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Prepared by Dr.Saira
PGR Medicine
Poisoning is a global issue occuring
all over the world involving people
of all ages and gender, from all
ethnic and economic backgrounds
More than 700,000 deaths
occur each year as a result of
poisoning!!!
General approach to a patient
with poisoning
…
 Quickly asses the potential danger.
 Consider decontamination to prevent
absorption.
 Treat complications if they occur.
 Observe the asymptomatic patients for
appropriate interval.
Asses the danger
 The drug to which person was exposed
 The amount ingested/degree of exposure
 The time since exposure
 The presence of any sign or symptoms
 Any premorbids
 Serum drug/toxin levels
In symptomatic patients,treatment
of life threatening complications
takes precedence over in-depth
diagnostic evaluation
1st and the foremost step is to stop
the further exposure of the patient.
Coma
Assesment and complications
Causative agents include
 Antihistamines
 Bezodiazepines
 Ethanol
 Opioids
 Anti-psychotic/anti-depressant drugs
Approach
 Airway
 Breathing
 Circulation
.. Drugs
Dextrose
In all comatose or convulsing patients give 50%
dextrose(in our hospital 25% is available),50-100
ml IV bolus unless a rapid bedside blood sugar
test is available.
Thiamine
In alcoholics/malnourished give thiamine 100mg
IM/IV.
 Nalaxone
..
0.4-2mg is empirically given to any comatosed
patient with depressed respiration.
Nalmefene,a newer opioid antagonist has a
duration of effect longer than nalaxone.
.. Flumazenil
0.2-0.5mg IV repeated as needed upto a
maximum of 3mg may reverse
benzodiazepine induced coma.Its use is not
commonly advised as the potential risks
outweight its benefits
Hypothermia
.. Hypothermia commomly accompanies
coma due to hypoglycemic agents,opioids
and other sedative-hypnotics.
 It may cause or aggravate hypotension.
 Gradual rewarming is usually preferred.
Hypotension
 Agents causing hypotension include carbon
mono-oxide,hydrogen sulphide,aluminium
phosphide,arsenic and many sedative-hypnotics.
 Empiric treatment with 200 ml boluses of 0.9%
normal saline upto a total of 1-2 litres.
 CVP guided fluids
 Inotropes
Hypertension
 Amphetamines,anti-cholinergics,cocaine
 Treat hypertension if patient is symptomatic
or diastolic BP >105-110 mmHg
 Sodiumnitroprusside,labetalol,phentolamin
e intravenously can be used.
Arrythmias
 Hypoxia,metabolic acidosis,or
electrolyte imbalance may trigger an
arrythmia.
 Treatment includes removal of
causative agent.If persists,amiodarone
or lidocaine etc can be used.
Seizures
 May be caused by a number of drugs and
metabolic disturbances.
 Administer 2-3mg lorazepam or 5-10mg
diazepam over 1-2min.
 If IV acess is not immediately available 510mg midazolam can be given
intramuscularly.
 For drug induced seizures phenobarbital is
preferred over phenytoin.
Hyperthermia
 Amphetamines,anticholinergic
agents,cocaine,salicylates,strychnine,TCA.
 Malignant hyperthermia with general
anesthetics and neuroleptic malignant
syndrome with antipsychotics.
 Remove clothings,spraying skin with cold
water,and fanning.
 Sedate,paralyze and place on mechanical
ventilation.
Decontamination
Decontamination of the skin /eyes
 Wash the affected areas with copious
amounts of lukewarm water or normal
saline
 For oily substances use soap/shampoo for
skin.
 For warfare agents use diluted hypochlorite
solution for skin.
Gastrointestinal decontamination
 Gastric lavage
 Activated charcoal
 Whole bowel irrigation
 Increased drug removal
• Urinary manipulation(alkalinization)
• Hemodialysis
• Repeat dose charcoal(gut dialysis)
ANTIDOTES
TOXINS
Antidotes
Toxic agent
Antidote
Acetaminophen
N-acetylcysteine
Anticholinergics
Physostigmine
Organophosphates
Atropine and pralidoxime
Benzodiazepines
Flumazenil
Carbon monoxide
Oxygen
Cyanide
Sodium nitrite
Digitalis glycosides
Digoxin specific Fab antibodies
Heavy metals
Chelating agents
isoniazid
Pyridoxine
Methanol
Ethanol
Opioids
Nalaxone
Snakebite
Anti-snake venom
Details of all the chemicals and
their antidotes can be seen in
MERCK index
https://www.rsc.org/merck-index
Diagnosis of poisoning
.. History may or may not be reliable.
 Physical examination
Blood pressure
Pulse
Temperature
Pupils
Sweating
Peristaltic activity
Sympathomimetic syndrome
 Blood pressure and pulse rate are elevated
 Temperature is raised
 Sweating with dry mucus membranes
 Agitated,anxious or frankly psychotic
Sympatholytic syndrome
 Blood pressure and pulse rate are low.
 Body temperature is reduced
 Pupils constricted or pinpoint
 Patient drowsy or comatosed
Cholinergic syndrome
 Bradycardia
 Miosis
 Sweating
 Bronchorrea
 Wheeze
 Excessive salivation
 Urinary incontinence
 Agitated and anxious
Anticholinergic syndrome
 Tachycardia
 Hypertension
 Raised body temperature
 Pupils widely dilated
 Skin hot flushed and dry
 Urinary retention
 Agitation/delirium
Laboratory tests
 Baselines
 Serum osmolality and osmol gap
 Electrolytes and anion gap
 BUN
 Urinalysis
 Electrocardiogram
 Abdominal radiographs
 Toxicology testing
When to admit?
..
 The patient has features that are not
expected to clear within 6-8 hours
observation period.
 Ingestion of delayed release preparations
 Continued administration of an antidote
is required
 Psychiatric or social services evaluation is
needed for suicidal attempt or suspected
drug abuse.
Observe the patient
 Asymptomatic or mildly symptomatic
patient should be observed for 4-6 hours.
 Longer observation is indicated if the
ingested substance is a sustained-release
preparation or is known to slow the
gastrointestinal motility or may cause a
delayed onset of symptoms.
Kala pathar intoxication
Introduction
 Paraphenylene diamine (PPD) has been
used internationally as a key ingredient in
different hair dye formulations to produce a
variety of shades depending on its
concentration.
PPD is used by women to color their
hair and as a dye when added to henna
(Lawasonia alba) to color the palms and soles
..
..
 Poisoning with Paraphenylene
Diamine (PPD) is emerging as an
important means of intentional self
harm in various developing countries
of Asia and Africa.
Mechanism of toxicity
 ParaphenyleneDiamine(PPD) is a coal-
tar derivative .
 On oxidation produces Bondrowski’s
base having allergenic, mutagenic and
highly toxic properties.
Systemic poisoning
Acute poisoning with PPD causes a
characteristic:
 Severe oedema of the face and neck
often requiring tracheostomy
 Swollen dry hard tongue.
..
..
 Chocolate brown color of the urine
 PPD intoxication is a multisystem
poison and can cause :
rhabdomyolysis,myoglobinuria and
acute renal failure (ARF)
..
 Asphyxia and respiratory failure are
the immediate threats to life under
such conditions.
 Endotracheal intubation, emergency
tracheostomy and ventilatory
assistance are needed.
..
 Shock is another important clinical
feature due to PPD
 Myocarditis, hypovolemia and sepsis
might be the underlying reasons for
severe hypotension.
 Myocardial injury and fatal cardiac
arrhythmias form the basis of sudden
cardiac death.
..
 Rhabdomyolysis and its consequences
(ARF, hyperkalemia, hypocalcemia,
hyperphosphatemia) are important
parameters predictive of mortality in the
syndrome of PPD intoxication.
 ARF form the basis of hyperkalemia.
 Hyperkalemia, with its arrhythmogenic
potential can also lead to sudden death.
..Intensive supportive care is the corner
stone of management.
..
Gastric lavage with saline and charcoal
oxygen
i/v fluids
diuretics
mannitol
Antibiotics
..
Inotropes(if hemodynamically unstable)
Steroids
Calcium gluconate
Sodium bicarbonate
Cardiac monitoring
Intake output monitoring
Methylene blue
Exchange transfusion
..
Consumption of amount, as low as 25ml
results in hepatitis. As there is no
specific antidote and the toxin is also
non-dialyzable, aggressive management
in collaboration with different
specialties is needed.
Formation of methaemoglobin
..
Use of methylene blue
Benzene poisoning
Introduction
 Benzene has been widely used as a
multipurpose organic solvent. This use is
now discouraged due to its high toxicity.
 Present uses include benzene as a raw
material in the synthesis of various
plastics and detergents.
 The tire industry and shoe factories use
benzene extensively.
.. Deaths from acute exposure to benzene
are often related to physical exertion
and release of epinephrine with
subsequent cardiac failure.
 Frequently, the person trying to rescue
a collapsed victim will die during the
effort of lifting the unconscious person
.
..
 Anesthesia may develop at concentrations
above 3,000 ppm
 At exposures of greater than 1,000 ppm
CNS symptoms include giddiness, euphoria,
nausea, and headaches; heightened cardiac
sensitivity to epinephrine-induced
arrhythmias may develop
.. Mild irritation to the eyes and mucous
membranes.
 Respiratory tract inflammation, pulmonary
hemorrhages, renal congestion, and cerebral
edema have been observed at autopsy in
cases of acute benzene poisoning .
.. People with existing hematologic disorders
may be more sensitive to the acute toxicity
of benzene to the bone-marrow.
 Females may be more sensitive to benzene
toxicity than males due to higher average
body fat content, which serves as a storage
reservoir for the chemical .
Management
 Oxygen
 Gastric lavage
 Nebulization
 Steroids
 PPI
 Sodium bicarbonate
 Fluids
 Intubation
 Methylene blue
 Exchange transfusions
Wheatpill
(aluminium phosphide)
poisoning
Introduction
 Wheat pill poisoning is a very serious but
unfortunately under-reported and underdiscussed problem.
 These pills are used as grain preservatives. In
wheat growing areas of Pakistan, these pills are
easily available over the counter without any
check or control on their sale.
Easy availability and no antidote,
makes it an ideal suicidal poison
..  .The spectrum of symptoms and
signs and their severity depends
upon the time lag between
aluminium phosphide ingestion and
hospitalisation.
 The reported in-hospital mortality
of aluminium phosphide poisoning
is 55-90%.
Mechanism of toxicity
They are available as tablets or
powder. Wheat pills mostly
contain aluminium phosphide
58% and inert ingredients 42%.
Phosphine is a very strong
reducing agent that inhibits
cellular enzymes involved in
several metabolic processes
..
 It cause ARDS and denaturing of
oxyhemoglobin.
 Local inflammation can cause gastritis
and esophagitis.
.. Less than 25% of patients are able to reach a
tertiary care hospitals.
only tip of the iceberg
Clinical presentation
 Patients with wheat pill poisoning
present typically with epigastric
pain, nausea, vomiting, cardiac
arrhythmias and cardiogenic shock.
 They worsen to develop severe
refractory hypotension and
metabolic acidosis.
…
 Most deaths occur within first 12-24
hours after exposure and are
cardiovascular in origin.
 After 24 hours usual cause of death is
liver failure.
.. Most common symptom seen in patients is
vomiting
 Most common sign is hypotension
Management
 As no antidote is available the
management of wheat pill poisoning
remains purely supportive.
 Aluminium phosphide can be
absorbed from exposed skin so
exposed skin and hair should be
flushed with water and then washed
with soap.
Protocol for wheatpill poisoning
 The protocol being mentioned here
has been circulated to all DHQs and
THQ s of Rawalpindi district by
Principal RMC and Allied hospitals.
 Maintain double IV line.
.. Keep NPO for 24-48 hours.
 Give fluids according to haemodynamic
status.
 Perform gastric lavage with edible oil 1-2
litres alongwith activated charcoal.
 Inj.Omeprazole 40mg stat then od
 Inj.mgs04 1gm iv stat then 1gm/hr for next 4
hours than 1 gm every 4 hourly for next 4872 hours.
 Inj.hydrocortisone 250mg iv stat then 100mg
….tds.
 Inj calcium gluconate diluted iv stat then od.
 Inj.amiodarone (if arrythmia).
 Vitals monitoring.
 Monitor with ECG and baseline labs.
 ICU care.
 Attendants counselling.
Organophosphate poisoning
Introduction
 Poisoning with organophosphorus
compounds (OP) is a global problem.
 World Health Organization estimates that
one million serious unintentional
poisonings occur every year and an
additional two million people are
hospitalized for suicide attempts with
pesticides.
..
Clinical presentation
 Muscarinic manifestations
Respiratory: Increased bronchial
secretions, bronchospasm, chest tightness,
dyspnoea, cough
Eyes: Blurred vision, conjunctival
injection, dimness of vision, miosis
Gastrointestinal: Cramping, diarrhea,
nausea, vomiting
..
Urinary: Incontinence
Cardiovascular: Bradycardia,
hypotension
Exocrine glands: Increased salivation
..
 Nicotinic manifestations
Muscle fasciculation, cramping,
weakness, diaphragmatic paralysis,
respiratory failure, tachycardia,
hypertension.
..Nausea and vomiting is
the most
common symptom reported by the
patients while miosis is the most
common sign observed
Management
 I/V line
 oxygen
 Gastric lavage with normal saline and
charcoal
…
 Inj.Atropine every 5 minutes till signs
of atropinization.
 Pralidoxime 1gm stat ;can be repeated
as needed.
 PPI
 Antibiotics
 I/V fluid
Famous poison victims
SOCRATES died of hemlock
Cleopatra VII of Egypt
Napoleone di Buonaparte died of
Arsenic
Bruce lee died of mixture of
overdose of sedative hypnotics
Michael jackson died of mixed drug
overdose
Scott Charles Bam Bam Bigelow
died of multiple drugs overdose
Adolf Hitler died of cyanide
BURDEN OF POISONING AT DHQ
NSAIDs 7
POISONING 239
Unknown 25
Paracetamol 6
Acid/corrosive
31
Kerosine oil 1
Wheat pill 35
Kalapathar 1
Mix…
Benzodiazepin
e 25
Opioid 3
Organophospha
te/Rat pill 104
In USA
Contact:
– American Association
of Poison Control
Centers at
http://www.aapcc.org/
– Your local poison
control center
– Poison Prevention
Week Council at
http://www.poisonprev
ention.org/
In Uk
UK National poisons information
centres contact number
087 0600 6266
PAKISTAN..????
Toxicology Advisory center??
Ordinance ???
Legislation ???
Protocol for wheatpill poisoning
 The protocol being mentioned here
has been circulated to all DHQs and
THQ s of Rawalpindi district by
Principal RMC and Allied hospitals.
 Maintain double IV line.
..
 Keep NPO for 24-48 hours.
 Give fluids according to haemodynamic
status.
 Perform gastric lavage with edible oil 1-2
litres alongwith activated charcoal.
 Inj.Omeprazole 40mg stat then od
 Inj.mgs04 1gm iv stat then 1gm/hr for next 4
hours than 1 gm every 4 hourly for next 4872 hours.
….
 Inj.hydrocortisone 250mg iv stat then 100mg
tds.
 Inj calcium gluconate diluted iv stat then od.
 Inj.amiodarone (if arrythmia).
 Vitals monitoring.
 Monitor with ECG and baseline labs.
 ICU care.
 Attendants counselling.
THANK YOU