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POISONING
Prepared by:
Nur Aqmar Abdul Najib
Lingeshwaran
INTRODUCTIO
N
• Development of dose related adverse effect following exposure to
chemicals, drugs or other xenobiotics
• Poisoning is a worldwide problem that consumes substantial health
care resources and causes many premature deaths
• Recognition of poisoning or drug overdose requires high index of
suspicion
• Routes of exposure :
Ingestion
Inhalation
Insufflation
Cutaneous / mucous membrane exposure
Injection
1. Resuscitation and
stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
Maintenance of adequate airway, breathing and
circulation
• In compromised airway patency or reduced respiratory drive,
mechanical airway and assisted ventilation is vital
• IV crystalloid bolus is first-line treatment of hypotension.
• Persistent hypotension despite an adequate volume infusion
may respond to a specific antidote. Otherwise, cautious
administration of an inotropic agent is indicated.
Antidote
• E.g. : naloxone for opiate toxicity, cyanide antidotes for
cyanide toxicity, and atropine for organophosphate
poisoning
RESUSCITATION
AND
STABLIZATION
 Toxin induced arrhythmia
• correction of hypoxia, metabolic/acid–base abnormalities and administration of an
antidote.
• sodium bicarbonate - wide QRS complex tachyarrhythmias.
Seizures
• titrated doses of IV benzodiazepines (isoniazid-induced seizures -pyridoxine)
• barbiturates - benzodiazepine-resistant seizures
Hypothermia / hyperthermia
• Hyperthermia - active cooling like ice water immersion; if ineffective, may need
sedation, neuromuscular paralysis, and intubation.
• several toxidromes associatedwith hyperthermia are treated with
pharmaceutical agents : sympathomimetic (benzodiazepines),
specific
serotoni
n
(cyproheptadine), and neuromuscular malignant syndrome (bromocriptine).
RESUSCITATION
AND
STABLIZATION
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
History taking
• from patient or reliable sources (family, friends,
police, bystanders)
• agent, amount, time & location, route, intake of other
substances
• environmental clues : drug paraphernalia, empty
bottles or suicide notes may aid in the diagnosis
CLINICAL
EVALUATION
Physical Examination
CLINICAL
EVALUATION
Toxicological
screening
• Blood, urine or
gastric aspirate
• Radio – opaque
drugs (CHIPS)
• Chloral hydrate
• Heavy metals
• Iron and iodide
• Psychotropics (TCA)
• Enteric coated
salicylates
CLINICAL
EVALUATION
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
1. Decontamination (internal & external)
• Skin decontamination
• Eye decontamination
• Induce emesis
• Gastric lavage / aspiration
2. Adsorbent (Activated charcoal, Fuller’s Earth)
3. Cathartics
4. Whole bowel irrigation
LIMITING
ABSORPTION
Skin
• Protect
• Remove clothing
• Copious irrigation with water or normal
saline
• Chemical neutralization and corrosive
agent further potentiate the injury
Eyes
• Remove contact lens
• Local anesthetic drop
• Flush with water or normal saline until
pH normal
1. Decontamination (external)
LIMITING
ABSORPTION
Induction of emesis
1. Decontamination (internal)
Syrup of ipecac NO
LONGER
recommended
 Prolonged vomiting
 Delay administration of
activated charcoal
 Pulmonary aspiration
LIMITING
ABSORPTION
Gastric lavage
1. Decontamination (internal)
LIMITING
ABSORPTION
Gastric lavage
LIMITING
ABSORPTION
Indications :
1. Evidence of potentially life-threatening amount of
poison that has been ingested
2. Procedure can be performed within 1 hour of
ingestion
3. Fully awake or intubated
Contraindications :
1. Unprotected airways
2. Esophageal pathology
Activated charcoal
2. Adsorbent
Children : 0.5-1g/kg
Adult : 25-100g
Minimum dilution : 30g in 240ml
Normally given as single dose
orally or via NG/OG tube
LIMITING
ABSORPTION
Activated charcoal
Contraindications :
• Unprotected airway
• Intestinal obstruction
• Ingestion of corrosive
substance
• GIT not anatomically intact
(perforation)
It is not effective in the following
substances :
 Alcohol
 Cyanide
 Iron
 Lithium
 Metal
 Hydrocarbons
LIMITING
ABSORPTION
Fuller’s Earth
• In paraquat poisoning
• Becomes deactivated after contact with soil/clay
LIMITING
ABSORPTION
• It decreases the absorption of poison by accelerating the
expulsion of the poison from GI tract.
• 2 types of osmotic cathartics :
• Saccharide cathartics – sorbitol
• Saline cathartics – magnesium citrate, magnesium
sulfate, sodium sulfate
3. Cathartics
Cathartics have NO ROLE in management of a poisoned
patient when used ALONE
LIMITING
ABSORPTION
• Polyethylene glycol-electrolyte solution
• Indications:
• Large ingestion of substances that are poorly
absorbed by activated charcoal
• Ingestion of sustained-release drugs
• Packed drugs in the body (bodypackers)
• Contraindications :
• Absent bowel sound, ileus, intestinal
obstruction, gut perforation
• Unprotected airway
4. Whole bowel irrigation
No conclusive evidences showing that this procedure
improves patient outcome in poisoning cases
Administer polyethylene
glycol-electrolyte solution
(CoLyte, GoLYTELY) at
2L/H by gastric tube until
rectal effluent is clear.
Stop administration after
4L if no rectal fluent
appeared.
LIMITING
ABSORPTION
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
ENHANCED
ELIMINATION
Who
needs it?
Methods :
1. Multiple dose activated charcoal
2. Ion trapping technique :
Urine alkalinization
Urine acidification – no longer use
3. Extracorporeal elimination :
Hemodialysis (HD)
Hemoperfusion (HP)
Continuous renal replacement therapy (CRRT)
ENHANCED
ELIMINATION
• MDAC should be considered only in patient who ingested life-
threating amount of : carbamazepine, dapsone, phenobarbitol,
theophylline, quinine, phenytoin
1. Multiple Dose Activated Charcoal (MDAC)
Optimum dose in unknown.
After initial dose (25g-100g in
adult), give at a rate less than
12.5g/hour
Pulmonary aspiration
Charcoal bezoar
Gut obstruction/perforation
Bowel infarction
ENHANCED
ELIMINATION
Urine alkalinization
• Prevents reabsorption of the ionized
drug across the renal tubular
epithelium thus enhancing excretion
through urine.
• Moderate to severe salicylate
toxicity when criteria for HD have not
been met.
• Also in phenobarbital, chlorpropamide
or phenoxyacetate herbicides
2. Ion Trapping Technique
ENHANCED
ELIMINATION
2. Ion Trapping Technique
Urine alkalinization
1. Correct hypokalemia
2. Administer IV Sodium bicarbonate 1-2 ampules OR 1 mEq/kg bolus
3. Infuse 100 mEq Sodium bicarbonate mixed with 1L of D5W at 250mL/H
4. 20 mEq of Potassium chloride may be added to solution to maintain
normokalemia
5. Monitor serum potassium and bicarbonate every 2-4 hours
6. Check urine pH regularly (every 15-30mins) , aim for pH 7.5-8.5
7. Another bolus of 1 mEq of IV NaHCO3 may be given in cases of insufficient
alkalinization
CONTRAINDICATED in :
♢Preexisting fluid overload ♢Renal impairment ♢Uncorrected hypokalemia
ENHANCED
ELIMINATION
Urine acidification
• NO LONGER RECOMMENDED
• produces metabolic acidosis, rhabdomyolysis and renal failure
2. Ion Trapping Technique
ENHANCED
ELIMINATION
• Have limited indications in poisoned patients
• A toxin must possess a number of properties to be
effectively removed by this technique
1. Low volume of distribution
2. Low molecular weight
3. Relatively low protein binding
4. Low endogenous clearance
3. Extracorporeal
Elimination
ENHANCED
ELIMINATION
3. Extracorporeal
Elimination
ENHANCED
ELIMINATION
HEMODIALYSIS HEMOPERFUSION CRRT
Dialyzable vs Non-dialyzable
DIALYZABLE NON -DIALYZABLE
Barbiturates Hydrocarbon
Salicylates Anticholinergics
Lithium Cyanide
Isoniazid Lead
Theophylline Opioid
Carbamazepine TCA
Methanol Arsenic
ENHANCED
ELIMINATION
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
ANTID0T
E
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
• Monitor vital signs
• IV fluids for replacement and
maintenance of adequate
blood volume
• Monitor fluid input and output
• Correction of metabolic
disturbances
• Frequent monitoring of urine
pH during alkalinization
therapy
• Intensive nursing care (ET tube)
• Manage underlying illnesses
SUPPORTIVE
THERAP
Y
1. Resuscitation and stabilization
2. Clinical evaluation
3. Limiting absorption
4. Enhanced elimination
5. Antidote
6. Supportive therapy
7. Disposition
GENERAL
MANAGEMENT
DISPOSITIO
N
ICU admission
ED Discharge
Inpatient Setting
Psychiatric
1. ACETAMINOPHEN
2. OPIODS
3. ORGANOPHOSPHAT
E
4. SALICYLATES
SPECIFIC
TOXILOGY
• Paraetamol is converted to a toxic metabolite, N-acetyl-p-
benzoquinonimine which is usually inactivated by conjugation by
reduced glutathione.
• However, in large overdose, the glutathione is depelted and causing
the toxic metabolite to bind to liver cells membrane and cause liver
necrosis. (can occur as little as 10g – 20 tablets)
ACETAMINOPHE
N
After ingestion of therapeutic amounts,
predominant metabolism by liver through
glucuronidation and sulfation. The small amount
of N-acetylp- benzoquinoneimine (NAPQI)
generated is conjugated with glutathione to a
nontoxic compound
After ingestion of large amounts, glucuronidation
and sulfation are saturated, and an increased
amount of NAPQI is generated. Detoxification of
NAPQI to a nontoxic compound soon depletes
glutathione stores, leaving excess NAPQI to
bind to intracellular proteins, causing cell death
• <24 HOURS – anorexia, vomiting and diaphoresis but
patient is still consious.
• Hepatic enzymes begin to rise 48 hours after ingestion
and peak at 72 hours.
• Recovery starts after 4 days unless hepatic failure
develops.
CLINICAL
FEATURES
OF
OVERDOSE
MANAGEMEN
T
• Determined the implication of a
measured acetaminophen
concentration
• The nomogram only directly applies to
an acetaminophen concentration
obtained after a single oral exposure
and during the window between 4
hours and 24 hours postingestion.
• Outcome prediction using this
nomogram cannot be applied to
acetaminophen concentrations
obtained outside this 20-hour window
or with chronic or recurrent
exposures
OPIOD
S
• Maintain airway and assist ventilattion if necessary
• Give oxygen
• Treat coma, seixures, hypotension and noncardiogenic
pulmonary edema if they occur – INTERMITTENT POSITIVE
PRESSURE VENTILLATION (not for diuretics)
• NALOXONE
MANAGEMEN
T
Watch out for signs of over treatment-
hyperventilation, muscle tremor, tachycardia and
hypertension
NALOXON
E
• Organophosphates insecticides
parathion, dichlorvos, and diazinon
include malathion,
• Organophosphates insecticides irreversibly inhibit the
acetylcholinesterase and nicotinic synapses
• Organophosphates can be absorbed through the
skin, lungs and the GI tract
ORGANOPHOSPHAT
ES
• Manifestations occur 30 min to 2 hour following exposure
• Musacrinic effects : nausea, vomiting, abdominal cramps,
urinary and fecal incontinence, salivation, and lacrimation
• Nicotinic effect : twitching, fasciculations, weakness and
cramps
• CNS effects : Anxiety, restlessness, tremor, convulsions and
coma
CLINICAL
MANIFESTATION
• Cholinsterase activity in plasma and in red blood cells
reduced than 50 % normal
• Insecticides may be identified in urine toxology
• FBC, BUSE, serum creatinine, blood sugar and ABG should
be done
INVESTIGATION
S
1. Remove clothing and wash skin thoroughly
2. If drug was ingested, induce vomiting, or gastric
lavage followed by activated charcoal
3. Give oxygen or ventilation to prevent hypoxia
4. Give atropine - a muscarinic receptor antagonist,
less effective for CNS toxicity and nicotinic effects
MANAGEMEN
T
• Salicylates poisoning can be due to ingestion of
aspirin or LMS (1ml of 25% LMS = 300mg salicylates)
• Ingestion of 10-20g of salicylates can be lethal
SALICYCLAT
ES
• Gastric lavage and activated charcoal
• Correct dehydration and alkalosis with 0.9% NS and
potassium as indicated . Correct eleytrolye imbalance
• Vitamin K for hypoprothrombinaemia
• Treat acidosis if severe
MANAGEMEN
T
• Forced alkaline diuresis if indicated ( salicylate level or more
than 50mg/dl and if clinical condition is poor
• Hemodialysis/haemoperfusion/ peritoneal dialysis is indicated
in severe cases, blood level of more than 100mg/dl, refractory
acidoses, severe CNS symptoms and pulmonary edema

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POISONING.pptx

  • 1. POISONING Prepared by: Nur Aqmar Abdul Najib Lingeshwaran
  • 2. INTRODUCTIO N • Development of dose related adverse effect following exposure to chemicals, drugs or other xenobiotics • Poisoning is a worldwide problem that consumes substantial health care resources and causes many premature deaths • Recognition of poisoning or drug overdose requires high index of suspicion • Routes of exposure : Ingestion Inhalation Insufflation Cutaneous / mucous membrane exposure Injection
  • 3. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 4. Maintenance of adequate airway, breathing and circulation • In compromised airway patency or reduced respiratory drive, mechanical airway and assisted ventilation is vital • IV crystalloid bolus is first-line treatment of hypotension. • Persistent hypotension despite an adequate volume infusion may respond to a specific antidote. Otherwise, cautious administration of an inotropic agent is indicated. Antidote • E.g. : naloxone for opiate toxicity, cyanide antidotes for cyanide toxicity, and atropine for organophosphate poisoning RESUSCITATION AND STABLIZATION
  • 5.  Toxin induced arrhythmia • correction of hypoxia, metabolic/acid–base abnormalities and administration of an antidote. • sodium bicarbonate - wide QRS complex tachyarrhythmias. Seizures • titrated doses of IV benzodiazepines (isoniazid-induced seizures -pyridoxine) • barbiturates - benzodiazepine-resistant seizures Hypothermia / hyperthermia • Hyperthermia - active cooling like ice water immersion; if ineffective, may need sedation, neuromuscular paralysis, and intubation. • several toxidromes associatedwith hyperthermia are treated with pharmaceutical agents : sympathomimetic (benzodiazepines), specific serotoni n (cyproheptadine), and neuromuscular malignant syndrome (bromocriptine). RESUSCITATION AND STABLIZATION
  • 6. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 7. History taking • from patient or reliable sources (family, friends, police, bystanders) • agent, amount, time & location, route, intake of other substances • environmental clues : drug paraphernalia, empty bottles or suicide notes may aid in the diagnosis CLINICAL EVALUATION
  • 9. Toxicological screening • Blood, urine or gastric aspirate • Radio – opaque drugs (CHIPS) • Chloral hydrate • Heavy metals • Iron and iodide • Psychotropics (TCA) • Enteric coated salicylates CLINICAL EVALUATION
  • 10. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 11. 1. Decontamination (internal & external) • Skin decontamination • Eye decontamination • Induce emesis • Gastric lavage / aspiration 2. Adsorbent (Activated charcoal, Fuller’s Earth) 3. Cathartics 4. Whole bowel irrigation LIMITING ABSORPTION
  • 12. Skin • Protect • Remove clothing • Copious irrigation with water or normal saline • Chemical neutralization and corrosive agent further potentiate the injury Eyes • Remove contact lens • Local anesthetic drop • Flush with water or normal saline until pH normal 1. Decontamination (external) LIMITING ABSORPTION
  • 13. Induction of emesis 1. Decontamination (internal) Syrup of ipecac NO LONGER recommended  Prolonged vomiting  Delay administration of activated charcoal  Pulmonary aspiration LIMITING ABSORPTION
  • 14. Gastric lavage 1. Decontamination (internal) LIMITING ABSORPTION
  • 15. Gastric lavage LIMITING ABSORPTION Indications : 1. Evidence of potentially life-threatening amount of poison that has been ingested 2. Procedure can be performed within 1 hour of ingestion 3. Fully awake or intubated Contraindications : 1. Unprotected airways 2. Esophageal pathology
  • 16. Activated charcoal 2. Adsorbent Children : 0.5-1g/kg Adult : 25-100g Minimum dilution : 30g in 240ml Normally given as single dose orally or via NG/OG tube LIMITING ABSORPTION
  • 17. Activated charcoal Contraindications : • Unprotected airway • Intestinal obstruction • Ingestion of corrosive substance • GIT not anatomically intact (perforation) It is not effective in the following substances :  Alcohol  Cyanide  Iron  Lithium  Metal  Hydrocarbons LIMITING ABSORPTION
  • 18. Fuller’s Earth • In paraquat poisoning • Becomes deactivated after contact with soil/clay LIMITING ABSORPTION
  • 19. • It decreases the absorption of poison by accelerating the expulsion of the poison from GI tract. • 2 types of osmotic cathartics : • Saccharide cathartics – sorbitol • Saline cathartics – magnesium citrate, magnesium sulfate, sodium sulfate 3. Cathartics Cathartics have NO ROLE in management of a poisoned patient when used ALONE LIMITING ABSORPTION
  • 20. • Polyethylene glycol-electrolyte solution • Indications: • Large ingestion of substances that are poorly absorbed by activated charcoal • Ingestion of sustained-release drugs • Packed drugs in the body (bodypackers) • Contraindications : • Absent bowel sound, ileus, intestinal obstruction, gut perforation • Unprotected airway 4. Whole bowel irrigation No conclusive evidences showing that this procedure improves patient outcome in poisoning cases Administer polyethylene glycol-electrolyte solution (CoLyte, GoLYTELY) at 2L/H by gastric tube until rectal effluent is clear. Stop administration after 4L if no rectal fluent appeared. LIMITING ABSORPTION
  • 21. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 23. Methods : 1. Multiple dose activated charcoal 2. Ion trapping technique : Urine alkalinization Urine acidification – no longer use 3. Extracorporeal elimination : Hemodialysis (HD) Hemoperfusion (HP) Continuous renal replacement therapy (CRRT) ENHANCED ELIMINATION
  • 24. • MDAC should be considered only in patient who ingested life- threating amount of : carbamazepine, dapsone, phenobarbitol, theophylline, quinine, phenytoin 1. Multiple Dose Activated Charcoal (MDAC) Optimum dose in unknown. After initial dose (25g-100g in adult), give at a rate less than 12.5g/hour Pulmonary aspiration Charcoal bezoar Gut obstruction/perforation Bowel infarction ENHANCED ELIMINATION
  • 25. Urine alkalinization • Prevents reabsorption of the ionized drug across the renal tubular epithelium thus enhancing excretion through urine. • Moderate to severe salicylate toxicity when criteria for HD have not been met. • Also in phenobarbital, chlorpropamide or phenoxyacetate herbicides 2. Ion Trapping Technique ENHANCED ELIMINATION
  • 26. 2. Ion Trapping Technique Urine alkalinization 1. Correct hypokalemia 2. Administer IV Sodium bicarbonate 1-2 ampules OR 1 mEq/kg bolus 3. Infuse 100 mEq Sodium bicarbonate mixed with 1L of D5W at 250mL/H 4. 20 mEq of Potassium chloride may be added to solution to maintain normokalemia 5. Monitor serum potassium and bicarbonate every 2-4 hours 6. Check urine pH regularly (every 15-30mins) , aim for pH 7.5-8.5 7. Another bolus of 1 mEq of IV NaHCO3 may be given in cases of insufficient alkalinization CONTRAINDICATED in : ♢Preexisting fluid overload ♢Renal impairment ♢Uncorrected hypokalemia ENHANCED ELIMINATION
  • 27. Urine acidification • NO LONGER RECOMMENDED • produces metabolic acidosis, rhabdomyolysis and renal failure 2. Ion Trapping Technique ENHANCED ELIMINATION
  • 28. • Have limited indications in poisoned patients • A toxin must possess a number of properties to be effectively removed by this technique 1. Low volume of distribution 2. Low molecular weight 3. Relatively low protein binding 4. Low endogenous clearance 3. Extracorporeal Elimination ENHANCED ELIMINATION
  • 30. Dialyzable vs Non-dialyzable DIALYZABLE NON -DIALYZABLE Barbiturates Hydrocarbon Salicylates Anticholinergics Lithium Cyanide Isoniazid Lead Theophylline Opioid Carbamazepine TCA Methanol Arsenic ENHANCED ELIMINATION
  • 31. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 33. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 34. • Monitor vital signs • IV fluids for replacement and maintenance of adequate blood volume • Monitor fluid input and output • Correction of metabolic disturbances • Frequent monitoring of urine pH during alkalinization therapy • Intensive nursing care (ET tube) • Manage underlying illnesses SUPPORTIVE THERAP Y
  • 35. 1. Resuscitation and stabilization 2. Clinical evaluation 3. Limiting absorption 4. Enhanced elimination 5. Antidote 6. Supportive therapy 7. Disposition GENERAL MANAGEMENT
  • 37. 1. ACETAMINOPHEN 2. OPIODS 3. ORGANOPHOSPHAT E 4. SALICYLATES SPECIFIC TOXILOGY
  • 38. • Paraetamol is converted to a toxic metabolite, N-acetyl-p- benzoquinonimine which is usually inactivated by conjugation by reduced glutathione. • However, in large overdose, the glutathione is depelted and causing the toxic metabolite to bind to liver cells membrane and cause liver necrosis. (can occur as little as 10g – 20 tablets) ACETAMINOPHE N
  • 39. After ingestion of therapeutic amounts, predominant metabolism by liver through glucuronidation and sulfation. The small amount of N-acetylp- benzoquinoneimine (NAPQI) generated is conjugated with glutathione to a nontoxic compound After ingestion of large amounts, glucuronidation and sulfation are saturated, and an increased amount of NAPQI is generated. Detoxification of NAPQI to a nontoxic compound soon depletes glutathione stores, leaving excess NAPQI to bind to intracellular proteins, causing cell death
  • 40. • <24 HOURS – anorexia, vomiting and diaphoresis but patient is still consious. • Hepatic enzymes begin to rise 48 hours after ingestion and peak at 72 hours. • Recovery starts after 4 days unless hepatic failure develops. CLINICAL FEATURES OF OVERDOSE
  • 41.
  • 43. • Determined the implication of a measured acetaminophen concentration • The nomogram only directly applies to an acetaminophen concentration obtained after a single oral exposure and during the window between 4 hours and 24 hours postingestion. • Outcome prediction using this nomogram cannot be applied to acetaminophen concentrations obtained outside this 20-hour window or with chronic or recurrent exposures
  • 44.
  • 46.
  • 47.
  • 48. • Maintain airway and assist ventilattion if necessary • Give oxygen • Treat coma, seixures, hypotension and noncardiogenic pulmonary edema if they occur – INTERMITTENT POSITIVE PRESSURE VENTILLATION (not for diuretics) • NALOXONE MANAGEMEN T
  • 49. Watch out for signs of over treatment- hyperventilation, muscle tremor, tachycardia and hypertension NALOXON E
  • 50.
  • 51. • Organophosphates insecticides parathion, dichlorvos, and diazinon include malathion, • Organophosphates insecticides irreversibly inhibit the acetylcholinesterase and nicotinic synapses • Organophosphates can be absorbed through the skin, lungs and the GI tract ORGANOPHOSPHAT ES
  • 52. • Manifestations occur 30 min to 2 hour following exposure • Musacrinic effects : nausea, vomiting, abdominal cramps, urinary and fecal incontinence, salivation, and lacrimation • Nicotinic effect : twitching, fasciculations, weakness and cramps • CNS effects : Anxiety, restlessness, tremor, convulsions and coma CLINICAL MANIFESTATION
  • 53. • Cholinsterase activity in plasma and in red blood cells reduced than 50 % normal • Insecticides may be identified in urine toxology • FBC, BUSE, serum creatinine, blood sugar and ABG should be done INVESTIGATION S
  • 54. 1. Remove clothing and wash skin thoroughly 2. If drug was ingested, induce vomiting, or gastric lavage followed by activated charcoal 3. Give oxygen or ventilation to prevent hypoxia 4. Give atropine - a muscarinic receptor antagonist, less effective for CNS toxicity and nicotinic effects MANAGEMEN T
  • 55. • Salicylates poisoning can be due to ingestion of aspirin or LMS (1ml of 25% LMS = 300mg salicylates) • Ingestion of 10-20g of salicylates can be lethal SALICYCLAT ES
  • 56.
  • 57. • Gastric lavage and activated charcoal • Correct dehydration and alkalosis with 0.9% NS and potassium as indicated . Correct eleytrolye imbalance • Vitamin K for hypoprothrombinaemia • Treat acidosis if severe MANAGEMEN T
  • 58. • Forced alkaline diuresis if indicated ( salicylate level or more than 50mg/dl and if clinical condition is poor • Hemodialysis/haemoperfusion/ peritoneal dialysis is indicated in severe cases, blood level of more than 100mg/dl, refractory acidoses, severe CNS symptoms and pulmonary edema