POISONING ‫رضا عزيزخاني‬ ‫استاديارطب اورژانس‬ ‫گروه طب اورژانس دانشگاه علوم by jennyyingdi

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									                             ‫رضا عزيزخاني‬
                         ‫استاديارطب اورژانس‬
‫گروه طب اورژانس دانشگاه علوم پزشکی اصفهان‬
Case Report1
 Woman 34 years old
 Hx = negative
 Finding= confused, agitated, dry skin, pupil dilatated,
 hypotension,
Case Report2
 Man, 42 years old
 Agitated with no problem
 No finding
 Hx of suicide
T.C.A POISONING

Is the most common cause of
 death due to drug overdose
High Mortality Rate
Antidepressants
•USES:
Anxiolytic & Antidepressive
Headach
Enuresis
Neuropathy
Chronic Pain
•EPIDEMIOLOGY :
 T.C.A Poisoning is common

 Poisoning is usually suicidal

 Toxic effects are typically moderate

 Severe toxicity or death may occur in
 large ingestion or co-ingestion
THE CAUSES OF THE
HIGH MORTALITY RATE

 USE   BY DEPRESSIVE PATIENTS

 SEVERE    CARDIOVASCULAR TOXICITY

 SEVERE    C.N.S TOXICITY

 LIMITED    TREATMENT
•PHARMACODYNAMIC:
 Serum peak                        2-8 h
 First pass hepatic metabolism: 20-70%
 High v/d                       10-20 l/kg
 High Tissue Concentration:     100 times
 metabolism:                   Liver
 Elimination:                  Kidney
  •MECHNISM
 T.C.A s   Inhibit Reuptake of Neurotransmitters:
   Norepinephrine
   Dopamine
   Serotonin
 Antihistaminic

 Anticholinergic
AT TERAPEUTIC DOSE :
      Have Different Anticholinergic &
      Antihistaminic Effects

AT TOXIC DOSE :
     Most Have Similar Effects
 Exceptions :
   Lofepramin : Minimum Toxicity
   Amoxapin : Max. Incidence of Seizure &
                Min. Cardiovascular Toxicity
   Maprotiline : High Cardiovas. Toxicity
AFTRE OVERDOSE :
 Onset of Toxicity is typically rapid

 Gastric emptying become slow & absorption
  delayed

 Most death occur within first 24 hrs

 Tissues distribution is very rapid

 Rapidly progression from no symptom to life-
  threatening cardiotoxicity or seizure occur in less
  than 1 hr
TOXIC EFFECTS:
 HEART :Myocardial Depression, Dysrhythmia
 , Conduction abnormality
 VASCULAR : Hypotention
 C.N.S : seizure, myoclonus, coma
 OTHERS         : G.I.T ,Urinary System, Hyperthermia ,
 Metabolic Acidosis , Mydriasis , Dry Skin , . . .
CARDIOVASCULAR EFFECTS

  Conduction Delay ( QRS Prolongation )
  Sinus Tachycardia
  Ventricular Arrhythmias
  Severe Hypotension
ventricular bigeminy     , right axis deviation , wide QRS complex
,       long Q-T interval , and right deviation of terminal 40-msec
QRS vector in limb leads    ,        with prominent R wave in aVR
 C.N.S TOXICITY
 Loss of consciousness :
   Confusion
   Drowsiness
   Lethargy & Coma
 Dellirium: Agitation, Disorientation,
 Psychotic behaviour

 Seizure & Myoclonus

 Hyperthermia
MECHANISM OF C.N.S TOXICITY

Block of cholinergic Receptors
Block of GABA Receptors in Brain
Inhibition of Fast Na Channel in
 Neurons
ANTICHOLINERGIC EFFECTS
 Sinus tachycardia
 Hyperthermia
 Illeus
 Urinary retention
 Pupil dilatation
 Seizure & Coma


* Alpha Blockade      Vasodilation &
                      Refractory Hypotension
HYPERTHERMIA
 Impaired Sweating


 Excessive heat generation
   Seizure
   Myoclonous
   Agitation
COMPLICATIONS :
A.R.D.S
RESPIRATORY DEPRESSION
ASPIRATION PNEUMONIA
A.R.F   (Rhabdomyolysis , Hypotension)
•TOXIC DOSE
  As low as 100 mg in children
  Ingestion of 2-3 times the daily dose in adult
  Ingestion of more than 1 gr is lifethreatening


  Ingestion of 300-1000 mg         Mild toxicity
               1-2 g             Moderate
              2-3 g              Severe ( lethal)
•DIAGNOSIS
 History Taking
 Physical Examination
       Dilated Pupil
       Dry Skin
       Seizure , Loss of consciousness
       Agitation , increased DTR , myoclonus
       Hyperthermia
 Serum Level
 ECG findings QRS Widening
B.L.S & A.L.S
  Air way Management
  Circulatory Support
     Treatment of Shock & Hypotension
     Fluid & Electrolyte Correction
     Acid - Base disturbances

  Antidotal therapy
   TREATMENT :
 Focused on aggressive airway management:


Endotracheal intubation should be performed

 if the patient is exhibiting a markedly decreased level of
  consciousness

 if the level of consciousness is rapidly deteriorating.
 Gasteric Lavage ( O.G.T, Char. - Lav. - Char )
 Activated Charcoal ( M.D.A.C )

 EMESIS is contraindicated

 Dialysis is not effective

 Flumazenil should not be used

 Physostigmine is contraindicated in CA overdose.
  Seizures, cardiac arrest, and death have occurred
  when physostigmine has been used in CA overdose."
 Hypertension is usually mild and transient and requires no
  treatment

 Hypotension



             begins with isotonic crystalloids, 10 cc/kg

             Second line : sodium bicarbonate

 If hypotension does not resolve, third line : norepinephrine or dopamine is
  recommended.·
         High-dose dopamine (20 to 30 mic g/kg/min)
         norepinephrine (2 to 20 mic g/min) may be necessary for the direct α,- agonist effect.
 For inotropic support alone, dobutamine is controversial
Antidote Therapy : Sodium Bicarbonate

 Ventricular dysrhythmia


 Refractory hypotension


 Wide QRS > 100 ms


 R terminal > 3 mm in AVR
 Antidote Therapy : Sodium Bicarbonate
 Serum alkalinization is clinically effective in decreasing CA-induced
  intraventricular conduction delays.

 The major effect of increasing pH seems to be increased sodium
  conductance through myocardial sodium channels rather than the
  increase in plasma protein binding.·

 NaHC03 is administered by intra- venous boluses of 1 to 2 mEq/kg until
  hypotension improves and the QRS narrows to 100 msec, or until serum
  pH increases to a maximum of 7.50 to 7.55.

 Speed of infusion : 2-3 cc/kg/min

 After obtaining the desired endpoint with intravenous NaHC0
  boluses initiating continuous isotonic intravenous infusion by
  adding three ampules of 8.4% NaHC03 (50 mEq/ampule, 100
  mOsm/ampule) to 1 L of 5% dextrose in water.
 Repeat boluses and continuous intravenous infusion should be guided by serial
  measurements of arterial pH and QRS duration.

 Sinus tachycardia is usually well tolerated and does not require specific therapy.


 β-Receptor antagonists and physostigmine are contraindicated.



 Determining the specific type of wide-complex rhythm is unnecessary
  because treatment in either case is intravenous NaHC03

 Lidocaine has not been consistently effective.


 Phenytoin has been shown to increase the frequency and duration of
  episodes of ventricular tachycardia and is not recommended as an
  anti dysrhythmic agent
 Type IA antidysrhythmics (quinidine, disopyramide, procainamide)
  and type IC antidysrhythmics (flecainide, moricizine, propafenone)
  are contraindicated because they also inhibit fast sodium channels.

 A transvenous pacemaker and over- drive pacing can be used for
  associated polymorphic ventricular tachycardia (torsades de pointes) not
  responsive to magnesium.

 Bradydysrhythmias are rare and late .


 Q-T prolongation, PR prolongation, do not mandate specific therapy


 Treatment    with NaHC03        , hypertonic sodium chloride, and
  hyperventilation does not resolve completely Q-T prolongation, which
  involves not only sodium channel blockade, but also protracted
  depolarization from potassium efflux blockade.
 Benzodiazepines should be used for agitation


 seizures usually respond to intravenous lorazepam or diazepam. '


 Seizures refractory to other benzodiazepines have terminated with intravenous
  midazolam boluses of 2.5 to 10 mg and continuous intravenous infusions."

 If benzodiazepines fail to terminate prolonged o repetitive seizures, phenobarbital
  may be administered in a loading dose of 20 mg/kg, given at a rate of up to 50
  mg/min in adults or up to 1 mg/kg/min in children.

 Propofol also has been used to treat refractory seizures successfully. A loading dose
  of 2.5 mg/kg is followed by continuous infusion of 25 to 200 µg/kg/min.

 Phenytoin may cause more and longer episodes of ventricular tachycardia.


 If maximal doses of benzodiazepines, phenobarbital, or propofol are ineffective,
  neuromuscular blockade and general anesthesia with continuous
  electroencephalogram monitoring are recommended to prevent rhabdomyolysis
  and hyperthermia caused by excessive muscle activity .
 Life-threatening hyperthermia (rectal temperature >40° C) is best treated
  with control of seizures and neumuscular blockade.

 A nondepolarizing neuromuscular blocker (e.g., rocuronium) is
  recommended if rabdomyolysis and hyperkalemia with ECG changes
  present.

 Evaporative cooling should be used until core temperature reaches 38.5° C.,
Treatment of Neurologic Complications
     of Antidepressant Poisoning
     Disposition
 Patients with known or suspected CA overdoses require 6 hours of observation
  with continuous cardiac monitoring and pulse oximetry.
 After 6 hours of obser vation, patients may be discharged for psychiatric
  evaluation if they do not develop :

       (1) ventilatory insufficiency,
       (2) desaturation on pulse oximetry,
       (3) QRS greater than 100 msec,
       (4) sinus tachycardia greater than 120 beats/min,
       (5) dysrhythmias,
       (6) hypotension,
       (7) decreased level of consciousness,
       (8) seizures,
       (9) abnormal or inactive bowel sounds.


 Patients who exhibit any of these findings should
               be admitted to an lCU

								
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