Prof.dr.H.Aznan Lelo PhD.

SpFK
dr.Datten Bangun MSc,SpFK

Dept.Farmakologi & Terapeutik

Fak.Kedokteran U S U
MEDAN
 Analgesic agents
Cosmetics/ personal care products
Household cleaning products
Sedative hypnotics/ antipsychotics
Foreign bodies/ toys
Cough/ cold OTC preparations
Topical preparations
Pesticides

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 Largely supportive !
oxygen, iv access & fluids
Decrease drug absorption
activated charcoal within 1 hour
( whole bowel irrigation )
( gastric lavage )
Increase drug elimination
urinary alkalisation
haemodialysis/perfusion /plasma
exchange
 A (Airway)
B (Breathing)
C (Circulation)
D (Disability-AVPU/ Glasgow Coma Scale)
DEFG ( Dont ever forget the Glucose)
GET A SET OF BASIC OBSERVATIONS

General Management -2
Use all your senses, search for the clues
LOOK -Track Marks
- Pupil Size
FEEL - Temperature, Sweating
SMELL - Alcohol
 Physiologically based abnormalities that are
known to occur with specific classes of
substances and typically are helpful in
diagnosis
Patterns of
Patterns of signs
signsand
andsymptoms
symptoms

Useful
Usefulto
to help
help in
in diagnosis andtreatment
diagnosis and treatmentof
of unknown
unknown poisons
poisons
Odor Poison
Bitter almonds cyanide
Eggs hydrogen sulfide,
mercaptans
Mothballs naphthalene, camphor
Wintergreen methylsalicylate
Garlic As, org- phosphates,
DMSO, Thallium

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 Supportive
Correct hypoxia, hypotension, dehydration,
hypo- hyperthermia, and acidosis
Control seizures
Monitor
TPR, BP, ECG, Oxygenation, GCS
General
Absorption
Elimination
Specific antidotes
Sympathomimetic
Anticholinergic
Cholinergic (muscarinic)
Narcotic

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Agents: cocaine, phencyclidine, ephedrine/pseudoephedrine,
theophylline, amphetamines, LSD, phenylpropanolamine,
caffeine
2. Presentation: mydriasis, tachycardia, hypertension,
hyperthermia, diaphoresis, seizure, central nervous system
(CNS) excitation
Similar to withdrawal toxidrome
Similar to anticholinergic toxidrome except:
Diaphoresis and normal bowel sounds with
sympathomimetic toxidrome
Dry skin and absent bowel sounds with anticholinergic
toxidrome
Vital signs: Tachycardia, hypertension,
hyperpyrexia.

Clinical appearance: diaphoresis (sweating),

piloerection, mydriasis and hyperreflexia. In
severe cases, seizures, hypotension (later effect)
and dysrhythmias may occur.

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Vital signs: Bradycardia, increased respiratory rate
(initially)
Clinical appearance: SLUDGE
Salivation
Lacrimation
Urination
Defecation Diaphoresis
Gastrointestinal distress
Edema (Pulmonary)

Also see: miosis (pinpoint pupils), muscle fasciculations,

CNS depression
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1.Initial management:
(2) Stabilization:
a.ABCs: airway protection most
commonly needed
b.Orogastric lavage or NG tube: if liquid
ingestion and pt has not vomited yet
c.IV access for antidotes and fluids
2.Antidotes
(1) Atropine:
a.effect:
competitive inhibition of Ach at
muscarinic receptors in smooth
muscles
and CNS
No effect on nicotinic receptor
(N-M junction):cant reverse muscle
weakness
b.bronchorrheahypoxiatachycardia
more atropin
(2) Pralidoxime (2-PAM,Protopam)
a.effect: form a complex of PAM-OP-AchE
PAM-OP released from
complex
AchE reactivation
metabolize Ach
b.decreases atropine effect
c.treatment as early as possible
decreased effect after 36-48 hrs
exposure
aging effect
Atropa belladonna (Solanaceae)
Vital signs: Tachycardia, hypertension,
hyperpyrexia

Clinical appearance: Hot, dry skin, mydriasis, diminished

or absent bowel sounds, urinary retention, confusion
and delirium. Sinus tachycardia is most common but
other cardiac conduction abnormalities may occur.
Seizures may occur with agents that enter the CNS.

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 Reassurance
Physical Containment
Sedation - benzodiazepines
Physostigmine
Close observation
Risk of medical complications
 Most common drug taken in overdose
Few symptoms or early signs
As little as 12g can be fatal
Hepatic and renal toxin
Centrolobular necrosis
More toxic if liver enzymes induced or
reduced ability to conjugate toxin
 General measures including
U&Es, LFTs, glucose, clotting ABG, bicarbonate,
paracetamol and salicylate levels
Activated charcoal
<8 hours
Take level after four hours
Start N-aceylcysteine if above treatment line
Patients are usually declared fit for discharge
from medical care on completion of its
administration. However, check INR, creatinine
and ALT before discharge. Patients should be
advised to return to hospital if vomiting or
abdominal pain develop or recur
 >8 hours
Urgent action required because the
efficacy of NAC declines progressively
from 8 hours after the overdose
Therefore, if > 150mg/kg or > 12g
(whichever is the smaller) has been
ingested, start NAC immediately,
without waiting for the result of the
plasma paracetamol concentration
>24 hours
Still benefit from starting NAC
 Precursors of glutathione
Dosage for NAC infusion - ADULT
(1) 150mg/kg IV infusion in 200ml 5%
dextrose over 15 minutes, then
(2) 50mg/kg IV infusion in 500ml 5%
dextrose over 4 hours, then
(3) 100mg/kg IV infusion in 1000ml 5%
dextrose over 16 hours
Side-effects
Flushing, hypotension, wheezing,
anaphylactoid reaction
Alternative is methionine PO (<12 hours)
 Aspirin (acetylsalicylic acid)
Methyl salicylate (Oil of Wintergreen)
5 ml = 7g salicylic acid
Herbal remedies
Fatal intoxication can occur after the ingestion
of 10 to 30 g by adults and as little as 3 g by
children
 Plasma salicylate concentration
Rapidly absorbed; peak blood levels usually occur
within one hour but delayed in overdose 6-35 hrs
Measure @ 4 hrs post ingestion & every 2 hrs until
they are clearly falling
Most patients show signs of intoxication when the
plasma level exceeds 40 to 50 mg/dL (2.9 to 3.6
mmol/L)
 Inhibition of cyclooxygenase results in decreased
synthesis of prostaglandins, prostacyclin, and
thromboxanes
Stimulation of the chemoreceptor trigger zone in the
medulla causes nausea and vomiting
Direct toxicity of salicylate species in the CNS,
cerebral edema, and neuroglycopenia
Activation of the respiratory center of the medulla
results in tachypnea, hyperventilation, respiratory
alkalosis
Uncoupled oxidative phosphorylation in the
mitochondria generates heat and may increase body
temperature
Interference with cellular metabolism leads to
metabolic acidosis
 Early symptoms of aspirin toxicity include tinnitus,
fever, vertigo, nausea, hyperventilation, vomiting,
diarrhoea

More severe intoxication can cause altered mental

status, coma, non-cardiac pulmonary oedema and
death
 directed toward increasing systemic pH by the
administration of sodium bicarbonate

IV fluids +/- vasopressors

Avoid intubation if at all possible ( acidosis)

Supplemental glucose (100 mL of 50 percent dextrose

in adults) to patients with altered mental status
regardless of serum glucose concentration to
overcome neuroglycopaenia

Hemodialysis
 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

 Antidote flumazenil
MOA: Benzodiazepine antagonist
IV administration 0.2 mg over 15 sec to max
3mg
S/E N&V; arrhythmias; convulsions
C/I concomitant TCAD; status epilepticus
Should not be used for making the diagnosis
Benzodiazepines may be masking/protecting
against other drug effects
 Deaths from poisoning with benzodiazepines alone are
rare, but may be lethal in combination with other CNS
depressants
Treatment is supportive and aimed at maintaining
adequate ventilation whilst supporting cardiovascular
depression
Flumazenil (specific benzodiazepine antidote) is not
licensed (in the UK) for routine use in benzodiazepine
overdoses
Flumazenil may induce seizures; particularly dangerous
where tricyclic antidepressants have been taken
Flumazenil, may however, be used in the differential
diagnosis of unclear cases of multiple overdoses but expert
advice is ESSENTIAL.
 PHARMACOLOGY
TCAs have several important cellular effects,
including inhibition of:
- Presynaptic neurotransmitter reuptake
- Cardiac fast sodium channels
- Central and peripheral muscarinic acetylcholine
receptors
- Peripheral alpha-1 adrenergic receptors
- Histamine (H1) receptors
- CNS GABA-A receptors
 Arrhythmias
- widening of PR, QRS, and QT intervals;
heart block; VF/VT
Hypotension
Anticholinergic toxicity
- hyperthermia, flushing, dilated pupils,
intestinal ileus, urinary retention, sinus
tachycardia
Confusion, delirium, hallucinations
Seizures
 History
Blood/urine toxicology screen
Levels not clinically useful
 ABC many require intubation
Consider gastric lavage if taken < 2hrs
Activated charcoal
Treatment of hypotension with isotonic saline
Sodium bicarbonate for cardiovascular toxicity
Alpha adrenergic vasopressors (norepinephrine)
for hypotension refractory to aggressive fluid
resuscitation and bicarbonate infusion
Benzodiazepines for seizures
 Carbon monoxide (CO) intoxication is one of the most
common causes of accidental and intentional poisoning
Atmospheric composition <0.001%
Blood carboxyhaemoglobin
Nonsmokers 1-3%
Smokers 10-15%
Sources of CO
Motor vehicle exhaust fumes
Heating systems
Inhaled smoke
Propane-powered forklift trucks
Methylene chloride
Pathophysiology
 CO is colourless, odourless, nonirritant toxic
gas
CO toxicity due to
Cellular hypoxia
Direct cellular injury

Cellular hypoxia
CO competes with O2 for binding to Hb
Affinity of Hb for CO x 200-250 > affinity for O2
O2-Hb dissociation curve shift to the left
Impaired tissue release of O2 and cellular hypoxia
 High level of clinical suspicion
Serum COHb level
Exhaled breath COHb level
Measured by spectrophotometry
Pulse oximetry cannot distinguish between
HbO2 and COHb
Comprehensive neurological and
neuropsychological assessment
CO Neuropsychological Screening Battery
CT brain to exclude other conditions
 High-flow, FiO2 ~100%, normobaric O2
O2 shortens the half life of COHb
21% O2 = 4-6 hours
100% O2 = 40-80 minutes
100% O2 2.5atm = 15-30 minutes
Continue O2 until COHb normal
Beware concomitant smoke inhalation and burn
injury
Normobaric v Hyperbaric O2 therapy
HBO hastens resolution of acute symptoms
Unclear evidence for effect of HBO on late
complications and mortality
 Irritant Poisons
Definition:
Those agents that set up an inflammatory process at the site of
application or contact. They do not destroy body tissues
The most common signs and symptoms of irritant and poisons are
due to their local action on the mucosa of the GIT, causing
inflammatory changes and partial desquamation of the intestinal
mucosa
This leads to burning pain, vomiting and diarrhea with bloody
stools
After absorption, the main symptoms of toxicity include rapid irregular
pulse, fall in blood pressure, convulsions and coma
Examples: mercuric chloride, silver nitrate, iodine, bromine, hydrogen
peroxide
 Poisoning by Silver
Silver nitrate is used as local styptic (astringent) and
antiseptic
Ingestion of a silver salt solution causes burning sensation
of GIT, abdominal pain, vomiting with black vomitus,
diarrhea, severe shock and convulsions
Repeated use of silver preparations may result in
deposition of greyish-blue metallic silver in the pigment
layer of the skin
Treatment:
1. Gastric lavage with NaCl to precipitate silver
2. Administration of demulcents, e.g., milk and egg
white which combines with sliver as proteinate
3. Administration of cathartics and cleansing enemas
 Poisoning by Iodine
Iodine is used in medicine as antiseptic and disinfectant
Ingestion of iodine causes gastric pain, vomiting (brown-
stained vomitus), diarrhea (bloody stool), collapse and
nephritis.
Inhalation of iodine causes inflammation of respiratory
tract, cough, and pulmonary edema.
Iodine produces inflammation, desquamation and
corrosion of mucous membranes
Treatment:
1. Gastric lavage with water or 1-1.5% solution of sodium
thiosulphate
2. Administration of starch solution and demulcents,
e.g., milk and egg white
 Poisoning by Bromine
Exposure to bromine vapor causes lacrimation,
pharyngitis, salivation, cough, pulmonary edema and
ulceration of eyelids and cornea pain, vomiting (brown-
stained vomitus), diarrhea (bloody stool)
Bromine produces yellow brown discoloration of the skin,
feeling of heat and ulcer
Treatment:
1. Transferring the patient to fresh air
2. Administration of oxygen
3. Treat bronchospasms and pulmonary edema by
aminophylline I.V.
 Poisoning by Hydrogen Peroxide
Hydrogen peroxide is used in medicine as antiseptic and disinfectant
Hydrogen peroxide has two mechanisms of toxicity; local tissue injury
and gas formation. The extent of local tissue injury is determined by
the strength of the hydrogen peroxide solution:
Dilute hydrogen peroxide (usually 3%) is an irritant
Concentrated hydrogen peroxide (10-30%) is a caustic
Gas formation results when hydrogen peroxide interacts with tissue
catalase, liberating molecular oxygen and water.
The main symptoms of toxicity are vomiting, abdominal pain and
gastric mucosal erosions
Treatment:
1. Give water or milk to dilute
2. Use gastric tube to prevent increased pressure
 Poisoning by Sulphuric Acid
Treatment:
Skin Contact
a. Remove acid by flooding with water for at least 15 minutes
b. Do not use chemical antidotes
c. Treat damaged areas as for thermal burns
Ingestion
1. Do not use gastric lavage or emesis because of the danger of
perforation
2. Ingested acid may be diluted by drinking large quantities of water or
milk
3. Treat shock by administration of 5% dextrose in saline
4. Give morphine sulphate to relieve pain
5. Treat asphyxia by maintaining an adequate airway
6. If perforation of the stomach or esophagus is suspected
Inhalation
a. Give artificial respiration
b. Treat bacterial pneumonia with organism specific chemotherapy
 Common chemical
Rapidly acting
Blood Agents is a misnomer
No direct effect in blood

Where is cyanide found?

Occurs naturally in foods (some fruits, lima beans)
Cyanide salts used in industry
(e.g. ore extraction)
Produced in smoke of burning plastics/synthetics
Electroplating
Metal polishing
Smells like bitter almonds
 Inhibits cellular respiration
Cytochrome a-a3
Tissues cannot utilize oxygen
Arterialization of venous blood
 Pulmonary
Dyspnea
Tachypnea
Pulmonary edema
Apnea

Gastrointestinal
Nausea, vomiting
Caustic effects
 Clinical picture
Lactic acidosis
ABG:
metabolic acidosis

ABG sample
Parameter Finding
PO2 Normal
Calc O2 Sat Normal
Venous O2 Sat Increased
 Remove from source
Oxygen
Cyanide antidote kit
Cyanide kit causes methemoglobinemia
 Amyl nitrite perle 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 kit

 Acute coronary syndrome (ACS) refers to a
spectrum of clinical manifestations associated with
acute myocardial infarction and unstable angina.
MONA:
M: morphine
O: oxygen
N: nitroglycerin
A: aspirin.
remember, the drugs arent given in the MONA
sequence. Theyre given in the order of OANM.
 Oxygen (O2) is given first in ACS, regardless of
the patients O2 saturation level. The heart uses
70% to 75% of the oxygen it receives, compared
to skeletal muscle, which uses roughly 20% to
25%.
 The standard recommended aspirin dosage to
treat ACS is 160 to 325 mg, given as chewable
baby aspirin to speed absorption.
Aspirin slows platelet aggregation, reducing
the risk of further occlusion or reocclusion of
the coronary artery or a recurrent ischemic
event.
 To help resolve chest pain from ACS, nitroglycerin
0.4 mg is given sublingually via a spray or rapidly
dissolving tablet.
If the first dose doesnt reduce chest pain, the dose
can be repeated every 3 to 5 minutes for a total of
three doses.
A potent vasodilator, nitroglycerin relaxes vascular
smooth-muscle beds. It works well on coronary
arteries, improving blood flow to ischemic areas. It
also decreases myocardial oxygen consumption,
allowing the heart to work with a lower oxygen
demand. In peripheral vascular beds, nitroglycerin
causes vasodilation and reduces preload and
afterload, resulting in decreased cardiac workload.
 If chest pain recurs once the initial pain
resolves or decreases, the patient may be
placed on a continuous I.V. infusion of
nitroglycerin. Because of the drugs
vasodilatory effects, be sure to institute
continuous blood-pressure monitoring.
 Metoprolol may be used in the initial treatment
of ACS. A cardioselective (beta1 receptor) drug,
its a beta-adrenergic blocker that dilates
peripheral vascular beds, in turn reducing
blood pressure, decreasing cardiac workload,
and lowering cardiac oxygen demands. It also
may have a mild analgesic effect in ACS-
related chest pain.
 If chest pain doesnt resolve with sublingual or I.V.
nitroglycerin, morphine 2 to 4 mg may be given
every 5 to 15 minutes via I.V. push. An opioid
acting primarily on receptors that perceive pain,
morphine also acts as a venodilator, reducing
ventricular preload and cardiac oxygen
requirements.
the patients blood pressure needs to be monitored
continuously. If hypotension occurs, elevate the
patients legs, give I.V. fluids as ordered, and
monitor for signs and symptoms of pulmonary
congestion.
 A systematic approach has proven to be the
most efficacious way to treat critically ill
poisoned patients.
Categorization of the poisoned patients
clinical appearance into a toxic syndrome
allows the clinician to initiate effective
treatment without knowing the specific
poison involved.
More research is needed to develop new and
more effective treatments for poisoning.
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Thank you for your attention