ACUTE POISONING

Out line
Definition
Epidemiology
Patient
approach
Management principles
Organophosphate poisoning
Hydrocarbon poisoning
Carbon monoxide poisoning
 DEFINITION
Poisons- Are substances that cause
disturbances to organisms, usually by
chemical reaction or other activity on the
molecular scale, when a sufficient quantity
is absorbed by an organism.
Epidemiology
Common pediatric emergency
 1 mill. Cases per year (USA)
 Age peaks
– 1-5yr…. accidental
– Adolescence… intentional, drug abuse
 Common poisoning agents and
routes of poisoning
Common poisons
Non drug substances (50%)
Cosmetics
Cleaning solutions
Forein bodies
Pharmaceutical preparations
analgesics
antimicrobials
Cough &cold products
Routes
– Ingestion -77%
– Dermal -7.5%
– Inhalation -6
– Ophtalmic -5%
 Approach to patient
History
– description of toxic agent -Product names and
ingredients along with their concentrations
– Amount ingested
– Time & rout of exposure
– Progression of symptoms
– Medical history
POISON SYNDROME ASSOCIATED SIGNS POSSIBLE TOXINS
sympathetic over activity Pyrexia ,flushing , Cough and decongestant
tachycardia ,hypertantion preparations…
Anti cholinergic activity pupillary dilation, dry Antiparkinsonian drugs,
mouth, hot, dry skin Antihistamines, Atropine
and nightshade,TCA…
cholinergic crisis Pupillary constriction, Organophosphate
Diarrhea, Urinary insecticides, Nicotine,
incontinence,Sweating Carbamate insecticides…
Metabolic acidosis Tachypnea, Kussmaul Ethanol,CO,TCA,Calycilat
breathing es,diabetic medications…
Chemical pneumonitis Respiratory Turpentine,essential
distress,cough,CNS oil,stoddard
depretion, solvent(white sprit)…
Renal failure Oliguria,hematuria,myogl Carbon tetrachloride,
obinuria Ethylene
glycol,mushroom,methan
 Physical Findings in poisoning
characterstics substances
ODOR
Bitter almonds Cyanide
Acetone Isopropyl alcohol, methanol, paraldehyde,
salicylates
Alcohol Ethanol
Garlic Arsenic, thallium, organophosphates
OCULAR SIGNS
Miosis organophosphates, muscarinic mushrooms,
clonidine, Narcotic
Mydriasis Atropine, alcohol, cocaine, amphetamines,

Lacrimation Organophosphates, irritant gas or vapors

CUTANEOUS SIGNS
 …cont
characterstics substances
CARDIAC SIGNS
Tachycardia Atropine, aspirin, amphetamines,
theophylline
Bradycardia Digitalis, narcotics, mushrooms,
clonidine, organophosphates
RESPIRATORY SIGNS
Depressed respiration Alcohol, narcotics, barbiturates
Increased respiration Amphetamines, aspirin, ethylene glycol,
CO, cyanide
CNS SIGNS
Ataxia Alcohol, antidepressants, barbiturates,
anticholinergics, phenytoin, narcotics
Coma Sedatives, narcotics, barbiturates ,lead
organophosphates, salicylates,TCA
 Lab tests
Qualitative
Quantitative
– blood
– urine
– Vomitus,etc
confirm substance ingested
evaluate the biochemical status of the Patient &
correlate with clinical condition.
 principles of Management
1. First aid measures
2. Prevention of absorption
3. Enhancement of elimination
4. Use of specific antidotes
5. Supportive care
 1. First aid measures

• Focus initialy on life support with primary

emphasise on cardiorespiratory care.

• Treat shock ,dysrhytmia and seizure like other

critically ill patients.
2. Prevention of absorption
Inhaled poisons (smoke, gas, fumes)
– Moving the patient to fresh air & if necessary oxygen
admnistration.

Poisons on the skin:

– Copious irrigation followed by soap wash.

Poison in the eye:

- Irrigate with tape water atleast for 10 minutes.
 Prevention of GI absorption
A. Activated charcoal
Use –to dicrease absorption and also inhance
elimination of already absorbed toxin.
Dose -10-50g(1g/kg) for a child
50-100g for an adolecent or adult
If severe symptoms are there cathartic should be
added only in the first dose to prevent major fluid
loss and dehydration .
...cont
B. Cathartics
Used with charcoal to hasten clearance of
charcoal-toxin complex.
The commonly used ones are
MgSo4 (250mg/kg)
Magnizium citrate(250ml/kg)
Sorbitol(1g/kg)
 ...cont
C.Emesis –ipecac syrup
Dose-depends on age
age Dose
6-12mo 10ml
1yr-12yr 15ml
Above 12yr 30ml
The onset of emesis is usually 20-30
minutes.
...cont
Contraindications to Emesis
• Age-less than 6mo
• Altered consciousness & convulsion
• Prior significant vomiting/ hematemesis
• Ingestion of caustics (acids/bases), hydrocarbons, and
agents that cause rapid onset of CNS or CV symptoms
...cont
D.Whole bowel irrigation
use to remove slowly absorbed substance,
foreign bodies,sustained release products.

E. Gastric lavage
Used only in older children
Contraindications
o Caustic/corrosive ingestion
o Convulsions/altered consciousness-unless
intubated with ETT
o Hydrocarbon ingestion
 3. Enhancement of elimination

– Forced diuresis (alkaline/acid)

– Dialysis
– Hemoperfusion
 4. Use of specific Antidotes
Antidot poison
Atropine Organophosphate and carbamate
pesticides,
β-blocking agents
Benztropine Acute dystonic reactions

Cyanide antidote kit Cyanide,Hydrogensulfide (nitrites only)

Deferoxamine Iron

Ethanol Methanol, ethylene glycol

Flumazenil Benzodiazepines

Methylene blue Methemoglobinemia

Glucagon β Blockers, calcium channel blockers,

hypoglycemic agents
oxygen Carbon monoxide
 Supportive care
Dictated by clinical circumstances and type of
poison:
1. Cardiorespiratory support
IV fluids
ventilatory support
Close monitoring
2. Control of seizures
diazepam and
long acting anticonvulsants
3. Rx of brain edema
Hyperventilation
Steroids
mannitol
Monitoring and correction of e- abnormalities
 PREVENTION
1. Safety closure
2. Keep out of the reach of children
3. Never store food and cleaning products together
4. Discard unused medicine and toxic products
together
5. Keep a bottle of syrup of ipecac and learn how to
use it
 Organophosphate poisoning
• Most occur as a result of accidental exposure
to insecticides
• 3 mil people exposed each year
• 300,000 deaths
 Pathophysiology
•Binds to cholinstrase enzymes preventing the
degradation of acetylcholine, resulting in
accumulation at nerve synapses and NMJ
•If left untreated, form a permanent bond to these

enzymes
Clinical presentation
Defecation
Urination
Miosis
Bradycardia
Bronchospasm =Muscarinic effects
Emesis
Lacrimation
Salivation…
...cont.
Muscle weakness
Fasciculation
Tachycardia =Nicotinic effects
Muscle cramp
Hypertension
Diaphoresis
…cont
 Acute toxicity
DUMBELS
Defecation
Urination
Miosis
Bronchorrhea/bronchospasm/bradicardia
Emesis
Lacrimation
Salivatiomn
…cont
• Fatality from acute toxicity generally results
from respiratory failure
 Intermediate syndrome
• 10 - 40% of patients develop a distinct neurologic d/o
24 – 96 hrs after exposure
Neck flexion weakness
Depressed DTR
Proximal muscle weakness
CN abnormality
…cont

 Delayed neurotoxicity
o Occurs 1 – 3 wks after exposure
Flaccid weakness of distal muscles
Sensory disturbances
Diagnosis

 Hx &P/E
 Atropine challenge
 Measurement of RBC acetylcholinstrase
 Management
• 1. General
 Airway : suction, ventilation support
 GI decontamination(lavage)
 Dermal decontamination
 Control seizure
2. Toxic specific
 Atropine: antagonizes the muscarinic

acetylcholine receptor
…cont

• Dose : 0.05mg/Kg, repeat every 15 min till

signs of atropinization (decease secretions)
• Maintain on atropine 0.05mg/Kg every 3 – 4

hrs for few days

 Pralidoxime: breaks the bond b/n OP &the

enzyme and enhancing the OP body clearance

• Dose ; 25 – 50mg/Kg over 30 min
 Hydrocarbon poisoning
• Found in thousands of commercial products
• Aspiration of hydrocarbons can lead to
serious, even life threatening toxicity
• aspiration depends on volatility, surface
tension & viscosity
• The most adverse effect is aspiration
pneumonitis
• Less than 2% of ingestions cause significant
pneumonitis
 …cont

Some halogenated hydrocarbons can sensitize

the myocardium to the effect of endogenous
catecholamine with the risk of dysrhythemia
& sudden death

• Hemolysis, hemoglobinuria & leukocytosis

• CNS depression
 Management

• Avoid induction of emesis and gastric lavage

due to the risk of aspiration
• Activated charcoal is also not useful
• So treatment is supportive
 Oxygen supplementation
 Inhaled B- bronchodilators
 Intubation
 NPO
 Carbon monoxide poisoning
• Produced during the combustion of any
carbon containing fuel
• The toxicity develops through 3 mechanisms:
1. It binds to hemoglobin, displacing oxygen with an
affinity for hemoglobin 250 times that of oxygen
2. It impairs the ability of hemoglobin to release
oxygen to tissue
3. It binds to cytochrome oxidase in tissue, impeding
oxygen use
 Clinical manifestations

• Symptoms are proportional to the Conc of

COHb in the blood
If > 15%- symptoms appear
If >20%- toxicity
If >40%-severe neurologic effects
 Management

• Administration of 100% oxygen

• Hyperbaric oxygen therapy (2.5 – 3 atm)
THANK YOU