1. Prep. By :
Dr.Alaa Eldeen Elmassry
Egyptian fellowship of internal medicine ( E.F.I.M.),
Palestinian board of internal medicine ( P.B.I.M. ),
Consultant internist
Head of the medical dept.,
Naser hospital.

2.  Recognize the epidemiology of drug
overdose?
 What are the different toxidrome pattern
seen in clinical practice?
 What are the general lines of therapy of
poisoned patient?
 Different specific poisoning that might face
in our practice.

3. 1-A 24-year-old male is brought to the
emergency department after taking cyanide in
a suicide attempt. He is unconscious on
presentation. What drug should be used as an
antidote?
A.A. Atropine
B.B. Methylene blue
C.C. 2-Pralidoxime
D.D. Sodium nitrite alone
E.E. Sodium nitrite with sodium thiosulfate

4. 2-Which of the following findings suggests an
opiate overdose?
A. Anion gap metabolic acidosis with a
normal lactate
B. Hypotension and bradycardia in an alert
patient
C. Mydriasis
D. Profuse sweating and drooling
E. Therapeutic response to naloxone

5. 3-A patient with metabolic acidosis, reduced
anion gap, and increased osmolal gap is most
likely to have which of the following toxic
ingestions?
A. Lithium
B. Methanol
C. Oxycodone
D. Propylene glycol
E. Salicylate

6. 4-Which of the following is true regarding drug
effects after an overdose in comparison to a
reference dose?
A. Drug effects begin earlier, peak earlier, and
last longer
B. Drug effects begin earlier, peak later, and last
longer
C. Drug effects begin earlier, peak later, and last
shorter
D. Drug effects begin later, peak earlier, and last
shorter
E. Drug effects begin later, peak later, and last
longer

7. 5-Which of the following statements
regarding gastric decontamination for toxin
ingestion is true?
A. Activated charcoal’s most common side effect is
aspiration.
B. Gastric lavage via NGT is preferred over
the use of AC in situations where therapeutic
endoscopy may also be warranted.
C. Syrup of ipecac has no role in the hospital setting.
D. There are insufficient data to support or exclude a
benefit when gastric decontamination is used more
than 1 h after a toxic ingestion.
E. All of the above are true.

8.  6-Which one of the following statements
regarding paracetamol overdose is false?
1. Metabolic acidosis with pH of <7.3 after
fluid resuscitation is an indication for liver
transplant
2. The first bag of NAC in treatment of
paracetamol overdose contains NAC
100mg/kg.
3. NAC has anti-oxidant property
4. Prognostic accuracy of Rumack-Matthew
nomogram decreases after 15hours
5. Paracetamol level is highest after 4 hours
after ingestion

9. Analysis of 2001 data from US poisoning centers
revealed the following statistics:
95 % caused minor or no effects
92 % were due to acute rather than chronic
ingestions
92 % involved a single substance
85 % were unintentional
59 % fatalities occurred in individuals aged 20
to 49
52 % occurred in children younger than 6 years
47 % involved pharmaceuticals

11. Adolf Hitler
Cyanide and gunshot simultaneously before capture

12.  Socrate (d. 399 BC) , Greek philosopher —
According to Plato, sentenced to kill himself
by drinking poison hemlock

13.  Is a former pediatric nurse who killed
somewhere between 11 and 46 infants and
children in her care.

14. British doctor acquitted in 1957 but suspected
of killing 163 patients via morphine and
barbiturates

15.  The Bhopal disaster (commonly referred to as
Bhopal gas tragedy) was a gas leak incident in
India , considered one of the world's worst industrial
catastrophes .
 The official immediate death toll was 2,259

16. When to suspect the poisoning ?
1.Rapid onset of symptoms like vomiting,
abdominal pain or depressed
consciousness.
2.Mass affection.
3.Psychiatric patients.
4.Specific toxic syndrome.

17.  Is often unreliable when provided by a
patient following intentional ingestion
 Knowledge of drugs prescribed for the
patient or the patient's family or friends
to which (s)he could have had access
 A thorough search of the exposure
environment should be conducted for
pill bottles or a suicide note

18.  The mental status, vital signs, and pupillary
examination are the most useful elements
and allow classification of the patient into
either a state of physiologic excitation or
depression
 Physiologic excitation, manifested by
central nervous system stimulation and
increased pulse, blood pressure, respiratory
rate and depth, and temperature, is most
commonly caused by anticholinergic,
sympathomimetic, or central hallucinogenic
agents, or by drug withdrawal states.

19.  Physiologic depression, manifested by
a depressed mental status, blood
pressure, pulse, respiratory rate and
depth, and temperature, is most
commonly precipitated by cholinergic
(parasympathomimetic),
sympatholytic, opiate, or sedative-
hypnotic agents, or alcohols

20.  Characteristic odors
 Pupillary findings
 Neuromuscular abnormalities
 Mental status alterations
 Skin findings
 Temperature alterations
 BP and heart rate alterations
 Respiratory disturbances

21. Odor Agent(s)
Acetone (fruity)
Ethanol, isopropyl alcohol,
chloroform, salicylates
Bitter almonds Cyanide
Garlic
Arsenic, organophosphates,
phosphorus, thallium, selenium
Mothballs Naphthalene, paradichlorobenzene
Kerosene Organophosphates, parathion
Freshly mown hay Phosgene
Rotten eggs Hydrogen sulfide
Wintergreen Methyl salicylate

22. Mydriasis
Sympathomimetics
Cocaine
Caffeine
Ephedrine
Amphetamines
Methylphenidate
Anticholinergics
Atropine
Scopolamine
TCAs
Antihistamines
Antiparkinson agents
Muscle relaxants
Antispasmodics
Phenothiazines
(some)
Plants (with
belladonna alkaloids)
Hallucinogens

23. Miosis
Opioids
Heroin
Morphine
Hydromorphone
Oxycodone
Hydrocodone
Codeine
Propoxyphene
Sedative-hypnotics
Barbiturates
Benzodiazepines
Organophosphate
insecticides
Carbamate insecticides
Pilocarpine
Edrophonium
Physostigmine
Sympatholytics
Clonidine
Oxymetazoline
Tetrahydrazoline
Antipsychotics
Miscellaneous

24. Nystagmus
Barbiturates
Carbamazepine
Phencyclidine
Phenytoin
Lithium
Ethanol
Toxic alcohols
Organophosphates
Strychnine
MAOIs
Serotonin syndrome

25. Cyanotic
Cyanide
Methemoglobinemia
Sulfhemoglobinemia
Hypoxemia

26.  Carbon monoxide
 Mushrooms
 Ethanol
 Scombroid fish poisoning
 Anticholinergic agents
 Antihistamines
 TCAs
 Atropine

29. Hypertension with tachycardia
Thyroid hormone
Anticholinergics
Drug withdrawal states
Organophosphates
Sympathomimetics

30.  MAOIs (foods with tyramine)
 Disulfiram reaction (early)
 Cholinergic agents
 Organophosphates
 Alpha-adrenergic agonists

31.  TCAs
 Theophylline
 Albuterol
 Toxic alcohols
 Beta-adrenergic agonists

32.  Barbiturates
 Beta-blockers
 Calcium-channel blockers
 Digoxin
 Cyanide
 Opiates

33. A toxidrome, or toxic syndrome, is a
constellation of clinical examination findings
that assists in the diagnosis and treatment of the
patient who presents with an exposure to an
unknown agent.
The toxicologic physical examination should
include documentation of vital signs, pupillary
diameter, skin findings (dry, flushed, or
diaphoretic), as well as the presence or absence
of bowel sounds and urinary retention.

34. There are five general toxidromes :
1.Sympathomimetic
2.Cholinergic
3.Anticholinergic
4.Opiate
5.Sedative hypnotic

35.  Hypertension
 Pyrexia .
 Pupillary dilatation,
 Diaphoresis
 Altered mental status.
Drugs that can cause this type of
toxidrome include : cocaine and the
amphetamines. vasopressors and β-
adrenergic agonists

36.  Bradycardia
 Respiratory depression due to paralysis
 Bronchoconstriction and bronchorrhea.
 Pinpoint pupils
 SLUDGE syndrome of salivation, lacrimation,
urination, defecation, gastrointestinal (GI)
distress, and emesis.
 Fasciculations and paralysis.
 Seizures and coma.
These agents include organophosphate
insecticides and nerve gases, as well as
carbamate pesticides.

37.  Tachycardia
 CNS effects include agitation, delirium, and
in severe cases, seizures.
 Mydriasis ,
 Dry , flushed skin
 Urinary retention
 Decreased intestinal motility.
Therapeutic agents that cause this toxidrome
include atropine, scopolamine, and
antihistamines.

38.  Respiratory depression and oxygen
desaturations
 Miosis
 Decreased GI motility, and
 Coma .
These agents include Morphine , Pethedin ,
Tramadol
Other agents that produce a similar toxidrome
include the imidazolines, including clonidine,
tetrahydrozoline, and oxymetazoline.

39.  Sedation or coma in the setting of
NORMAL vital signs.
 A common misconception is that ingested
benzodiazepines cause respiratory
depression.
 While this may be true in the setting of
intravenously administered
benzodiazepines, patients with a
benzodiazepine ingestion generally do not
develop respiratory compromise.

40.  Blood sugar : This test should be considered
one of the vital signs in the patient with
altered mental status.
 Chemistry (bicarbonate and the creatinine)
 Blood gases.
 Serum drug screen: In general, the studies
included on this panel include
acetaminophen, salicylate, and ethanol
concentrations. Some laboratories include a
tricyclic antidepressant (TCA) screen as
well.

41.  Rarely contributes to the management of the patient
◦ Amphetamines: commonly cross-reacts with over-the-
counter cold medications.
◦ Opioids: This assay frequently misses the presence of
the synthetic opioids such as fentanyl and meperidine
◦ Cocaine: This assay is not directed at the parent
compound which is very short lived
◦ Cannabinoids: its presence does not have any bearing
upon the diagnosis of intoxication.
◦ Benzodiazepines: detection of oxazepam; however,
some commonly used benzodiazepines (such as
lorazepam) don’t produce it and therefore often
missed by this screening

42.  Cardiac toxins tend to prolong the :
1. PR interval (reflecting nodal blockade)
2. The QRS (reflecting sodium channel
blockade)
3. The QT interval (potassium channel
blockade).

43.  May reveal radiodense material in the
stomach or gut in the following ingestions :
◦ Chloral hydrate
◦ Heavy metals
◦ Iron
◦ Phenothiazines
◦ Enteric-coated preparations
◦ Sustained-release preparations
(Goldfrank's Toxicologic Emergencies. 8th Ed. 2006:62)

44. 1- Prevention of absorption
Gastric lavage
Activated charcoal (AC)
Whole-bowel irrigation
Cathartics.
Ipecac syrup.
2- Increased elimination:
Forced diuresis
Urinary alkalinization
Hemodialysis and hemoperfusion
3- Antidote

45. Endoscopy
Surgery
Dilution

46. AC is an insoluble, nonabsorbable,
inert, fine carbon powder.
AC is often the only GI
decontamination measure needed
to treat an overdose.

47.  The greatest benefit from AC is seen
when it is administered within one
hour of ingestion, and when used AC
should be administered as soon as
possible after patient presentation.
 The decision to use AC is not
algorithmic and depends upon the
toxin ( BLAST ), the clinical status of
the patient, and the time since
ingestion.

48. AC administration is not recommended:
1. In patients who have ingested nonabsorbable
acidic or alkaline corrosives (hydrochloric or
sulfuric acid)
2. Pt who require endoscopy because charcoal
will obstruct the view of the endoscopist.
3. In patients who have ingested low-viscosity
hydrocarbons (eg, gasoline, kerosene, liquid
furniture polish) and who are at high risk for
aspiration.
4. If the agent ingested is not bound by
charcoal.

49. Corrosives Arsenic
Acids Lead
Alkali Mercury
Hydrocarbons Iron
Alcohols Sodium
Acetone Calcium
Ethanol Potassium
Ethylene glycol Magnesium
Isopropanol Fluoride
Methanol Iodide
Essential oils
Drugs not absorbed by AC

50.  Common side effects include:
 Nausea , vomiting, abdominal cramps,
and diarrhea, particularly when the
drug is used with sorbitol .
 Aspiration
 Constipation
 Mechanical bowel obstruction

51.  Dose — The recommended dose of
activated charcoal (AC) is 1 g/kg
 The usual single adult dose is 25 to 100 g
mixed with water and administered as a
slurry by mouth or nasogastric tube.
 Doses larger than 100 g are
not recommended in obtunded patients
due to the increased risk of vomiting
and aspiration.

52.  Routine use of gastric lavage in the
management of poisoned patients is not
recommended by the American Academy of
Clinical Toxicology or the European
Association of Poison Centres and Clinical
Toxicologists
 Controlled studies in animals and human
volunteers show that gastric lavage
decreases the absorption of ingested poison
by an average of 26 percent when performed
30 minutes after ingestion and 12 percent
when performed at 60 minutes

53.  Gastric lavage is less effective activated
charcoal (AC) in reducing the
absorption
 Gastric lavage in combination with AC
(administered either following lavage
or both before and after) is more
effective in reducing drug absorption
than AC given alone

54.  A corrosive agent (eg, strong alkali,
concentrated acids, such as hydrochloric or
sulfuric)
 Low viscosity hydrocarbons (eg, gasoline,
kerosene, liquid furniture polish)
 The patient has a depressed mental status and
tracheal intubation has not been performed
 There is a risk of hemorrhage or perforation
due to esophageal or gastric pathology or
recent surgery
 The patient is unable to cooperate with the
procedure

55. 1. Aspiration
2. Laryngospasm
3. Hypoxia and hypercapnia,
4. Esophageal and gastric erosions ,
bleeding, perforation
5. Inadvertent tracheal insertion and
pulmonary lavage,
6. Cardiac arrhythmias, cardiac ischemia,
7. Pneumothorax,
8. Fluid and electrolyte imbalances, and
9. Hypothermia

56.  Syrup of Ipecac (SOI), which is derived
from the dried rhizome and roots of the
ipecacuanha, induces emesis in more than
90 percent of overdose patients with a mean
time of onset of 20 minutes
 Ipecac should NOT be administered
routinely in the management of poisoned
patients since there is no evidence from
clinical studies that it improves important
outcomes

57.  Refers to the enteral administration of a
polyethylene glycol balanced electrolyte
solution (PEG-ELS) in order to rapidly
cleanse the gastrointestinal (GI) tract of its
contents and prevent intoxicant absorption.
 An effective means of GI decontamination
following ingestion of drug packets,
sustained-release or enteric-coated
preparations, or agents not well adsorbed by
activated charcoal (AC).

58.  Isosmotic high molecular weight
polyethylene glycol (PEG-3350) electrolyte
lavage solution is administered by mouth or
nasogastric tube at a rate of 2 L per hour in
adults until the rectal effluent is clear;
volumes required to accomplish this vary
from 5 to 50 L
 Complications — Abdominal cramps,
bloating, nausea, vomiting, and aspiration
pneumonitis

59.  Cathartics are intended to decrease poison
absorption by enhancing rectal evacuation
of the poison-activated charcoal complex.
 Two types of osmotic cathartics are used to
treat poisoned patients:
1. Saline cathartics (eg, magnesium citrate,
magnesium sulfate, sodium sulfate).
2. Saccharide cathartics (eg, sorbitol,
mannitol).

60. Recommended adult doses of commonly used
agents are:
 1 g/kg (1 to 2 mL/kg) of 70 percent
sorbitol (0.9 g/mL)
 4 mL/kg or 250 mL of magnesium citrate
 250 mg/kg or 15 to 20 g of magnesium
sulfate

61.  Dilution is recommended following the
ingestion of acidic or alkaline corrosives
 Dilution must be performed within minutes
of exposure to be effective and does not
prevent the absorption of poison.
 The recommended volume for adults is up
to 5 mL/kg or 250 mL of water or milk.

62. Antidote administration is appropriate
when:
1. There is a poisoning for which an
antidote exists.
2.The actual or predicted severity of
poisoning warrants its use.
3.Expected benefits of therapy outweigh
its associated risk.
4.there are no contraindications.

63. Poison/syndrome Antidote(s) Adult dose
Acetaminophen
N-acetylcysteine (Mucomyst 20
percent)
Initial oral dose: 140 mg/kg, then 70
mg/kg q 4 h x 17 doses
Anticholinergic
agents
Physostigmine (Antilirium)
Initial dose: 0.5-2.0 mg slow IV over
3-5 min
Benzodiazepines Flumazenil (Romazicon)
Initial dose: 0.1-0.2 mg IV over 30-60
sec, repeat 0.1-0.2 mg IV every minute
prn up to 1.0 mg
Beta-blockers
1) Glucagon
1) Initial dose: 5-10 mg IV bolus, then
2-10 mg/hr IV infusion
2) Calcium
2) Calcium chloride 10 percent: 1 gm
(10 cc) IV; repeat as necessary
3) Insulin + dextrose
3) Insulin load: 0.5 units/kg IV bolus,
then 0.5-1.0 U/kg/h IV
Dextrose 10 percent IV infusion (with
KCl) - titrate to euglycemia
Calcium-channel
blockers
1) Calcium
1) Calcium chloride 10 percent: 1-4 gm
(10-40 cc) IV; repeat as necessary
2) Glucagon
2) Initial dose: 5-10 mg IV bolus, then
2-10 mg/hr IV infusion
3) Insulin + dextrose
3) Insulin load: 0.5 units/kg IV bolus,
then 0.5-1.0 U/kg/h IV

64. Carbon monoxide Oxygen ± hyperbaric chamber
100 percent oxygen by ventilator or
NRB; high-flow oxygen by tight-
fitting facemask
Crotalid snakebite
Wyeth polyvalent crotalidae antivenin
(equine)
Mild: 3-5 vials; moderate: 6-10 vials;
severe: 10-20 vials
Mix reconstituted antivenin in 1000 mL
NS over 4-6 hours
Cyanide
1) Amyl nitrate pearls
1) One ampule by inhalation for 15 sec
every 3 min until IV access
2) Sodium nitrite (3 percent solution) 2) 10 mL (300 mg) IV over 3 min
3) Sodium thiosulfate (25 percent) 3) 50 mL (12.5 g) IV over 10 min
Digitalis Digoxin immune Fab (Digibind)
1) (# mg ingested x 0.8) ÷ 0.6 = #vials
needed
2) (Dig concentration [in ng/mL] x 5.6 x
kg [weight]) ÷ 600 = #vials
3) Empiric dose: 10 vials (acute
poisoning); 1-3 vials (chronic)
4) Reconstitute Digibind in NS and
administer IV over 5-30 min
Ethylene glycol
Methanol
1) Ethanol 10 percent in D5W ±
hemodialysis
1) Initial load: 10 mL/kg IV of 10 percent
ethanol over 30 min, then 1.5 mL/kg IV
infusion (titrate drip to serum ethanol 100
mg/dL); double to triple infusion during
hemodialysis
2) Fomepizole [4-MP] (Antizol) ±
hemodialysis
2) Initial load: 15 mg/kg IV over 30 min,
then 10 mg/kg every 12 hours IV over 30

65. Poison/syndrome Antidote(s) Adult dose
Heparin Protamine sulfate
1 mg neutralizes 90-115 U heparin; Initial
dose: 1 mg/min to total dose 200 mg in 2
h
Iron Deferoxamine (Desferol)
15 mg/kg/h IV infusion until urine color
clears or patient clinically well (not to
exceed 6 gm/24 h)
Isoniazid Pyridoxine (Vitamin B6)
Initial dose: 1 gm pyridoxine for every gm
INH ingested or empiric 5 gm IV over 10
min if amount ingested unknown
Lead
2,3-dimercaptosuccinic
acid [DMSA] (Succimer);
100 mg cpsl
30 mg/kg po in three divided doses x 5
days, then 20 mg/kg in twice daily doses x
14 days; repeat therapy prn after 2 week
rebound
Mercury
Arsenic
Gold
British antilewisite,
dimercaprol (BAL); in
peanut oil
Initial dose: 4-6 mg/kg IM every 4-6 h x 2
days

66. Methemoglobinemia
Methylene blue (1
percent solution)
Initial dose: 1-2 mg/kg (0.1-0.2
mL/kg) IV over 5 min; repeat prn
Opiates
Naloxone (Narcan)
Nalmefene,
naltrexone
Initial dose: 0.1-2.0 mg IV push
(opioid dependent patients should
receive 0.1 mg IV every 30-60 sec until
clinical response); synthetic opiates
may need up to 10 mg for initial
reversal dose
Organophosphates
Carbamates
Nerve agents
1) Atropine
1) Initial dose: 0.5-2.0 mg IV; repeat q
3-5 min until sweat and secretions
clear
2) Pralidoxime [2-
PAM] (Protopam)
2) Initial dose: 1 gm IV over 15 min,
then IV infusion of 3-4 mg/kg/h for
24-72 hrs or until clinical toxicity
resolves
Sulfonylurea
Octreotide
(Sandostatin) +
dextrose
Initial dose: 50-100 mcg SQ or IV,
then 50 mcg q 12 h until euglycemia
maintained without supplemental
dextrose
Tricyclic
antidepressants
Sodium bicarbonate
(NaHCO3)
Initial dose: 1-2 ampules (50-100
mEq) IV push, then IV infusion to
maintain blood pH 7.45-7.55 and
PCO2 30 mmHg (Usual drip: 3≅
amps NaHCO3 in 1 L D5W infused
at 200-250 mL/h)

67. ◦ Patients who have taken an overdose as a
suicidal gesture should all receive a
psychiatric evaluation prior to discharge.
◦ In cases where the patient is stable and
asymptomatic, a brief period of
observation may be all that is necessary.
◦ In cases where potentially toxic agents
have been ingested, patients should be
monitored for 4 to 6 hours before
discharge.

68.  N-acetyl-para-aminophenol (APAP) is the leading
cause of toxicologic fatalities per year in the
United States, and
 APAP-induced hepatotoxicity is the most frequent
cause of acute liver failure
 APAP is often sold in combination preparations
together with nonsteroidal anti-inflammatory
drugs (NSAIDs), opiate analgesics, or sedatives
 In general, a dose of 150 mg APAP per kilogram is
the potentially toxic limit that requires therapeutic
intervention.

70.  Decreased glutathione stores (fasting,
malnutrition, anorexia nervosa, chronic
alcoholism, febrile illness, chronic
disease).
 P450 enzyme inducers (ethanol, INH,
phenytoin and other anticonvulsants,
barbiturates, smoking).

71.  First 24 hours—asymptomatic stage:
◦ Early symptoms are very nonspecific and
primarily related to the GI tract (nausea,
vomiting, anorexia).
◦ High-dose APAP can cause pallor or
lethargy in some patients.
◦ This initial phase is rare in symptoms
and patients appear pretty unremarkable.
◦ Always think of other coingestants if a
patient exhibits extreme vital sign
abnormalities or other significant
symptoms during the first 24 hours.

72. 24 to 48 hours—hepatotoxic stage:
◦RUQ tenderness is the most
common symptom.
◦Transaminitis, bilirubinemia, and
elevated PT/INR are also
common findings during the
second phase.

73.  2 to 4 days—fulminant hepatic failure stage:
Significant hepatic dysfunction develops
(i.e., a peak in hepatic enzyme elevation
along with jaundice, coagulopathy with high
risk of spontaneous bleeding, hypoglycemia,
anuria, and cerebral edema with coma or
even death).
 4 to 14 days—recovery stage: If stage 3 is
survived, the hepatic dysfunction usually
resolves over the following days/weeks.

74.  Assess airway, breathing, and
circulation (ABCs) and mental status.
 Especially in patients who are
nauseated or vomiting, the assessment
of mental status is crucial to intervene
with airway protection in time.

75.  Obtain an APAP serum level at 4 hours or
later after ingestion.
 Plot the APAP concentration on the
Rumack-Matthew nomogram.
 LFT—AST is a relatively sensitive
nonprognostic marker for hepatic injury.
 PT/INR, serum bicarbonate, blood pH,
serum lactate, renal function panel, and
serum phosphate level are the prognostic
markers for hepatic injury.

77. ◦ pH < 7.3 two days post ingestion Or ,
◦ All of the following: PT > 100, serum
creatinine > 3.3 mmol/L, severe hepatic
encephalopathy (grade III or IV).
Additional criterion
 Elevated serum phosphate levels > 1.2
mmol/L on days 2 to 4
 Arterial serum lactate > 3.0 mmol/L after
fluid resuscitation

78.  Gastric lavage is not useful in APAP
overdose; however, it may be indicated in
presence of certain other coingestants.
 Activated charcoal
 N-acetylcysteine (NAC)
NAC replenishes depleted GSH glutathione
stores.
It should be administered early (i.e., within 8
hours after ingestion) to prevent any liver
damage

79. ◦ Any patient after acute poisoning with a toxic
APAP level according to the nomogram.
◦ Patients who present more than 24 hours after
acute ingestion and still have a detectable
serum APAP level or elevated AST.
◦ Patients with chronic APAP exposure (i.e., >4
g/d in adults, > 120 mg/kg/d in children) who
present with elevated transaminases.
◦ Patients with signs of fulminant hepatic failure.

80. ◦ Oral dosing: Loading dose of 140 mg/kg PO,
then 70 mg/kg PO every 4 hours for a total of 17
doses (i.e., 1,330 mg/kg over 72 hours).
◦ IV dosing ( 20 h protocol ) : Load with a dose of
150 mg/kg NAC IV over 1 hour. Then 50mg/kg
over 4hours then 100 mg / kg over 16 h
◦ IV dosing : as oral dosing ( 72 h protocol )
Treatment can be stopped when the serum
acetaminophen concentration is undetectable,
the ALT is clearly decreasing or in the normal
range, and the INR is less than two.

81.  Salicylate toxicity may result from acute or
chronic ingestion of acetylsalicylic acid.
 Toxicity is usually mild after acute
ingestions of <150 mg/kg, moderate after
ingestions of 150 to 300 mg/kg, and
generally severe with overdoses of 300 to 500
mg/kg.
 Toxicity from chronic ingestion is typically
due to intake of >100 mg/kg/d over a
period of several days

82.  Nausea, vomiting, tinnitus, tachypnea,
hyperpnea, and malaise are common.
 Hyperthermia
 Severe intoxications may include lethargy,
convulsions, and coma
 Noncardiogenic pulmonary edema may
occur and is more common with chronic
ingestion

83.  Obtain electrolytes, BUN, creatinine,
glucose, and salicylate concentration.
 ABGs may reveal an early respiratory
alkalosis, followed by metabolic acidosis.
 Serum salicylate concentrations
◦ Salicylate concentrations > 70 mg/dL at
any time represent moderate to severe
intoxication.
◦ Salicylate concentrations > 100 mg/dL are
very serious and often fatal.
 Imaging : may shows Salicylate concretions

84.  Administer 50 to 100 g AC if presentation is
within 1 hour of ingestion
 Alkaline diuresis is indicated for symptomatic
patients with salicylate blood concentrations
> 40 mg/dL.
Administer 150 mEq (three ampules) sodium
bicarbonate in 1,000 mL D5W at a rate of 10 to
15 mL/kg/hr (target urine pH, 7 to 8)
Give 40 mEq potassium chloride IVPB over 4
to 5 hours to maintain serum potassium
concentration above 4 mEq/L.

85.  Treat altered mental status with IV dextrose,
despite normal blood glucose.
 Treat cerebral edema with hyperventilation
and osmotic diuresis.
 Treat seizures with a benzodiazepine
(diazepam, 5 to 10 mg IV q15min up to 50
mg) followed by phenobarbital, 15 mg/kg
IV.
 Hemodialysis if : persistent acidosis, severe
CNS symptoms, progressive clinical
deterioration, pulmonary edema, or renal
failure.

86.  Organophosphates (OPs) are
commonly used as pesticides and
insecticides (e.g., parathion). Some of
them also have medical indications
(e.g., malathion in lice shampoo).
 In the developing world, OP and other
pesticide poisonings represent the
most common causes of death from
intoxications

87.  Inhibition of ACh breakdown through blocked
AChE leads to accumulation of ACh at
nicotinic and muscarinic receptors resulting in
excessive cholinergic stimulation
 Most OPs bind AChE initially in a reversible
way. Some OPs, however, become permanently
bound over time, a phenomenon known as
“aging.” If aging occurs, the only way to
overcome the inhibitory effect is for the body
to synthesize new enzyme.
 OPs are hepatically metabolized.

88.  The cholinergic toxidrome is a result of overstimulation
of nicotinic and muscarinic receptors
 Muscarinic effects:
◦ SLUDGE syndrome: Salivation, Lacrimation,
Urination, Diarrhea, GI cramping, Emesis.
◦ Bradycardia, bronchorrhea,
bronchoconstriction
◦ Other effects: miosis, diaphoresis.
◦ NOTE: intoxicated patients may present
with tachycardia instead of bradycardia due
to hypoxia (bronchoconstriction,

89. ◦ Ganglionic: tachycardia, hypertension,
diaphoresis, mydriasis.
◦ Neuromuscular: neuromuscular
depolarization, fasciculations, motor
weakness, paralysis with respiratory failure
(analogous to succinylcholine, which is
related to ACh).
◦ Central: confusion, agitation, lethargy,
seizures, coma.

90. Cholinesterase levels
relatively useless in assessing the
severity of exposure in acute
intoxications because of its wide
range of normal values.

91.  Remove patient from potential source of
poisoning.
 All clothing, especially leather, should be
removed from the patient and discarded in a
ventilated area
 Skin and hair decontamination requires
thorough irrigation with water and might be
enhanced through use of alcohol-based soaps.
 Ocular decontamination should be irrigated
with water only.
 Gastric lavage might be indicated in stable
patients who ingested contaminated fluids

92.  Is an Antimuscarinic agent which competes with
ACh for receptor binding
 GOAL: Atropinization, that is, drying of bronchial
secretions with normalized oxygen saturation (which
may require 10 to 100 times of usually common
atropine doses):
1. A heart rate > 80 bpm
2. A systolic BP > 80 mm Hg
The initial adult dose is 1 to 3 mg IV as a bolus. Then
titrate according to persistence of bronchorrhea by
giving the double of the previously used dose every 5
minutes until atropinization achieved

93.  forms a complex with OPs that are bound to
AChE. The pralidoxime-OP complex is then
released from the enzyme and thus regenerates
AChE function.
 Once the AChE bound OPs start aging,
pralidoxime is rendered ineffective. Therefore it is
crucial to start pralidoxime therapy early.
 Dose : 1 to 2 g of pralidoxime in 100 mL NS IV
over 20 minutes, then infusion of 500 mg/hr
 Cardiac and respiratory failure have been reported
after administration of pralidoxime

94. 1- Intermediate syndrome (IMS):
◦ This syndrome is a post-acute paralysis from
persistent ACh excess after the acute cholinergic
phase has been controlled.
◦ occurs hours to days after treatment of acute OP.
2- OP-induced delayed neurotoxicity (OPIDN):
◦ OPs also inhibit other neurotoxic esterases, resulting
in polyneuropathy or spinal cord damage due to
demyelination of the long nerve fibers.
◦ OPIDN usually occurs several days to weeks after
acute OP poisoning leading to temporary, chronic or
recurrent motor or sensory dysfunctions

95. Generally speaking,
benzodiazepines have a wide safety
margin so its overdose rarely
represent a medical problem.

96.  The typical presentation of a pure oral
benzodiazepine overdose is coma with
normal vital signs.
 Respiratory depression is exceedingly
unusual in oral overdose of
benzodiazepines.
 The differential diagnosis includes
barbiturate overdose, hypoglycemia,
ethanol intoxication, CNS, and other
metabolic causes of coma.

97.  Supportive care with observation is the
mainstay of therapy.
 In patients with co-ingestions and
respiratory depression, intubation and
ventilation may be required.
 Since this is a benign overdose, gastric
lavage and AC are not necessary.
 These interventions may cause aspiration in
an otherwise stable patient.

98.  Traditional recommendations include the use
of flumazenil; however, given the propensity to
precipitate seizures and acute benzodiazepine
withdrawal in patients on long-term
benzodiazepine therapy, this therapy should be
avoided.
 In special cases such as reversal of
iatrogenically induced respiratory depression,
reversal of sedation, flumazenil may be given
as a 0.1 mg/min dose intravenously.
 Repeat injections may be given as resedation
occasionally reoccurs.

99.  Multiple TCAs are on the market,
including Amitriptyline, Clomipramine,
Doxepin, Imipramine, Trimipramine,
Desipramine, Nortriptyline, and
Amoxapine.

100.  TCAs interact with a wide variety of receptors
with many consequent effects
 It has a:
1. Anticholinergic effect : dry mouth , urinary
retention, and GI motility and mydriasis.
2. Antihistaminic effect : sedation
3. Central sympatholytic effect : hypotension and
reflex tachycardia
4. Anti serotoninergic effect
5. Antagonism of CNS gamma-aminobutyric acid
(GABA) A receptors

101.  In one classic study, one-third patients
with a QRS of ≥100 milliseconds
developed seizures.
 Fifty percent of patients with a QRS of
≥ 160 milliseconds developed
ventricular dysrhythmias
 Prolongation of the QT interval.

102. After the patient's airway is protected, a dose
of AC 1 g/kg is warranted .
Sodium bicarbonate has been demonstrated
to narrow the QRS, A bolus of 1 to 2 mEq/kg
every 3 to 5 minutes ,continuous ECG
monitoring until the QRS narrows or the BP
improves.
Serial VBGs should be obtained with a goal of
maintaining the blood pH at 7.50 to 7.55.

103.  Norepinephrine is the pressor of choice in
hypotensive patients who do not respond to
alkalinization because of its direct effects on
the vasculature.
 Lidocaine may be considered in the presence
of ventricular dysrhythmias precipitated by
TCA toxicity. However, class Ia and Ic
antidysrhythmics are contraindicated in the
management of TCA-poisoned patients.
 Benzodiazepines are the mainstay of treatment
for seizures. Phenytoin should be avoided.

104.  The toxicity associated with an overdose of
β-blockers is largely due to the effects of
antagonism at catecholamine receptors.
 In general, selectivity is lost in overdose, so
bronchospasm may occur in the setting of
β1-selective antagonists.

105.  Patients with a significant ingestion of an
immediate-release product will exhibit signs
of toxicity within 6 hours.
 The exception to this rule is sotalol, which
in overdose, can have delayed toxicity and
prolonged effects
 With the exception of propranolol and
sotalol, β-blocker overdose in healthy people
tends to be benign, with significant number
of patients remaining asymptomatic after
ingestion

106.  Patients with significant ingestions present
with:
1. Bradycardia
2. CHF.
3. Patients with propranolol ingestions may
develop coma, seizures, and hypotension.
4. Propranolol overdoses have a high mortality
In patients with symptomatic bradycardia
also consider overdose of CCB, clonidine, or
digoxin.

107.  The ECG may reveal sinus bradycardia
or atrioventricular block.
 In propranolol ingestions, a wide QRS
manifesting sodium channel blockade
may be present.
 With sotalol, QTc prolongation may
appear as a delayed presentation and
torsades de pointes may develop.

108.  Patient should have an IV placed, and
continuous cardiac monitoring should be
instituted.
 Hypoglycemia should be treated with 50 mL
of 50% dextrose.
 Consider AC if patients present within 1
hour of ingestion.
 Intubation and ventilation should be
instituted in patients with altered mental
status.

109.  Atropine 1 mg IV may be given up to 3 mg for
symptomatic bradycardia; however, this is usually
ineffective as the bradycardia is not vagally
mediated.
 A fluid bolus of 20 mL/kg should be given and may
be repeated; monitor for the development of fluid
overload.
 Glucagon 2 to 4 mg IV may be given over 1 to 2
minutes. Then start infusion of 2 to 5 mg/hr—not to
exceed 10 mg/hr.
 Calcium gluconate 3 to 9 g IV may be given through
a peripheral line in patients with hypotension.

110.  Any patient with hypotension is a candidate
for high-dose insulin euglycemia therapy.
 This involves a bolus of 1 U/kg of regular
insulin, followed by an infusion of 0.5 to 1
U/kg/hr of regular insulin. This should be
accompanied by a dose of 50 mL of 50%
dextrose and a dextrose drip at 1 g/kg/hr of
dextrose.
 Glucose should be obtained every 30
minutes, and potassium levels should be
followed every 2 hours

111.  Catecholamines should be approached with
caution in these patients because α-
stimulation in conjunction with β-blockade
may precipitate acute heart failure.
 Therefore, hemodynamic monitoring should
be instituted with careful titration of
epinephrine at 0.02 mcg/kg/min or
norepinephrine at 0.1 mcg/kg/min.
 Isoproterenol at 0.1 mcg/kg/min may be
useful as well

112. QUESTIONS
??

113.  Most of poisoning events pass uneventfully without
significant harm.
 The most important clinical approach is to try to
classify the patients toxidromes
 ABCDE approach is the first priority in management
of poisoned pt.
 Gastric lavage is ineffective if done after one hour of
exposure.
 AC is an effective mode of decontamination but not
in all overdoses


114.  ECG is important investigation in poisoned
pat.
 Paracetamol poisoning is a common cause
of drug overdoses and is the most common
cause of acute hepatic failure in western
countries.
 The use of paracetamol nomogram is the
best mode to determine the need for NAC
use

115.  The goal of GOAL of Atropinization is
1. A heart rate > 80 bpm
2. A systolic BP > 80 mm Hg
but not dilated pupils.
 The classic presentation of Benzodiazepine
overdoses is sedation with normal vital signs


116. Thank you