Engidaw Ambelu

1. SEMINAR ON POISONING
By :MERON GIRMA
ENGIDAW AMBELU
MODERATOR:
DR.GETA

2. OUTLINES:
• DEFINITION, TYPE AND EPIDEMIOLOGY
• HISTORY AND PHYSICAL EXAMINATION
• CLINICAL DIAGNOSIS
• PRINCIPLE OF MANAGEMENT
• COMMON SELECTED POISONINGS

3. Definition
Poison:
“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.

4. Poisoning:
“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%

5. Types:
Deliberate (intentional)
Suicide & homicide
 Accidental (unintentional)
Dosage error
Recreational use
Environmental:
• Plants
• Food
Venomous stings/bites
Industrial exposures

6. • Epidemiology
• Each day a child is exposed to potential toxin
• Age
• most common in<5yrs(50-60%)
• Cause
• most(93-99%) are accidental

7. 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.

8. 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

9. 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
time.

10. 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

11. Medical history
Underlying diseases
Concurrent drug therapy

12. The effects of poisoning maybe None, Mild or Severe
depending on:
• 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.

13. PHYSICAL EXAMINATION
ODOR
• Bitter- almonds Cyanide
• Acetone -Isopropyl alcohol,
Methanol, Paraldehyde,
Salicylates
• Alcohol-Ethanol
• Wintergreen -Methyl
Salicylate
• Garlic -Arsenic, Thallium,
Organophosphates
OCULAR SIGNS
• Miosis -Narcotics (except
meperidine),Organophosphates,
muscarinic,mushrooms,phenoth
iazine's,barbiturates (late), PCP
• Mydriasis -Atropine, alcohol,
cocaine,CO
• Lacrimation-
Organophosphates, irritant gas
or vapors
• Poor vision- Methanol,
botulism, CO

14. CUTANEOUS SIGNS
• Dry, hot skin -Anticholinergic
agents, botulism
• Diaphoresis-
Organophosphates, nitrates,
muscarinic mushrooms,
aspirin, cocaine
• Erythema- Boric acid,
mercury, cyanide,
anticholinergics
ORAL SIGNS
• Salivation -Organophosphates,
salicylates, corrosives,
strychnine
• Dry mouth- Amphetamines,
anticholinergics, antihistamine
• Burns- Corrosives, oxalate-
containing plants
• Gum lines- Lead, mercury,
arsenic
• Dysphagia -Corrosives, botulism

15. INTESTINAL SIGNS
• Cramps -Arsenic, lead, thallium,
Organophosphates
• Diarrhea -Antimicrobials, arsenic,
iron, boric acid
• Constipation -Lead, narcotics,
botulism
• Hematemesis -Aminophylline,
corrosives, iron, salicylates
CARDIAC SIGNS
• Tachycardia Atropine, aspirin,
amphetamines, cocaine, cyclic
antidepressants, theophylline
• Bradycardia -Digitalis,
narcotics, mushrooms,
clonidine, Organophosphates,
β blockers,CCB
• Hypertension- Amphetamines,
LSD, cocaine, PCP
• Hypotension Phenothiazines,
barbiturates, cyclic
antidepressants, Fe, β blockers,
CCB

16. RESPIRATORY SIGNS
• Depressed respiration
Alcohol, narcotics,
barbiturates
• Increased respiration -
Amphetamines, aspirin,
ethylene glycol, CO, cyanide
• Pulmonary edema
Hydrocarbons, heroin,
Organophosphates, aspirin
CNS SIGNS
• Ataxia -Alcohol,
antidepressants,
barbiturates,
anticholinergics, phenytoin,
narcotics
• Coma -Sedatives, narcotics,
barbiturates, PCP,CO
Organophosphates,lead
• Hyperpyrexia
Anticholinergics, cocaine

17. CNS sign…
• Muscle fasciculation -
Organophosphates,
theophylline
• Muscle rigidity- Cyclic
antidepressants, PCP,
phenothiazines, haloperidol
• Paresthesia- Cocaine,
camphor, PCP, MSG
• Altered behavior- LSD, PCP,
amphetamines, cocaine,
alcohol, anticholinergics,
camphor
• Peripheral neuropathy-
Lead, arsenic, mercury,
organophosphates

18. Clinical Diagnosis
• CBC
• serum electrolyte
• LFT, RFT
• screening
• RBS
• SO2

19. 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

20. 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.
E Emergency
P Priority
Q Queue (non-urgent)
Categories after
Triage
Action required
EMERGENCY CASES Need immediate
emergency treatment
PRIORITY CASES Need assessment and
rapid attention

21. Emergency Management of Triaged Children
If any sign positive: give treatment(s) for ABCDO
Emergency Signs
A: Airway problem
B: Breathing problem
C: Circulation or shock
Cm: Coma or Unconscious
Cn: Convulsion
D: Dehydration, Severe
Ds: Disability
O: Bleeding child, poisoning (immediate), open fracture

22. SELECTED POISONS
• Drugs
Acetaminophen
Phenobarbitone
Salicylate
Iron
Digoxin
• Insecticides (pesticides)
Organophosphate
Carbamates
• Hydrocarbons
• Venomous stings/bites
Snake bite

23. • Toxic substances have seven common major
pathophysiologic
mechanisms that may produce symptom
1. Interfere with the transport or tissue utilization of O2
e.g. CO
2. Depress or stimulate CNS e.g. MDMA
3. Affect autonomic nervous system e.g. Organophosphate

24. 4.Affect the lungs by aspiration e.g. Hydrocarbon
5.Affect the heart and vasculature myocardial dysfunction
e.g.Antidepressant
6.Produce local damage e.g. Corrosive
7.Effect on the liver e.g. Acetaminophen

25. Organophosphate poisoning
• Less common (< 1%) in children
• Mostly accidental and unintentional
• More common in lower socioeconomic class
• Used in agriculture(crop sprays) and home as insecticides &
pesticides
e.g.
Insecticides – malathion(MLT), parathion, ethion, diazinon
Nerve gases - sarin, tabun
ophthalmic agents - echothiophate, isoflurophate
Herbicides - tributes [DEF], merphos

26. Pathophysiology:cholinesterase inhibitor
bind to the enzyme preventing degradation of Ach
accumulation of Ach at nerve synapses affecting:
• CNS
• Neuromuscular junctions
• Sympathetic & Parasympathetic NS

27. NORMAL
PHYSIOLOGY

28. Clinical Manifestations:
• Muscarinic s/Sx (Parasympathetic NS)
Diaphoresis, emesis,
Incontinence (urine, fecal),
Tearing, bronchorrhea & bronchospasm
Meiosis, hypotension, bradycardia
MUSCARINIC SIGNS
SLUDGE/BBB DUMBELS
S=Salivation D=Diarrhea &
diaphoresis
L=Lacrimation U=Urination
U=Urination M=Miosis
D=Defecation B=Bronchocorrhe
a,bronchospasm,
bradycardia
G=GI symptoms E=Emesis
E=Emesis L=Lacrimation
B=Bronchorrhea S=Salivation
B=Bronchospasm
B=Bradycardia

29. • Nicotinic S/S(Sympathetic NS)
Muscle weakness, tremors, fasciculation,
Hypoventilation, HTN, tachycardia, dysarhythmias
• CNS effects
confusion, delirium, coma, Seizure, anxiety, restlessness,
Emotional lability, Confusion, Ataxia, Tremors,impaired
memory, lethargy, psychosis

30. the balance between stimulation of muscarinic and nicotinic
receptor depend on the
- Type of organophosphate
- Dose
- Route and rate of absorption
- Individual factor

31. Management:
Supportive
GID
Antidotes (atropine)

32. Hydrocarbon Poisoning
• 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

33. • Type of toxic response depends on:
• amount of ingestion
• volatility(viscosity)

34. • Pathophysiology
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.

35. b. Systemic effects
• volatile or low viscosity → degenerative changes in
various organs (mostly CNS)
Clinical Manifestations:mainly respiratory
Choking, Coughing

36. vomiting & diarrhea, which may be bloody
 dyspnea and cyanosis
mild tracheobronchitis, severe necrotizing
bronchopneumonia & pul.hemmorrhage
atelectasis , pneumatocele, bacterial infection (secondary),
pneumomediastinum
 mild to moderate fever within 48hrs
CNS -tremors, irritability, confusion, drowsiness, sz,&
coma

37. management
Correction of hypoxia & acidosis
 NO emesis
 NO lavage
 NO prophylactic Antibiotic
 NO STEROIDS

38. 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
of ingestion

39. 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

40. Pathophysiology:
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

41. Risk factors in children — Liver damage caused by excess N-
acetyl-p-benzoquinoneimine (NAPQI) can occur in four
circumstances :
• Excessive intake of acetaminophen
• Decreased capacity for glucuronidation or sulfation
• Increased cytochrome P450 (CYP2E1) activity
• Depletion of glutathione stores

42. Clinical Manifestations:
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
amylase, lipase)

43. • 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

44. Management:
- Supportive
-Emesis/lavage
-NAC/Mucomyst

45. PHENOBARBITONE POISONING
• Pathphysiology
• 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

46. •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
2-6days

47. Clinical Manifestations:
 Early
Euphoria
Disinhibition
Ataxia
Dysarthric
Nystagmus
slow respiration but adequate
superficial reflexes disappear
corneal reflexes present
pupils react briskly to light

48. Late
limbs become flaccid
DTR disappear
pupils become constricted
Sometimesbullous eruptions
Terminal phase
shallow & periodic respiration
decreased BP-Shock

49. Management
Supportive
GID
AC
Saline catharsis
Diuresis
Alkalinization
Dialysis

50. Snake Bite
• 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
negligible envenomation.
• In the world 3000 species, 500 poisonous

51. 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
painless.

52. Local Symptoms and Signs
• Local pain
• Local bleeding
• Bruising
• Lymphangitis
• LN Enlargement
• Blistering
• Local infection&Abscess formation
• Necrosis

53. Systemic Symptoms
General
• Nausea
• Vomiting
• Malaise
• Abdominal pain
• Weakness
• Drowsiness
• Prostration

54. Cardiovascular(vipridae)
• Visual disturbances
• Dizziness
• Faintness
• Collapse
• Shock, Hypotension
• Cardiac arrhythmias
• Pulmonary oedema
• Conjunctival oedema
Bleeding and clotting disorders
( vipridae)
• Bleeding from recent wounds
(including fang marks,
venepunctures etc) and from
old partlyhealed wounds
• Spontaneous systemic
bleeding

55. Neurological (Elapidae,Russell’s viper)
• Drowsiness
• Paraesthesiae
• Abnormal taste and smell
• “Heavy” eyelids,Ptosis,Ext. ophthalmoplegia
• Facial paralysis
• Aphonia
• Difficulty in swallowing secretion
• Respiratory and generalised flaccid paralysis

56. Rhabdomyolisis
• Generalised pain, stiffness and tenderness of muscles, trismus,
myoglobinuria, hyperkalemia, cardiac arrest, acute renal failure
• Occur with sea snakes, Russell’s viper

57. Renal (Viperidae, Sea snakes)
• Loin (lower back) pain
• Haematuria
• Haemoglobinuria
• Myoglobinuria
• Oliguria / Anuria
• Symptoms and signs of Uraemia

58. Endocrine
• 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

59. Management of Snake Bite
• First aid treatment
• Transport to hospital
• Rapid clinical assessment
and resuscitation
• Detailed clinical assessment
and species diagnosis
• Investigations/laboratory
tests
• Antivenom treatment
• Observation of the response
to antivenom:
• decision about the need for
further dose(s) of antivenom
• Supportive/ancillary
treatment
• Treatment of the bitten part
• Rehabilitation
• Treatment of chronic
complications

60. • 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.