TOXICOLOGY IN EMERGENCY

Dr.Yasa Asmara, Sp.PD

MECHANISM OF SUBSTANCE TOXICITY

Factors that influence clinical

manifestation
Time of exposure
Route of exposure
Pharmacodynamic (absorption,
metabolism, excretion)
Age
Concomitant disease

Route of exposure

Clinical feature toxic ingestion

TOXIC SYNDROME

Diagnosis of Toxic ingestion

History and physical examination

Vital sign
Ocular finding
Mental status, behaviour and muscle tone
Laboratory evaluation:

Anion gap
Osmolal gap
Oxygen saturation

Toxicology screening
Poison control center consultation

Diagnosis
Anamnesis : Substance taken
Check the pharmacy label
Physical examination
Toxic syndrome
Eye finding
Neuropathy
Abdominal finding
Skin finding
Odors

Diagnosis-cont
Essential clinical laboratory tests

Osmolar gap
Anion gap
Serum glucose
Renal and hepatic function
Urinalysis
Electrocardiogram
Pregnancy test (female childbearing)

Specific laboratorium

Osmolar gap =
Mesured - calculated
osmolality (05)

Calculated Osmolality =
2(Na) + glucose + BUN
18
2.8
= 290 mOsm/l

Anion gap =
(Na) (Cl +HCO3) =
8 12 meq/L

Elevated anion gap metabolic

acidosis

Elevated osmolal gap

Substance toxicity
Acute Intoxication is emergency for treatment
Diagnosis poisoning some time difficult
Treatment must quickly, begin with life saving
treatment, sequential, many step may be
simultaneously
Do not think antidote as first priority

Management of acute poisoning

ABCDES

Airway
Breathing
Circulation
Decontamination (prevention of absorption):
Emesis
Gastric empetying
Activated charcoal
Catharsis
Whole Bowel Irrigation
Enhancement Elemination
Forced Diuresis, urinary pH manipulation
Extracorporeal removal ( HD, Hemoperfusion, Hemofiltrasion)
Specific Antidote

Specific Antidotes

Disposition
All patients serious overdose should be
observed at least 6 hours before discharge
or transfer to psychiatric facility
Most poisoned/drug overdosed patients
need close observation in ICU, especially
potential for serious cardiorespiratory
complication

Criteria for admission to the ICU

SPECIFIC POISONING

CAUSTIC INJURY

Acid and alkaline poisoning

Pathophysiology
Alkaline agent
Acid agent
liquifaction

coagulation necrosis

thrombosis
of blood vessels

superficial injury

deep injury

Factors contributing injury

pH
Volume caustic ingested
Contact time
Preexisting state of stomach (full/empty)
Time course of injury
Location of injury (esophagus/stomach)

Clinical presentation

Symptom : Pharyngeal pain

Dysphagia
Physical Examination :
Erythema
Pseudomembrane
Hypotension
Respiratory distress
Sepsis

Complication

Acute : Upper airway obstruction

G I hemorrhage
Gastric perforation
Sepsis
Mediastenitis, pleuritis, pericarditis,
Tracheobronchoesophageal fistula
Chronic: Obstruction
Stenosis
Vocal cord paralysis
Squamous cell Ca (?)

Management

A. Stabilization: ABC
B. Initial management : decontamination surface
Contraindication for :
Neutralizing agent
Gastric lavage
Emesis
Cathartics
Charcoal

Disposition

Surgery : perforation
Burn unit : epidermal burn
ICU
: caustic burn to GI tract
Monitoring : repeat endoscopy and Upper GI
series (3 week postingestion) to detect stricture
formation.
Upon discharge : return immediately if
dysphagia develop

ORGANOPHOSPHATE

Toxicity through inhibition

acetylcholinesterase

Organophosphates bind to and phosphorylate

carboxylic esterase enzyme, including RBC
cholinesterase.
Phosphorylation is time-dependent, relatively
irreversible
Caused incapable degrading acetylcholine, then
resulting excessive accumulating acetylcholine
in neuroeffector junction (muscle, autonomic and
CNS), produced inhibitory effect of
neurotrasmission

Sign and symptom

Stimulation muscarinic receptor : DUMBLS

Defecation
Urination
Miosis
Bradycardia, bronchospasm
Lacrimation
Salivation
Stimulation nicotinic receptor : MATCH
Muscle weakness and fasciculation
Adrenal Medulla activity increase
Tachycardia
Cramping skeletal muscle
Hypertension
CNS effect : agitation, psychosis, coma, seizure depression
cardiorespiratory centers

Therapy:

Stabilization: A, B dan C
Decontamination: eye, skin, gastrointestinal
Elemination: (-)

Antidote :

Atropin (competitive block Ach)

Anticholinergic (glycopyrrolat)
Pralidoxim
Target atropinisation (mydriasis,dry mouth, tachycardi)