Dr. TAHER A. SULIMAN

1. PRINCIPLES OF
MANAGEMENT OF
ACUTE POISONING

2. IMPORTANT RULE
All poisoned patients should be
managed as if they have a
potentially life-threatening
intoxication, although they
appear normal

3. 1. Initial assessment & stabilization of VFs
2. Definitive care of poisoning cases:
a) Measures to identify the toxic agent.
I. PreventioHistory and circumstantial evidence
II. Symptoms and signs (including toxidromes)
III. Investigations
IV. Postmortem picture
b) Decrease further absorption.
c) Antidote therapy (if available).
d) Enhance elimination (excretion) of the toxic substance.
e) Treatment of systemic complications resulting from poisoning
3. A secondary survey for: INFECTION, TRAUMA,
METABOLIC DISTURBANCE

4. STABILIZATION OF
THE PATIENT• The initial approach to the poisoned patient
should be essentially similar in every case,
irrespective of the toxin ingested.
• Similar to the initial approach to the trauma
patient
• Applied as initial approach to all patients in
ED irrespective of the mechanism of injury.
• This approach can be termed as routine
poison management

5. INITIAL ASSESSMENT & STABILIZATION
The Basic Life Support including ABCDE
should be applied before all other
considerations.
 Many toxic substances can lead to
potentially life-threatening changes that
should be identified and treated quickly.
Many poisoned patients require only
supportive therapy alone.

6. A= Airway Patency
Airways should be kept patent and any suspicion for
obstructing material must be removed
The most common factor contributing to death
from poisoning is loss of airway-protective
reflexes with subsequent airway obstruction
caused by:
• Flaccid tongue
• Pulmonary aspiration of gastric contents
• Respiratory arrest
All poisoning patients should be suspected of
having a potentially compromised airway.

7. • The most common cause of airway
obstruction in an unconscious patient is
passive obstruction by the tongue.
• The neck lift with jaw thrust may be the
first maneuver performed by the
physician on the unconscious poisoned
patient followed by endotracheal
intubation

8. Loss of consciousness is often accompanied by loss of muscle tone
(A)Occlusion of the airway by the tongue can be relieved by
a head-tilt chin-lift (B)
or a jaw thrust (C).
In patients with possible cervical spine injury, the angles of the jaw should be
lifted anteriorly without hyperextending the neck.

9. Indications for endotracheal intubation
in the poisoned patient include:
1) Protection of the airway in the obtunded or comatose
patient with a depressed or absent gag reflex to
prevent aspiration during gastric lavage
2) Controlled ventilation in patients who demonstrate
respiratory depression or failure
3) Removal of secretions in patients who develop
pulmonary edema secondary to a toxic substance
4) Institution of positive end-expiratory pressure (PEEP)
therapy for those patients who are at risk for
developing adult respiratory distress syndrome
(ARDS).

10. The other issues to keep airways patent:
1. Aspiration of secretions and
regurgitated food and stomach
contents.
2. Removal of foreign bodies,
dentures, or mucous from mouth.
3. Prevent falling back of the tongue
in comatose patient by
oropharyngeal tube.

11. B= Breathing
assisted ventilation is done according to the situation:
Monitoring of RR is important.
Patients may have one or more of the
following complications: bradyapnea,
ventilatory failure, hypoxia, or
bronchospasm.

12. Normal Respiratory Rates
AGE BREATHS/MIN
Newborn to 6 weeks 30 - 60
Infant (6 weeks to 6 months) 25 - 40
Toddler ( 1 to 3 years) 20 - 30
Young Children ( 3 to 6 years) 20 - 25
Older Children (10 to 14 years) 15 - 20
Adults 12 - 20

13. C= Circulation
A. Check blood pressure and pulse rate and
rhythm.
B. Begin continuous ECG monitoring
C. Secure venous access
D. Draw blood for routine studies.
E. Begin intravenous infusion If the patient is
hypotensive, normal saline or another isotonic
crystalloid solution is preferred

14. Disability (Neurological):
A decreased level of consciousness is the most
common serious complication of drug
overdose or poisoning.
• Coma
– C.N.S depressant: barbiturate, benzodiazepine and opiate
– Hypoglycemic agent and alcohol.
– Hypoxic agent (CO).
– Metabolic agent (Salicylate, methanol).
– Other as organophosphate.
For patients with altered consciousness or respiratory depression of
unknown cause give "coma cocktail“:
– Dextrose (Hypoglycemia)
– Thiamine (Alcohol-related Amnestic Syndromes)
– Naloxone (Opiates)
– O2 (Hypoxia)

15. Coma Cocktail
• if the patient’s mental status is altered
or if hypotension exists, give……
coma cocktail:
1. 100% oxygen
2. Naloxone
3. Glucose
4. Thiamine
• Coma cocktail is administered for a
diagnostic and therapeutic reasons.

16. Seizures
• seizures caused by specific toxins can exhibit certain
specific properties.
• Strychnine is unique in that it can cause generalized
seizures while the patient is alert. ‘‘spinal seizure.’’
• Other drug-induced seizures will respond only to
specific antidotal therapies and not to conventional
antiseizure medication.
– anticholinergic-induced seizures may respond to
physostigmine
– isoniazid-induced seizures, which respond to pyridoxine.
– theophylline-induced seizures rarely respond to
phenytoin alone and often only to multidrug therapy

17. DEFINITIVE
CARE WITH
POISONING

18. Try to identify the poison
• Accurate and complete history
• History from sources other than patient
(family, friends, pharmacist, & pill
bottles at the scene).
• Attempt to establish the time and
amount of the ingestion

19. CAREFULPHYSICAL EXAM
• Based on knowledge of drug pharmacology
& effects on ANS
• The vital signs should be monitored
accurately.
• Level of consciousness (AVPU), pupillary
size and reaction to light.
• Skin examination and breath odors
• Recognizing toxidromes.
• Exam should include evaluation for head
trauma, focal neurological findings, needle
track marks.

20. Breath odors & Skin Findings
BREATH ODORS
• Bitter almonds: cyanide
• Fruity: DKA,
isopropranolol
• Oil of wintergreen:
methylsalicylate
• Rotten eggs: sulfur
dioxide, hydrogen
sulfide
• Pears: chloral hydrate
• Garlic:
organophosphate,
arsenic
• Mothballs: camphor
SKIN
• Diaphoretic Skin
Sympathomimetics
Organophosphates
Salicylates
• Red Skin
CO, boric acid
• Blue Skin
Cyanosis
methemoglobinemia

21. EXAMPLES OF TOXICVITAL SIGNS
• Bradycardia (PACED)
P propranolol
A anticholinesterase
C clonidine, Ca ch. blocker
E ethanol + alcohols
D digoxin, dravon (opiates)
• Tachycardia(FAST)
F free base (cocaine)
A anticholinergic,
antihistamin
S sympathomimetic
T theophylline
• Hypothermia (COOLS)
C CO
O opiates
O oral hypoglycemics, insulin
L liquor (Alcohols)
S sedative hypnotics
• Hyperthermia (NASA)
N neuroleptic malignant syndome
A antihistamines
S salicylates, sympathomimetics
A anticholinergics, antidepressant
• Hypotension (CRASH)
C clonidine
R reserpine
A antidepressants
S sedative hypnotics
H heroin (opiates)
• Hypertension (CTSCAN)
C cocaine
T theophylline
S sympathomimetics
C caffeine
A anticholinergics, amphetmine
N nicotine

22. Toxic Physical Findings
• Miosis (COPS
C cholinergics, clonidine
O opiates,
organophosphates
P phenothiazines,
pilocarpine, pontine
hemorrage
S sedative hypnotics
• Midriasis (AAAS)
A antihistamines
A antidepressants
A anticholinergics,
atropine
S sympathomimetics
(amphetamine)
• Seizures
Organophosphates
TCA
Insulin
Sympathomimetics
Camphor
Cocaine
Amphetamine
Theophylline
Beta blockers
Lithium
Lead
Lidocaine

23. TOXIDROMES
Opioids
• Triad: respiratory
depression, PPP,
decreased level of consc
• Bradycardia,
hypotension,
hypothermia
Cholinergics:
carbamate and
organophosphate
• SLUDGE
• Seizures, coma
• Muscle fasciculations
• Miosis
Serotonin Syndrome:
fluoxetine,
trazadone,
meperidine
• Irritability, agitation, altered mental
status
• Hyperreflexia, tremor, myoclonus,
trismus
• Ataxia, incoordination
• Flushing, diaphoresis, fever
• Diarrhea
Extrapyramidal:
haloperidol,
phenothiazines
• Rigidity, tremor
• Opisthotonus, trismus
• Choreoathetosis
• Hyperreflexia

24. EXAMPLE 1
• Acute Phenothiazine Toxicity
– Blocking dopamine, alpha-adrenergic, serotonin
receptors
– In cases of hypotension unresponsive to fluids,
alpha-adrenergic (norepinephrine) can be given
but……
– Dopamine (α & β adrenergic stimulator) if given
will exaggerate hypotension because of
stimulation of β receptors while α-receptors are
blocked by phenothiazines

25. EXAMPLE 2
• Scorpion Sting
Scorpion Venom Epinephrine & NE &
Angiotensin II
α- receptor stimulation
Hypertension
selective alpha-blocker (prazocin)

26. 1. TOXICOLOGY SCREENING
2. ESSENTIAL CLINICAL
LABORATORY TESTS
INVESTIGATION
S

27. • Quantitative serum levels of
Acetaminophen, Salicylates, Digoxin, Iron,
Lithium, Methanol, Theophylline,
Phenobarb, Ethylene glycol may influence
therapy.
– Toxico screening provides direct evidence of
ingestion, but must not affect initial
management (first 6-8 hrs) and should not
await results.
– The management must depend mainly on the
clinical status and available lab studies
Toxicology
Screening

28. TOXICOLOGY SCREENING
Comprehensive blood and urine screening is of little
practical value in the initial care of the poisoned patient.
On the other hand, specific toxicologic analyses and
quantitative levels of certain drugs may be extremely
helpful.
Urine and gastric specimens are the best samples for
broad qualitative screening.
Blood samples should be saved for possible quantitative
testing, but blood is not a good specimen for screening for
many common drugs, including psychotropic agents,
opiates, and stimulants.

29. LIMITATIONS OF TOXICOLOGY
SCREENS1. Comprehensive toxicology screens may look
specifically for only 40–50 drugs out of more
than 10,000 possible drugs or toxins (or 6
million chemicals).
• However, these 40–50 drugs account for more than 80% of
overdoses.
2. The time factor for reading toxicology
screening is very long .
3. If the initial urine screen is done too soon
after ingestion. The drugs found on the
screen may not be responsible for the
symptoms seen, especially if the drugs are
not quantitated.

30. DRUGS COMMONLY INCLUDED IN A
COMPREHENSIVE URINE SCREEN
Alcohols
1. Acetone
2. Ethanol
3. Isopropyl alcohol
4. Methanol
Analgesics
1. Acetaminophen
2. Salicylates
Anticonvulsants
1. Carbamazepine
2. Phenobarbital
3. Phenytoin
4. Primidone
Antihistamines
1. Benztropine
2. Chlorpheniramine
3. Diphenhydramine
4. Pyrilamine
5. Trihexylphenidyl
Opiates
1. Codeine
2. Dextromethorphan
3. Hydrocodone
4. Meperidine (Pethidine)
5. Methadone
6. Morphine
7. Oxycodone
8. Pentazocine
9. Propoxyphene

31. DRUGS COMMONLY INCLUDED IN
A COMPREHENSIVE URINE
SCREENPhenothiazines
1. Chlorpromazine
2. Promethazine
3. Thioridazine
4. Trifluoperazine
Sedative-hypnotic drugs
1. Barbiturates
2. Benzodiazepines
3. Chloral hydrate
4. Glutethimide
5. Meprobamate
6. Methaqualone
Stimulants
1. Amphetamines
2. Caffeine
3. Cocaine and benzoylecgonine
4. Phencyclidine (PCP)
5. Strychnine
Tricyclic antidepressants
1. Amitriptyline
2. Desipramine
3. Doxepin
4. Imipramine
5. Nortriptyline
6. Protriptyline
Other drugs
1. Diltiazem
2. Lidocaine
3. Procainamide
4. Propranolol
5. Quinidine and quinine
6. verapamil

32. DRUGS COMMONLY INCLUDED
IN A COMPREHENSIVE BLOOD
SCREENAlcohols
• Acetone
• Ethanol
• Isopropyl alcohol
• Methanol
Analgesics
• Acetaminophen
• Salicylates
Anticonvulsants
• Ethosuximide
• Carbamazepine
• Phenobarbital
Sedative-hypnotic drugs
• Barbiturates
• Diazepam
• Ethchlorvynol
• Glutethimide
• Meprobamate

33. Investigations1. CBC
2. LFT
3. RFT
4. Electrolytes, CPK
5. Blood Sugar
6. Arterial Blood Gas
– CO, MetHgb, Cyanide toxicity
– Respiratory or metabolic acidosis Example (Salicylates)
7. Urinalysis
– Ferric chloride test for salicylates
– Ketones ( salicylates, ketoacidosis )
– Calcium oxalate crystals (ethylene glycol and oxalic acid )

34. EXAMPLE: Potassium
Changes
Hyperkalemia
Alpha-adrenergic agents
Digitalis glycosides
Fluoride
Lithium
Potassium
Renal failure
Hypokalemia
Barium
Beta-adrenergic drugs
Caffeine
Diuretics (chronic)
Epinephrine
Theophylline
Toluene (chronic)
Salicylates

35. Osmolal Gap
OG = (measured serum osmolality) –
(calculated osmlality)
 Calculated osmolality: [2(Na+) + (Glucose/18) +
(BUN/2.8)].
 Normal Serum osmolality is 285-300 mOsm/kg.
 Normal osmolal gap is 8-12 mOsm/kg.
 Elevation due to presence of unmeasured, low-
molecular weight molecules that are osmotically
active:
 Methanol
 Ethylene glycol
 Diuretics, such as glycerol, manitol, sorbitol
 Isopropanol
 Ethanol

36. Anion Gap
• AG is an indirect measure of phosphates,
sulfates, & organic acids.
Na + unmeasured cations = (Cl + HCO3) + unmeasured anions
Na – (Cl + HCO3) = unmeasured anions – unmeasured cations
Anion gap = (Na ) – (Cl + HCO3)
• Normal anion gap is 12-16 mEq/L.

37. a. An elevated anion-gap acidosis is usually caused by an
accumulation of lactic acid but may also be caused by other
unmeasured acid anions such as formate (eg, methanol poisoning) or
oxalate (eg, ethylene glycol poisoning).
b. In any patient with an elevated anion gap, also check the osmolar
gap; a combination of elevated anion and osmolar gaps suggests
poisoning by methanol or ethylene glycol.
Note: Combined osmolar- and anion gap elevation may also be seen
with severe alcoholic ketoacidosis and diabetic ketoacidosis.
c. A narrow anion gap may occur with an overdose by lithium,
bromide, or nitrate, all of which can increase the serum chloride
level measured by some laboratory instruments.

38. • Causes of high anion gap
metabolic acidosis:
excessive acid production or with addition of exogenous
acids:
– Carbon monoxide, Cyanide.
– Alcoholic ketoacidosis
– Toluene
– Methanol
– Uremia
– Diabetic ketoacidosis
– Paraldehyde, Phenformin
– Iron, Isoniazid
– Lactic acidosis
– Ethylene glycol
– Salicylates

39. Causes of low anion gap with acidosis
• Acetazolamide
• Amiloride
• Ammonium chloride
• Amphotericin B
• Bromide
• Iodide
• Lithium
• Polymyxin B
• Spironolactone
• Toluene

40. Oxygen Saturation Gap
• The difference between the oxygen saturation
calculated from routine blood gas analysis and the
oxygen saturation measured by pulse oximetry.
• Others use this term for the difference between the
calculated oxygen saturation from a standard blood gas
machine and the measured value from a co-oximeter.
• An oxygen saturation gap is present when there is more
than a 5% difference.
• Causes of elevated oxygen saturation gap include
– carbon monoxide
– Methemoglobinemia
– hydrogen sulfide
– Cyanohemoglobin does not result in this finding. Although
cyanide poisoning may result from smoke inhalation, it is
not associated with an oxygen saturation gap, but rather
with an elevated serum lactate and a severe metabolic
acidosis.

41. PREVENTION OF FURTHER
ABSORPTIONA- Dermal Exposure
• Remove all clothing.
• Washing skin gently with soap and water for at least 30 minutes.
• Forceful washing may damage skin and promotes further
absorption.
• Protection of medical staff
B- Eye Exposure
• Washing conjunctiva with running water or normal saline for 20
minutes. Solid corrosives should be removed by forceps.
C- GIT Exposure
Gastrointestinal Decontamination Intestinal Decontamination
Induction of emesis
Gastric lavage
Activated Charcoal
Activated charcoal
Cathartics
Whole bowel irrigation

42. INDUCTION OF EMESIS
Syrup Ipecac
• The only safe method for induction of
vomiting. Poison Treatment in the Home. Pediatrics 2003;112;1182
 From the root of Cephalus Ipecachuana: emetine &
cephaline
 Early phase: within 30 minutes by direct GIT stimulation.
 Late phase: after 30 minutes through action on CTZ.
 Dose: Adults: 30 ml; 15 ml for children more than 2 Yrs,
5-10 ml for children 6 months to 2 yrs. Not more than 2
doses
 If emesis does not occur within 30 minutes, move around
the patient, if no emesis a second dose can be given.
• Syrup of ipecac should no longer be used routinely as a
poison treatment intervention in the home.

43. INDUCTION OF
EMESISContraindications
1.Convulsions.
2.Corrosives.
3.Hydrocarbons.
4.Sharp objects (e.g. needles).
5.Coma or impending coma
6.Decreased gag reflex.
7.Severe CVS disease or respiratory distress or
emphysema.
8.Recent surgical intervention.
9.Hemorrhagic tendencies (varices, active peptic ulcer,
thrombocytopenia).
10.Previous significant vomiting (spontaneously).
11.Less than 6m of age (not well developed gag reflex).

44. GASTRIC LAVAGE• used in hospitals when emesis was failed or
there was contraindication for it.
• Gastric lavage is effective in the first 4-6 hrs
after ingestion.
Technique:
1. An assistant with suction machine should be
available.
2. Dentures, mucous, vomitus should be
removed from patient's mouth.
3. Proper tube size to be selected according to
the patient age.

46. Complications:
1. Bradycardia, especially, in cases of organophosphate or digitalis
toxicity.
2. Laryngospasm and cyanosis.
3. Vomiting & Aspiration pneumonia.
4. Stress reaction that may cause hypertension, and or
tachycardia.
5. Hyponatremia, if tape water is used in children.
6. Mechanical gut injury.
7. Faulty introduction of the tube in the trachea
Contraindications:
• Absolute contraindications:
1. Corrosives
2. Froth producing substances as shampoo or liquid soap.
3. Oesophageal varices or peptic ulcer
• Relative contraindications
1. coma.
2. Convulsions.
3. Petroleum distillates.

47. ACTIVATED CHARCOAL
• Adsorption of a wide variety of drugs
and chemicals.
• It is not digested; it stays inside the
GI tract and eliminates the toxin
when the person has a bowel
movement.
• Adult dose is 1 gm/kg.

48. Substances not adsosorbed by AC
1. Corrosives
2. Alcohols
3. Cyanide
4. Oils
5. Glycols
6. Metals (Iron, Lithium, Lead, Mercury,..)
7. Petroleum distillates
8. Sodium chloride
9. Sodium hypochlorite bleach

49. ACTIVATED CHARCOAL
Contraindications
1) Coma
2) Intestinal obstruction.
3) Corrosives
4) If an oral antidote is given
5) Hydrocarbons

50. Multiple-dose Activated Charcoal
• Multiple-dose activated charcoal is defined as the
administration of more than 2 doses of activated
charcoal in the treatment of a given poisoning
• The recommended indications for the use MDAC are:
(1) the patient has ingested a potentially life-
threatening amount of carbamazepine, dapsone,
phenobarbital, quinine, or theophylline
(2) in the clinical judgment of the clinician the benefits
outweigh the risks
(3) alternative methods of treatment are not effective.

51. CATHARTICS (laxatives)
These are substances that enhance the passage of
material through GIT and decrease the time of
contact between the poison and the absorptive
surfaces of the stomach and intestine.
a) Osmotic cathartics: increase osmotic pressure in
the lumen, as Mg sulfate.
b) Irritant cathartics: act by increasing motility,
such as caster oil.
Contraindications:
• GIT hemorrhage.
• Recent bowel surgery.
• Intestinal obstruction.
• Renal failure for magnesium salts.

52. WHOLE BOWEL IRRIGATION
The goal of WBI is to clean GIT from nonabsorbed ingested toxins.
Polyethylene glycol electrolyte solutions are used, should be
administered by gravity.
Indications
• Ingestion of a toxin that is known to be poorly adsorbed by A
charcoal.
• Ingestion of massive amounts of drugs / impractical AC
• Ingestion of sustained-release or enteric-coated preparations
(e.g. aspirin)
• Removal of ingested packets of illegal drugs (body packers).
• Ingestion of large amount of drugs that may form concretions
or bezoars
• Treatment of suspected drug concretion
– Continual rise in measurable toxin concentrations despite charcoal
administration).
– Drugs that may form concretions: Salicylates, Barbiturates,
Carbamazepine, Enteric coated or sustained release tablets,
Meprobamate.

53. ANTIDOTE
S

54. DEFINITION
• according to
– International Programme on Chemical Safety
– United Nations Environmental Programme
– WHO
A THERAPEUTIC SUBSTANCE USED TO
COUNTERACT THE TOXIC ACTION(S) OF A
SPECIFIED XENOBIOTIC

55. ANTIDOTES Classification
According
to mode
of action
1- Physical
2- Chemical
3- physiological
According to mechanism of
action
1- Interacts with the poison to form a
nontoxic complex that can be excreted
e.g. chelators
2- Accelerate the detoxification of the
poison: N-acetylcysteine, thiosulfate.
3- Decrease the rate of conversion of the
poison into its toxic metabolites:
Ethanol, Fomepizole.
4- Compete the poison for certain
receptors: Naloxone.
5- Block the receptors through which the
toxic effects of the poison are mediated:
atropine
6- Bypass the effect of the poison: O2
treatment in CO and cyanide toxicity.
7- Antibodies to the poison: digiband,
antivenoms.

56. 1- Physical Antidotes
Agents used to interfere with poisons
through physical properties, not change
their nature
a) Adsorbing: the main example is
activated charcoal.
b) Coating: a mixture of egg & milk makes
a coat over the mucosa. It can be
effective in corrosives, but not in cases
of organophosphate. It decreases
efficacy of AC.
c) Dissolving: 10% alcohol or glycerine for
carbolic acid.

57. 2- Chemical Antidotes
a) Oxidizing: Amyl Nitrite is used in cyanide toxicity.
b) Reducing:
• Methylene Blue: it is used with MetHb producers:
nitrates, nitrites, phenacetin, chlorates,
sulfonamides.
• Vitamin C: used for drugs causing Met-Hb.
c) Precipitating:
• Starch: it makes blue precipitate with iodine. 50
gm in glass water.
• Egg albumin, gelatin, skimmed milk: in mercury
but should be rapidly washed as the precipitate
dissolves in excess albumin.

58. 3- Physiological (Pharmacological)
Antidotes
a) Antagonism
1- Competitive Antagonists
Naloxone:
Naltrexone: Opiate dependence; longer action with
affinity for mu receptors.
Flumazenil: antagonist for benzodiazepines
Atropine: organophosphate, carbamate, and other
parasympathomimetic (pilocarpine, muscarine). It is
used as antidote to correct bradycardia caused by
morphine, digitalis, aconitine, β-blockers, and calcium
channel blockers.
.

59. 2) Non-Competitive Antagonism
Anticonvulsants: for treatment of convulsants.
Calcium gluconate: used for:
a) Calcium channel blockers especially verapamil.
b) Black widow spider bite.
c) Lead colic
d) Oxalic acid.
Pralidoxime (2-PAM): ChE activator by breaking the
alkylphosphate-ChE bond. It is used in organophosphate
toxicity to form an oxime-phosphate complex and leaves
the ChE enzyme activated. Contraindicated in carbamate
toxicity because of short duration of action.
Diacetyl Monoxime (DAM): same action as PAM with more BBB
penetration and reactivation of ChE in CNS.
Physostigmine: counteract the anticholinergic effects such as
in severe atropine or TCA toxicities.

60. b) Chelating Agents:
Unite metallic poisons to form soluble, nonionizable, less toxic, and
easily excreted chelates.
1- Dimercaprol (BAL)
• prototype chelator (bisulfide molecule)
• removes intracellular and extracellular lead
• lipid-soluble drug and must be administered IM only
• It has the typical sulfide odor and patients often complain of the taste
• It is the first chelator used in encephalopathic individuals. Rapidly
crosses the BBB.
Adverse effects
fever, pain at the injection site, nausea, vomiting, headache, and
sterile abscess formation. It is recommended to alkalinize urine as
the chelate may dissociate in acidic urine.
Indications:
Lead, Arsenic, inorganic Mercury, Copper, Gold.
Contraindications:
a) Liver failure as metallic chelate is excreted mainly through the bile.
b) G6PD deficiency.
c) Transtoxicity or concurrent iron supply.
d) Organic Mercury; risk of neurotoxicity.

61. 2- Calcium disodium edentate (Ca Na2 EDTA)
• Unites with the metal which takes place of its calcium.
• It is water soluble and may be used IM or IV
• It allows extracellular lead to be renally eliminated
• In cases of lead encephalopathy, BAL should be given first
to avoid redistribution of lead mobilized by CaNa2EDTA to
CNS.
•
3- D-Penicillamine: Hydrolysis product of penicillin
approved for the treatment of Wilson disease and
cystinosis. Effective orally and has few adverse effects.
• a) It can chelate lead even in low blood levels.
• b) It is effective in children with blood levels 20-40
µg/100ml.

62. 4- Succimer (Di-Mercapto Succinic Acid; DMSA)
The best for lead chelation in children with a lead level
higher than 45 µg/dL. An effective oral chelator that
approaches the effect of both CaNa2EDTA and BAL.
5- Dimerval (DMPS)
Has become antidote for most heavy metal
intoxications. In the oral form and in a water-based
parenteral form.
6- Cobalt edetate (Kelocyanor)
Cobalt compounds directly chelate cyanide, thus
reducing its toxicity, bypassing the formation of a
toxic (methemoglobin) intermediate. Kelocyanor is
thought to work faster than any of the MetHb-
formers.

63. N-Acetyl Cysteine (NAC):
Antidote in acetaminiophen toxicity:
1-Precursor for glutathione. NAC is converted to cysteine,
which can replenish glutathione stores.
2- NAC also directly detoxifies acetaminophen toxic
metabolite to nontoxic metabolites.
3-NAC can provide a substrate for sulfation
a) Oral NAC: It is effective in preventing hepatotoxicity
regardless of the initial acetaminophen level if it is
started within 8 hrs of ingestion.
b) Intravenous NAC: IV administration of NAC is
recommended for selected patients, including those with
GIT bleeding or obstruction, potential fetal toxicity, or an
inability to tolerate oral NAC.

64. d) Antibodies (Immunology-based Antidotes)
1- Digoxin Specific Antibody Fragment (FAB fragments,
Digiband):
Life-threatening arrhythmias
Initial potassium level >5 mEq/l.
Digoxin SL >10 ng/mL at 6-8 h postingestion
Digoxin SL >15 ng/mL in an acute ingestion
Ingestion >10 mg in healthy adults or > 4 mg in childre
2- Polyvalent Snake Antivenom:
3- Scorpion Antivenom: Indications include:
a) All children and old patients presenting with any of
systemic manifestations.
b) Patients with CV disease.
4- Antibotulism Serum:

65. 4) Other Antidotes
a) Vitamins
Vitamin K:
a) Agents causing hypoprothrombonemia: organic
arsenic, salicylates, coumarin.
b) Vitamin A toxicity: inhibits flora, antagonism of
hepatic action of vit K.
Vitamin B12 (Hydroxycobalamin):
contains cobalt ion, able to bind to cyanide with
greater affinity than cytochrome oxidase to form
nontoxic cyanocobalamin that is excreted in
urine.
Glucagon:
is used in β-blocker poisoning to stimulate the β-
adrenergic nerves on a receptor different from
that occupied by the β-blocker.

66. Cyanide Antidote Kit
• Step I
Amyl nitrite & Sodium nitrite: induce
methemoglobinemia so that cyanide, with high
affinity for ferric iron (Fe3+), may attach to it to form
cyanomethemoglobin, rather than to the iron of the
cytochrome, thus restoring or allowing cellular
respiration
• Step II
Sodium Thiosulfate: detoxification of the formed
cyanomethemoglobin compound so that it can be
excreted. The presence of thiosulfate in the blood
allows rhodanese to detoxify Cyano-MetHb by
catalyzing the formation of thiocyanate, which is
nontoxic and rapidly excreted in the urine.

67. ENHANCEMEN
T OF
EXCRETION
OF ABSORBED
POISONS

68. Forced Diuresis
It is a simple method for some poisons.
It is effect is increase with manipulation of urine
pH.
It is efficient only in poisons with the following
properties:
 Substances excreted mainly by kidneys.
 Substances with low volume distribution.
 Substances with low protein binding.
Types:
1- Fluid Diuresis
2- Osmotic Diuresis: mannitol 10%, which is
excreted by renal tubules leading to increases
in its osmotic pressure

69. Manipulation of Urine pH
This method acts depending on the extent of
ionization (pKa)
a) Forced alkaline diuresis
b) Acid diuresis
It is uncommonly used method for certain
substances such as amphetamine. It is a
dangerous method because of the risk of
myoglobin precipitation in renal tubules.

70. Dialysis
by allowing toxic substances to pass through semi-
permeable membrane depending on the
concentration gradient. It is beneficial when
renal function is impaired. Dialyzable
substances for good results must have:
A) Low volume distribution.
B) Low molecular weight.
C) Low protein binding.
Examples for dialyzable substances: alcohols,
barbiturates, salicylates.
Examples for nondialyzable substances: opiates,
atropine, antidpressants.

71. a) Peritoneal dialysis
Acts by considering peritoneum as
semipermeable membrane.
Complications: intra-abdominal
bleeding, perforation of
abdominal organs, peritonitis,
dehydration or overhydration.
Contraindications: pregnancy,
abdominal hernia, or respiratory
distress.

72. b) Hemodialysis
The semipermeable membrane is a cellulose
bag (artificial kidney).
Indicated when the condition is deteriorating
despite proper treatment, or in toxicities
with potentially lethal blood levels.
Complications:
Hypotension.
Bleeding tendency (due to heparin).
Electrolyte imbalance.
Cross infections.
Muscle cramps.
Air embolism.

73. Hemoperfusion
Using equipment and vascular access similar to that for
hemodialysis, the blood is pumped directly through a
column containing an adsorbent material (either
charcoal or Amberlite resin). Systemic anticoagulation is
required, often in higher doses than for hemodialysis,
and thrombocytopenia is a common complication.
1. Because the drug or toxin is in direct contact with the
adsorbent material, drug size, water solubility, and
protein binding are less important limiting factors.
2. For most drugs, hemoperfusion can achieve greater
clearance rates than hemodialysis. For example, the
hemodialysis clearance for phenobarbital is 60–80
mL/min, whereas the hemoperfusion clearance is 200–
300 mL/min.

74. Contraindications:
Patients with coagulopathy.
Patients with uncorrected hypotension.
Complications:
Thrombocytopenia.
Hypocalcemia.
Hypoglycemia.
Hypotension.
Adsorption of therapeutic drugs.