SEMINAR ON POISONING
By :MERON GIRMA
• DEFINITION, TYPE AND EPIDEMIOLOGY
• HISTORY AND PHYSICAL EXAMINATION
• CLINICAL DIAGNOSIS
• PRINCIPLE OF MANAGEMENT
• COMMON SELECTED POISONINGS
“Poison is a substance ( solid/ liquid or gaseous ),that produce
ill health or death, by its constitutional or local effects or both,
by altering cell structure or functions.”
The branch of medicine that deals with the detection and
treatment of poisons is known as toxicology.
“The development of dose related adverse effects following
exposure to chemicals, drugs or other xenobiotics.”
It occurs when any substance interferes with normal body
functions after it is
Swallowed; ingested poisons => 78%
Inhaled; breathed in poisons => 5.4%
injected ;IV, IM, SQ or Intra Dermal => 0.3%
Absorbed; poisons taken in through unbroken skin =>6.8%
Enter through Opthalmic; => 5.9%
• Each day a child is exposed to potential toxin
• most common in<5yrs(50-60%)
• most(93-99%) are accidental
Hx content of poisoned patient
Identification of the patient and toxic agent.
What? Description of the toxin.
Product names (brand, generic, chemical) and
ingredients, along with their concentrations
Bring container to hospital with patient.
How much? Magnitude of the exposure.
determine as accurately as possible how much of the
substance has been consumed by counting the remaining
tablets or measuring the remaining volume of liquid or gas
after we ask the previous amount.
It is better to overestimate than to underestimate
When ?Time of exposure.
Knowing the time lapse between exposure and the onset of
symptoms and/or medical evaluation w influence decisions of
diagnostic testing as well as therapeutic intervention.
Period of exposure
• First time use or chronic user
• If unknown—estimate the shortest and longest possible
Progression of symptoms.
Knowing the nature and progression of symptoms is very
helpful for assessing the need for immediate life support, the
prognosis, and the type of intervention needed
What interventions have been done?
– Traditional home remedies may be harmful
Concurrent drug therapy
The effects of poisoning maybe None, Mild or Severe
• The amount of poison ingested.
• The nature of the substance.
• The age of the child.
• The nutritional status of the child.
• The state of the stomach-whether empty or full of food.
Principle of Management
1. Initial resuscitation and stabilization
2. Removal of toxin from the body
3. Prevention of further poison absorption
4. Enhancement of poison elimination
5. Administration of antidote
6. Supportive treatment
7. Prevention of re - exposure
The management principle is applied based on triage
• Triage is the process of rapidly examining all sick children
when they first arrive in hospital in order to place them in one
of three categories.
Q Queue (non-urgent)
EMERGENCY CASES Need immediate
PRIORITY CASES Need assessment and
Emergency Management of Triaged Children
If any sign positive: give treatment(s) for ABCDO
A: Airway problem
B: Breathing problem
C: Circulation or shock
Cm: Coma or Unconscious
D: Dehydration, Severe
O: Bleeding child, poisoning (immediate), open fracture
• Toxic substances have seven common major
mechanisms that may produce symptom
1. Interfere with the transport or tissue utilization of O2
2. Depress or stimulate CNS e.g. MDMA
3. Affect autonomic nervous system e.g. Organophosphate
4.Affect the lungs by aspiration e.g. Hydrocarbon
5.Affect the heart and vasculature myocardial dysfunction
6.Produce local damage e.g. Corrosive
7.Effect on the liver e.g. Acetaminophen
• Less common (< 1%) in children
• Mostly accidental and unintentional
• More common in lower socioeconomic class
• Used in agriculture(crop sprays) and home as insecticides &
Insecticides – malathion(MLT), parathion, ethion, diazinon
Nerve gases - sarin, tabun
ophthalmic agents - echothiophate, isoflurophate
Herbicides - tributes [DEF], merphos
bind to the enzyme preventing degradation of Ach
accumulation of Ach at nerve synapses affecting:
• Neuromuscular junctions
• Sympathetic & Parasympathetic NS
• Most commonly ingested hydrocarbons - gasoline,
lubricating oil, motor oil, mineral spirits, lighter
fluid/naphtha, lamp oil,and kerosene.
• Other common sources of hydrocarbons -dry cleaning
solutions, paint, spot remover, rubber cement, and solvents
• Type of toxic response depends on:
• amount of ingestion
o Cause toxicity in 2 ways :
a. Aspiration (most common) results in
→ Spasm, edema, inflammatory rxn, and necrosis of
the respiratory passages & alveoli.
→ Vascular thrombosis & hemorrhage with chemical
pneumonitis, atelectasis, & emphysema.
b. Systemic effects
• volatile or low viscosity → degenerative changes in
various organs (mostly CNS)
Clinical Manifestations:mainly respiratory
vomiting & diarrhea, which may be bloody
dyspnea and cyanosis
mild tracheobronchitis, severe necrotizing
bronchopneumonia & pul.hemmorrhage
atelectasis , pneumatocele, bacterial infection (secondary),
mild to moderate fever within 48hrs
CNS -tremors, irritability, confusion, drowsiness, sz,&
Correction of hypoxia & acidosis
NO prophylactic Antibiotic
Paracetamol (Acetaminophen) Poisoning
• mostly used & available at home
• analgesic and antipyretic
• overdose cause fatal and nonfatal hepatic necrosis with
certain risk factors ,but is nearly always good if the antidote,
N-acetylcysteine (NAC), is administered within 8 to 10 hours
Patterns of exposure could be:
1) Intentional: more common in older children and
adolescents with a single event and high dose.
2) Unintentional: common among younger children. occur
through "exploratory" behavior or inappropriate dosing
due to toxic metabolite N-acetyl-P-benzoquinonemine
(NAPQI), produced by P450 enzyme.
Paracetamol → conjugation (sulfate,Glucuronide)
Reactive Metabolite → Gluthatione → NAC (NAPQI)
Binding to Hepatic macromolecules → Necrosis
Risk factors in children — Liver damage caused by excess N-
acetyl-p-benzoquinoneimine (NAPQI) can occur in four
• Excessive intake of acetaminophen
• Decreased capacity for glucuronidation or sulfation
• Increased cytochrome P450 (CYP2E1) activity
• Depletion of glutathione stores
if untreated, poisoned patient passes through 4 stages;
• Stage I (up to 24 hrs) – Asymptomatic, but less commonly:
nausea, vomiting, and, in large doses, lethargy and malaise
• Stage II (24 to 72 hours after overdose) – RUQ pain, elevation
in liver enzymes, prothrombin time (PT) and, in severe cases,
evidence of nephrotoxicity (elevated blood urea nitrogen,
creatinine, oliguria) and/or pancreatitis (elevated serum
• Stage III (72 to 96 hrs) – Evidence of liver failure and, in
severe cases, renal failure and multi-organ failure;
death most commonly occurs in this stage
• Stage IV (4 to 14 days) – Recovery
• 50% of phenobabitone is non-protein-bound,
available to equilibrate with tissues.
• ability to cross cell memrane(BBB) is inversely
correlated with its degree of ionization.
• cause depression of the brainstem RAS with
resultant generalised depression of the CNS
•May result in :
mild sedation, sleep or
high doses—coma,& respiratory arrest
Absorbed from oral ingestion
onset of effects in 20-60min.
Slowly metabolized by liver microsomal
enzymes & are eliminated –half-lives of
slow respiration but adequate
superficial reflexes disappear
corneal reflexes present
pupils react briskly to light
limbs become flaccid
pupils become constricted
shallow & periodic respiration
• Majority of the bites being on the lower extremities.
• Males:Female: 2:1
• 50% of bites by venomous snakes are dry bites that result in
• In the world 3000 species, 500 poisonous
Early Signs and Symptoms of Venomation
• Increasing local pain (burning, bursting,throbbing) at the site
of the bite
• Local swelling that gradually extends proximally up the
bitten limb and tender
• painful enlargement of the Regional Lymph nodes.
However, bites by kraits and sea snakes may be virtually
Local Symptoms and Signs
• Local pain
• Local bleeding
• LN Enlargement
• Local infection&Abscess formation
• Acute pituitary/adrenal insuff.
• with Russell’s viper
• Acute phase: Shock, Hypoglycaemia
• Chronic phase (mnths to yrs after): Weakness,
• Loss of 2ry sexual hair, Amenorrhoea,
• Testicular atrophy, Hypothyroidism etc
Management of Snake Bite
• First aid treatment
• Transport to hospital
• Rapid clinical assessment
• Detailed clinical assessment
and species diagnosis
• Antivenom treatment
• Observation of the response
• decision about the need for
further dose(s) of antivenom
• Treatment of the bitten part
• Treatment of chronic
• Antivenom is immunoglobulin (usually the enzyme refined F(ab)2
fragment of IgG) purified from the serum or plasma of a horse or
sheep that has been immunised with the venoms of one or more
species of snake.
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