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SPECIFIC THERAPY FOR ACUTE

INTOXICATION
Hendra Wana Nur’amin, dr., M.Sc
Department of Pharmacology and Therapy
Faculty of Medicine
Lambung Mangkurat University
This topics

 Insecticides
 Snake venoms
 Ethanol
 Chlorine
 Opiates
 Paracetamols
 Cyanides

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Insectisides

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Insecticide
Symptoms:
• Excessive salivation
• Tearing of the eyes
• Diarrhea
• Vomiting
• Difficulty breathing
• Abdominal pains
• Agitation, irritability or even
seizures
• Confusion or even
hallucinations
• Headache
• Generalized weakness
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Insecticide

Management
• Basic life support
• Clean airway
• Gastric Lavage
• Atropine IV 2mg. Repeat
every 10-15 minutes if
needed.
• Recovery: flushing,
hypersalivation (-), normal
heart rhytm (increase)
• Observe

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 Atropine vs
organophosphate /
Carbamate intoxication

OP / carmabate  inhibitAChE
 let ACh accummulated in theSC
 stimulation of r-M and r-N
(predominantly stimulation of r-M)
 symptoms & sign ofintoxication

Atropine block r-M

 prevent stimulation of r-M byACh

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SNAKE VENOM

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 Snake Venom
• It is modified saliva
• Mostly comprised of proteins
• Has about 20 different enzymes, of
which, a species usually has between 6
and 12
Kinds of Toxins
• Neurotoxins: have the ability to damage
and or destroy nerve tissues
• Haematoxins: affects the blood and
causes Haemolysis and Hemorrhage
• Myotoxins: these cause muscle pain and
turn urine brown to black because of the
protein Myoglobin that is present
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Ethanol

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Alcohol

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 Alcohol
Management
• Basic life saving
– Establish and maintain the airway.
– Give high concentration oxygen.
– Assist ventilations as necessary.
– Establish vascular access.
• symptomatic
• Emetic
• Administer glucose and Thiamine (B1) 
Prevention of Wernicke–Korsakoff syndrome

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 Wernicke Korsakoff encephalopathy
• eye/vision issues
• confusion
• difficulty walking
• memory loss

• B1 deficiency because of longterm alcoholism

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Moderate alcohol consumption as risk factor
for adverse brain outcomes and cognitive
decline: longitudinal cohort study. BMJ
2017;357:j2353 doi: 10.1136/bmj.j2353
Chlorine

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Chlorine

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 Chlorine
Management:
• Avoid exposure
• Symptomatic
Controversial
• If ingested  milk, antacid Mg(OH)3 or Al(OH)3
Don’t force emesis or gastric lavage

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CO intoxication

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 Carbon monoxide
Symptom of intoxication :
• No symptom COHb < 2% (non-smoker), < 5% (smoker)
• Cardiovascular symptoms : COHb > 5%
• Fatal symptom : COHb > 50%

Symptoms :
• COHb  cherry red skin and mucous membrane
• Respiratory tract (there is no dyspnea) PO2 very little to change
(decrease 1/245) but transportation of O2 decrease up to 50%
• chemoreceptors are not stimulated,
• Hypoxia  reflextory COP (tachycardy)

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Carbon monoxide

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 Carbon monoxide
Therapy of intoxication :
1. Terminate the contact,
2. Artifial respiratory (inspiration = expiration)
3. Oxygen
- t1/2 (half recovery time) at 1 atm. : 80’
- t1/2 at O2 1 atm: 30 minutes
- t1/2 at O2 3 atm(hyperbaric): 23 minutes
4. It is necessary to ad CO2 5 - 7% (to stimulate
resp. centre)
5. Exchange transfusion for moribund
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 Narcotics, Opiates, and Opioids
• Narcotic: drug that produces sleep or altered
mental status
• Opiate: natural drugs derived from opium
• Opioid: non-opium-derived synthetics
• Pathophysiology
– Bind with receptor sites in the brain and tissues
– Effects are lessened when taken orally.
– A dose of naloxone may not permanently reverse
the effects of heroin.

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Opioids

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 Narcotics, Opiates, and Opioids
• Assessment
– Classic presentation
features:
• Euphoria
• Hypotension
• Respiratory depression
• Pinpoint pupils
– Produce a dreamlike
state
• Management
– Establish a patent airway
and vascular access.
• Administer naloxone.
– If the patient does not
respond to naloxone:
• They may have taken a
potent synthetic drug.
• They may have taken
multiple drugs.
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Opioid Poisoning
 Opiates
• Antidote – naloxone
• MOA: Pure opioid antagonist competes and displaces
narcotics at opioid receptor sites
• I.V. (preferred), I.M., intratracheal, SubQ: 0.4-2 mg every
2-3 minutes as needed
• Lower doses in opiate dependence
• Elimination half-life of naloxone is only 60 to 90 minutes
• Repeated administration/infusion may be necessary

• S/E BP changes; arrhythmias; seizures; withdrawal

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 Paracetamol
• Widely available
• Potential toxicity underestimated
• Toxicity unlikely to result from a single dose
of less than 150 mg/kg in child or 7.5 to 10 g
for adult
• Toxicity is likely with single ingestions greater
than 250 mg/kg or those greater than 12 g
over a 24-hour period
• Virtually all patients who ingest doses in
excess of 350 mg/kg develop severe liver
toxicity unless appropriately treated

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 Clinical features
Stage I (0.5 to 24 hours)
• No symptoms; N&V Malaise
Stage II (24 to 72 hours)
• Subclinical elevations of hepatic aminotransferases (AST, ALT)
• right upper quadrant pain, with liver enlargement and tenderness.
Elevations of prothrombin time (PT), total bilirubin, and oliguria and
renal function abnormalities may become evident
Stage III (72 to 96 hours)
• Jaundice, confusion (hepatic encephalopathy), a marked elevation
in hepatic enzymes, hyperammonemia, and a bleeding diathesis
hypoglycemia, lactic acidosis, renal failure 25%, death
Stage IV (4 days to 2 weeks)
• Recovery phase that usually begins by day 4 and is complete by 7
days after overdose

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 N-acetylcysteine

• Antidote – MOA: a glutathione precursor

• Limits the formation and accumulation of NAPQI
• Powerful anti-inflammatory and antioxidant effects
• IV infusion or oral tablets (also oral methionine)
• 150mg/Kg over 15 min; 50mg/Kg over next 4 hrs; 100mg/kg over next 16
hrs up to 36hrs
• Beyond 8 hours, NAC efficacy progressively decreases
• S/Es nausea, flushing, urticaria, bronchospasm, angioedema, fever, chills,
hypotension, hemolysis and rarely, cardiovascular collapse

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Cyanides

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Mechanism of action of Cyanide

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 Cyanide
Clinical manifestations
• Time to onset of symptoms, as well as additional signs of
exposure, depends on dose and route of exposure:
– Inhalation
• Rapid onset: seconds to minutes
• Additional signs: Metallic taste; burning sensation in GI / respiratory
tract
– Ingestion
• Delayed onset: 15 to 30 minutes
• Additional signs: Sore throat; burning sensation in GI / respiratory
tract; diarrhea
– Skin contact
• Delayed onset: 15 to 30 minutes
• Additional signs: Erythema, pain at site of contact

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 CYANIDE
TOXICITY
INGESTION

LETHAL DOSES
Hydrogen Cyanide
60- 90 mg
(HCN)
200 mg Potassium Cyanide (KCN)

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 CYANIDE
TOXICITY
INHALATION

Concentration (mg.m-3) Effect

300 immediately lethal
200 lethal after 10 minutes
150 lethal after 30 minutes
120-150 lethal after 30-60 minutes
50-60 20 minutes to 1 hour without effect
20-40 light symptoms after several hours

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 Cyanide
Management
1. Remove from source
2. Oxygen
3. Cyanide antidote kit
• Amyl nitrite until IV established
• Sodium Nitrite (300mg IV)
– Peds: 0.33 ml/kg of 10% solution)
• Sodium Thiosulfate (12.5gm IV)
– Peds: 1.65 ml/kg of 25% solution)

Cyanide
antidote 44
kit
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 Anaphylaxis
• Anaphylaxis is a rapidly
progressing, life-
threatening allergic
reaction
• Common triggers include
venom from insect bites
or stings, foods, and
medication
• The cause remains
unknown in 32–50% of
cases, referred to as
"idiopathic anaphylaxis.

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 References
• Hoffman RS, et al. Goldfrank’s Manual of Toxicologic
Emergencies. McGraw-Hill Companies, Inc 2007
• Katzung BG, et al. Basic and Clinical Pharmacology 13th
Ed. San Fransisco: McGraw Hill, 2015
• Klaassen CD, Watkins III JB. The Basic Science of Poison 8th
Ed. McGraw-Hill Companies, Inc, 2013
• KLaassen CD. Casarett & Doull’s Essentials of toxicology 3rd
Ed. McGraw-Hill Companies, Inc, 2015
• Ngatidjan. Specific Therapy of Acute Intoxication.
Department of Pharmacology and Therapy, Facultu of
Medicine, Univesitas Gadjah Mada

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THX

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