate poisoning
Organophosphate poisoning
Organophosphate poisoning
     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
                  Conclusions

   The key to successful management in a
    poisoning is early recognition and appropriate
    management

   Remember common toxidromes

   OP poisoning very common in our part of the
    world

   Role of oximes still not established
THANK YOU
Is there a role?- nature of OP
          compound
    Human poisoning by OP bearing two
    methoxy groups eg. malathion,
    paraoxon-methyl, dimethoate and
    oxydemeton-methyl is generally
    considered to be rather resistant to
    oxime therapy.

    Failureattributed to megadose
    intoxications and to prolonged time
    intervals between poison uptake and
    oxime administration

    Dimethylphosphoryl-inhibited human cholinesterases:
    inhibition, reactivation, and aging kinetics. Arch. Toxicol
     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 in
    severe cases of OP poisoning”

   Case reports where even with high dose -
    course is prolonged

        MK Johnson et al. Evaluation of antidotes for poisoning by
        organophosphorus pesticides. Emergency Medicine (2000)
        12:22-37.
Is there a role?- time of
     administration
 Electrophysiological
 improvements…(present) when
 obidoxime administered within 12
 hours of poisoning. Minimal or no
 improvement if treatment delayed
 more than 26 hours.


    Efficacy of obidoxime in human organophosphorus
    poisoning: determination by neuromuscular
    transmission studies. Besser R et al. Muscle Nerve
    1995; 18:15-22


          in vitro study - re-activation
 Vellore -
 of AChe is poor if P2 AM is
Is there a role?- time of
     administration
 “…Obidoxime was   quite ineffective in
 oxydemetonmethyl poisoning when
 the time elapsed between ingestion
 and oxime therapy was longer than 1
 day…..when obidoxime was
 administered shortly after ingestion (1
 h) reactivation was nearly complete…”

 Cholinesterase status, pharmacokinetics and laboratory
 findings during obidoxime therapy in organophosphate
 poisoned patients. Thiermann H et al (Germany). Hum Exp
 Toxicol 1997; 16:473-80
Is there a role?- ageing of OP
   “…..believed that 1 day after
   intoxication with a dimethyl OP
   insecticide, virtually all the AChe will
   be in the aged inhibited form, so that
   oxime therapy will be useless after this
   time.”

   Ageing  characteristics different for di-
   methyl (half life 3.7 hours) and di-ethyl
   (half life 33 hours) - therapeutic
   window five times the half life
Is there a role?- toxicity

  Formationof stable phosphoryl oximes
  (POXs) with high anticholinesterase
  activity

  Obidoxime andother pyridinium-4-
  aldoximes form these POXs


  The phosphoryl oxime-destroying activity of human
  plasma. Arch. Toxicol 2000; 74:27-32
      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 with
    obidoxime

								
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