Principles of Management of Poisoning (PMC)

Principles of Management of Poisoning
Pradeepa Jayawardane
MBBS, PhD
Senior Lecturer in Pharmacology
Epidemiology of Poisoning
•Acute self poisoning is a major public health issue

in many countries around the world
•In developing countries such as Sri Lanka the
reported mortality of 10%
•Developed countries mortality is low - 0.5%
•In Sri Lanka, acute poisoning is among the
leading ten causes of hospital death
Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•The highest incidence is reported from rural

districts.
•The high mortality reflects the wide availability of
highly toxic compounds such as pesticides and
limited resources to treat poisoned patients in rural
primary hospitals
•Recent studies in urban Sri Lanka demonstrate an
increase in poisoning with pharmaceuticals

•The type of poisoning is influenced by

–availability
–prior knowledge about the poison and its effects
gained through different means of communication
and information including media
•Studies from both developed and developing
countries demonstrate that young people,
particularly women, below 30 years are over
represented in self harm

Classification of Poisons
•Drugs
•Industrial, Household, and Environmental
Toxicants
•Natural Products
•Warfare agents

•Poisoning may be acute or chronic
•Acute poisoning
–Accidental
–Deliberate
–Iatrogenic
–Environmental
–Occupational
•Poisoning in young children is usually accidental.
It may be iatrogenic (example,over-treatment with
paracetamol)

Routes of Exposure
•Oral
•Inhalational
•Dermal
Less commonly
•Intravenous

General Principles of Management of a
Poisoned Patient
•Resuscitation
•Antidotes
•Decontamination
Patient should be resuscitated and stabilized

(Supportive care and antidote treatment) before
decontamination

Poisoned Patient
Resuscitation
•Airway
•Breathing
•Circulation

Poisoned Patient
The most important first aid measure to minimize
morbidity and mortality from ingestion is the
removal of poison from the GI tract
–Gastric aspiration and lavage

–Emesis
–Activated charcoal
–Whole bowel irrigation

Poisoned Patient
Gastric aspiration and lavage
•If conscious obtain consent

•Instructions to the patients
•No GL in struggling and uncooperative pts

Poisoned Patient
Technique- Gastric aspiration and lavage

1. Protect airway (endotracheal intubation) if
patient is comatose
2. Lie patient on their left lateral head down
position
3. Insert a large bore orogastric tube
The tube end should be lubricated with water
or soluable jelly

Poisoned Patient
Technique- Gastric aspiration and lavage
3. Insert a large bore orogastric tube

Position of the tip of the tube should be confirmed by air
insufflation while listening over the stomach
4. Aspirate stomach contents
5. Use a small cycle lavage of 50-100 mL (and then

aspirate). Can use water or 0.9% Sodium chloride

Contraindications for gastric aspiration and
lavage
•Corrosive ingestions (concentrated acids, alkali etc)

petroleum products such as kerosene
•Oesophageal disease
•Should not be performed in individuals where the

airway protective mechanisms are impaired or
expected to be affected due to impaired consciousness
coma or convulsions.
•These patients can be lavaged following intubation with a

cuffed endo-tracheal tube
Complications of gastric aspiration and
lavage
•Gastric lavage may potentially increase gastric

delivery of tablets into the small bowel, especially
those that have formed into large clumps. This
could lead to increased absorption
•Aspiration of gastric contents occurs in about 3%

of patients leading to aspiration pneumonia
•Laryngospasms and hypoxia

Complications of gastric aspiration and
lavage
•Fluid and electrolyte imbalance
•Oesophageal rupture is a very rare but potentially

fatal complication.
•Profound bradycardia, cardiac arrest

Poisoned Patient
Emesis
Induced by giving syrup of ipecacuanha
•Should only be given to conscious and alert

patients, who had ingested a potentially a toxic
amount of poison
•Initiation of emesis is slow
•Thus in severe poisoning lavage is considered
better
Poisoned Patient
Contraindications for emesis
•Non-toxic ingestions - emesis should not be used as a
method of punishment
•Prior significant vomiting - ipecac induced emesis is no

better than "natural" emesis, and would not be expected to
recover additional material
•Any patient who is comatose,seizing,hypotensive,or has

lost his/her protective airway reflex

Poisoned Patient
•The patient who is presently awake, but may be

expected to rapidly deteriorate before emesis has
been completed.
•Examples of this type of ingestion include TCA,
beta blockers, camphor, and many others.
•Caustic agents may cause additional injury during

emesis.
Poisoned Patient
•Aspiration risk: ingestions of poorly absorbed
hydrocarbons
•Need for rapid administration of oral antidotes,

such as NAC, especially approaching 6-8 hours
after ingestion.
•Late in pregnancy
•Hypertensive crisis or intracranial hypertension

Poisoned Patient
Complications of emesis
•Intractable vomiting (rare)

•Diarrhea
•Aspiration
•Neuromuscular weakness
•Mallory-Weiss tear of the esophagus

Poisoned Patient
Activated Charcoal
Activated charcoal is made from material burnt in a

super heated high oxygen atmosphere creating small
holes throughout the grain of the charcoal. This
effectively increases the charcoal's surface area .
Toxic compounds that are not effectively absorbed by

activated charcoal are
–Iron
–Lithium
–Alcohols
–Glycol
Poisoned Patient
Indications for charcoal

•Activated charcoal is indicated for most if not all
poisonings that fulfill the following criteria:
–Drug ingested is adsorbed by charcoal and has

significant potential for toxicity
and
–Time since ingestion is less than 1-2 hours
–The drug has significant enterohepatic circulation

Poisoned Patient
Indications for charcoal

•The drug delays gastric emptying and time since
ingestion is less than 4 hours
•The drug is in a controlled release preparation
and time since ingestion is less than 12-18 hours

Poisoned Patient
Dose:
•Over 12 y: 50-100g
Administration of charcoal
After gastric lavage, charcoal is normally put
down the tube prior to removal

Poisoned Patient
Contraindications for activated charcoal
•If patients consciousness is impaired

•If use increase the severity of aspiration

Poisoned Patient
Whole Bowel Irrigation
•A technique that uses large volumes of an iso-

osmolar solution (polyethylene glycol) that is not
absorbed.
• It has been shown the most efficient means of

gastrointestinal decontamination in some
circumstances.
Poisoned Patient
Indications for whole bowel irrigation
•Medications not absorbed by charcoal (e.g. iron

and lithium)
•Sustained release preparations (e.g. theophylline

and verapamil)

Poisoned Patient
Mechanism of action
It physically flushes tablets from the gastrointestinal

tract. Interrupts enterohepatic circulation.
Dose
•15 mL/kg per hour of polyethylene glycol (colonic lavage
solution). If tolerated increase to 25 mL/kg/hr

Poisoned Patient
Whole bowel irrigation
Administration
Oral or by nasogastric tube
If the patient agrees to drink the solution, they should be

reassessed after 15 minutes to determine their
compliance, Most patients require nasogastric tubes
Some patients may require an antiemetic if they are
vomiting. Initially the fluid rate may be turned down until
the vomiting is controlled

Poisoned Patient
Administration
•The end point of administration of polyethylene

glycol is to have a clear rectal effluent which
usually occurs after 4 - 5 litres of fluid (2-4 hours).
•Tablets will often be noted in the effluent.

Poisoned Patient
Duration
•There are also little data to make firm
recommendations on the time over which this
strategy should be followed.
•In all but the most serious cases this is usually

less than 12 hours after treatment commences

Poisoned Patient
Elimination
•Alkaline and acid diuresis

•Peritoneal dialysis
•Haemodialysis

Poisoned Patient
•Before, during and after decontamination
procedures it is essential to check that patient
breaths properly, the airway is clear.
•Secretions should be sucked out.
•If cyanosed oxygen should be given
•If respiration is impaired, intubation and assisted

ventilation should be considered
Poisoned Patient
Supportive Therapy
•Maintenance of a fluid balance chart

•Adequate oral and IV fluids
•Monitoring of the patient
•Anticipate cardiac, hepatic , renal failure
•Anticipate respiratory failure

Antidotes and Chelating Agents
Mechanisms of Action
Antidotes may exert a beneficial effect by:

• Forming an inert complex with the poison
•(e.g. desferrioxamine, D-penicillamine, dicobalt
edetate, digoxin-specific antibody fragments,
dimercaprol, hydroxocobalamin, protamine,
Prussian blue)

Mechanisms of Action Contd

•Accelerating detoxification of the poison (e.g.
N-acetylcysteine)
•Reducing the rate of conversion of the poison

to a more toxic compound (e.g. ethanol)

Mechanisms of Action
•Competing with the poison for essential
receptor sites (e.g. oxygen, naloxone)
•Blocking essential receptors through which

the toxic effects are mediated (e.g. atropine)
•Bypassing the effect of the poison (e.g.

oxygen, glucagon).
Acute Organophospate (OP) Poisoning
Pathophysiology

Acute OP Poisoning
Symptoms and signs
–Acute cholinergic syndrome

–Intermediate syndrome
–Organophosphate induced delayed
polyneuropathy

Management of acute OP poisoning
Initial stabilization
Severe acute OP poisoning is a medical
emergency
Airway
Breathing
Circulation
•oxygen - at the first opportunity

•left lateral position, with the neck extended
Muscarinic antagonist drugs
Atropine
0.6 – 3 mg bolus dose of atropine depending on severity
Monitor
Air entry to the lungs
HR
BP
Signs of increased secretions
Pupil size

Muscarinic antagonist drugs
Double the dose, and continue to double each

time that there is no response

Target end-points for atropine therapy
•Clear chest on auscultation with no wheezes

•Heart rate >80 beats/min
•Pupils no longer pinpoint
•Dry axillae
•Systolic blood pressure >80-100 mmHg

Once the targets are achieved
– Maintain on an atropine infusion

–Observation of the patient
•for recurrences of cholinergic signs
•signs of atropine toxicity
•respiratory failure

Pralidoxime
Mechanism of action
•Oximes reactivate inhibited AChE
Pralidoxime chloride and iodide are used widely

•Lack of good evidence for the clinical effectiveness of

oximes
•WHO recommends that PAM should be given to all

symptomatic patients requiring atropine
•30 mg/kg loading dose of pralidoxime chloride,

followed by 8 mg/kg/hr by continuous infusion (often
simplified to a 1-2g loading dose over 20-30 mins,
followed immediately by 500mg/hr)

•Seizures
–Diazepam

•Decontamination should only occur after the
patient has been stabilized and treated with
oxygen, atropine, and oxime
•Current practice is to only perform lavage on

patients who present within two hrs of ingesting
a substantial amount of OP and who are
intubated or conscious and willing to cooperate
•Activated charcoal

Acute Paracetamol poisoning
Mechanism of toxicity
N-acetyl-p-benzoquinonimine

•After 8 hours of significant overdose glutathione

stores are depleted and toxic metabolite binds to
sulphydryl groups in phospholipid membranes and
tissue proteins causing disruption of cell
membranes
•Liver, kidney, heart and pancrease

Patients who have a higher risk of paracetamol

induced liver damage
•Malnutrition and eating disorders
•Chronic alcohol abuse
•Recent or ongoing viral illness
•Use of enzyme inducing drugs
–Carbamazepine
–Phenytoin
–Rifampicine
–Isoniazid

Acute Paracetamol Poisoning
Clinical Features
Most patients are asymptomatic initially (including those

who will develop hepatic injury)
Early protracted vomiting is associated with higher

ingestions
Hepatic and organ injury usually begins at about 10

hours after poisoning
Most patients who develop hepatotoxicity will have

abnormal transaminases by 24 hours
Clinical features of untreated paracetamol

poisoning
Phase I(0-24 hrs)

•Asymptomatic
•Features of gastrointestinal irritation-nausea,
vomiting and abdominal pain
•Rarely- metabolic acidosis, cardiac arrhythmias


Poisoning
Phase II (24-72 hrs)

•Hepatotoxicity – increased hepatic enzymes,
bilirubin and prothrombin time
•Right upper quadrant abdominal tenderness


Poisoning
Phase III (72-96 hrs)

•Peak transaminase levels are seen on 3rd -5th days
•Bleeding manifestations
•Hepatic encephalopathy
•Elevated bilirubin level
•Renal insufficiency
•Acidosis
•Electrolyte imbalances


Poisoning
Phase III (72-96 hrs)

•Thrombocytopaenia
•Hypoglycaemia
•DIC
•Hypokalaemia
•Pancreatitis
•Myocarditis
•Renal failure


Poisoning
Phase IV (96 hrs -2 weeks)

•Hepatic failure and death
Or
•Complete resolution of hepatic damage and
recovery

Risk assessment and prognosis

–History
–Single overdose of >10g or >150mg/Kg is generally
regarded as hepatotoxic
–Blood levels
–If PCM levels available send blood after 4 hours of
overdose up to 16 hours
–Look for biochemical evidence of hepatotoxicity
–Clinical assessment

Interpretation of the plasma paracetamol level

Interpretation of the plasma paracetamol level
•Is designed to use for acute ingestion. It is of no

use in chronic ingestions
•Do not discontinue treatment if the initial level is

above the treatment line and the subsequent
levels fall below the treatment line
•Beyond 15 hrs risk assessment is less reliable

and clinical judgment become more important

Management
On admission
•Liver function tests
•FBC
•PT or INR
•Renal function tests
•Blood glucose
•Serum electrolytes
•Repeat these tests daily

Reduce absorption
–Gastric lavage within 1-2 hour of
overdose ??? Contraversial
–Single dose of 50g activated charcoal in 200
ml of water for those who present within 2
hours of a toxic dose

Antidotes
–Most effective if started within 8 hours but still
effective even later
–N acetylcystein (i.v. or orally) and methionine
(orally)

Antidote use
Commence an antidote if an adult has ingested a

single overdose of more than 150mg/Kg or more
than 10g.
Oral methionine or IV NAC

Dosage for NAC infusion i.v.
•Adults and children over 20 kg

–150 mg/kg in 200 ml of 5% dextrose over 15 minutes
–Followed by 50 mg/kg i.v. in 500 ml of dextrose over
4 hours
–Followed by 100 mg/kg i.v. in 1000 ml of dextrose
over 16 hours
–If liver dysfunction or coagulopathy develops,
maintain an infusion at a dose of 100mg/kg , until INR
falls below 2

Side effects of NAC
–15% of patients receiving NAC develop dose

related analaphylactoid reaction due to histamine
release
–Most commonly occurs within 1 hour of starting
the infusion

Side effects of NAC
Management
–usually responds to temporarily
discontinuation or slowing the infusion
–Recommence once the reaction has settled
–An antihistamine is rarely needed

•Once commenced NAC should be continued

–Exceptions
•Reliable plasma PCM level below the Rx
line for the patient
•Anaphylaxis
•If NAC is started for progressive liver dysfunction it should
be continued until INR begins to fall
•After the regime blood for PT/INR & basic LFT

Oral Methionine
•Adults and children weighing over 20 kg

–2.5g followed by 3 more doses of 2.5 g given at 4
hourly intervals

Staggered overdose or multiple supratherapeutic

Ingestions
•Often occur following accidental ingestion of higher doses
frequently
•It is defined as more than one ingestion of paracetamol
over a period exceeding 8 hrs that results in a cumulative
dose more than 100mg/kg/day
•Damage occurs due to lack of time for glutathione stores
to regenerate
•Treated with NAC if
–INR>1.3
–AST> 50mg/dl

Yellow Oleander Poisoning

•Yellow oleander seeds

•highly toxic cardiac glycosides including thevetins
A and B and neriifolin,
•unidentified substances
•The number of yellow oleander seeds ingested is

a poor guide to the degree of poisoning


•Cardiac glycosides bind to and inactivate the

Na+/K+ ATPase pump on the cytoplasmic
membrane of cardiac cells
•As a result intracellular Na+ concentration
increases
•This affects the Na+/ Ca+ exchange channels
resulting in an increase in intracellular Ca+ that
leads to increased force of contraction

Mechanism of Toxicity
•The increase of intracellular Ca+ ions also raises

the resting membrane potential of the cell, leading
to increasing rates of spontaneous cellular
depolarization and myocardial automaticity

•Enhanced vagal activity by central and peripheral

mechanisms
•Reduced conduction through AV and SA nodes
Reduced heart rate
•Increased Ca causes increased contractility

Management of Yellow Oleander Poisoning
Assessment and initial management

•Airway, breathing, and circulation should be
checked and stabilized
•Assess
–level of hydration – fluid resuscitation
–level of consciousness
–ability to protect their airway,
–hemodynamic stability (pulse rate, blood
pressure),
–evidence of aspiration should be assessed
Assessment and initial management
•12-lead ECG with rhythm strip

•Continuous cardiac monitoring
•Careful observation of cardiac rhythm should
continue for a minimum of 24 h

Supportive Care
Vomiting, diarrhoea Hypovolaemia
Fts of dehydration
Postural drop of BP Hypotension
Resuscitate with normal saline

•intravenous metoclopramide10 mg
Electrolytes
Serum Potassium- check every 6 hours
Hypokalaemia worsens toxicity, thus correct
< 3 mEq/L – 500mL of Hartmann’s solution infused over 4
hours
Or Intravenous potassium
If serum potassium > 5.5 - indications for anti-digoxin Fab if
available.
In the absence of anti-digoxin Fab,
insulin/dextrose

Gastric Decontamination
Gastric lavage
•No longer considered routine practice in the
treatment of poisoning (AACT/EAPCCT position
statements on gastric lavage)

Gastric Decontamination
Activated charcoal
Single dose Vs Multiple dose

Pharmacological management
•Treat marked hypotension (systolic < 70 mmHg)

or bradycardia (<40 bpm) with bolus doses of
atropine (2–3 mg)
•Otherwise give small bolus of atropine (0.3–0.6
mg) or an infusion (0.6 mg/h) to keep the heart
rate around 70–80 bpm

Temporary cardiac pacing
•Heart rate below 40/min, with any form of sick

sinus syndrome or heart block

Management of Tachyarrythmias
•More dangerous and are more difficult to treat
•Ventricular tachyarrhythmias are best treated with

lidocaine

•In the absence of anti-digoxin Fab, treat VF with

low energy DC cardioversion

Digoxin-specific antibody fragments
•Digoxin-specific antibody fragments have been

demonstrated in a randomized controlled trial
(RCT) to be effective in reversing life-threatening
cardiac arrhythmias and correcting hyperkalemia
in yellow oleander poisoning

Digoxin-specific antibody fragments
•A single dose (800-1,200 mg) of digoxin-specific

antibody fragments is dissolved in 100 mL of
normal saline and given by intravenous infusion
over 20 min irrespective of age, sex or body weight

Methanol Poisoning
Methanol (methyl alcohol, wood spirits) is used

as a
–fuel in high performance engines
–solvents
–antifreeze
–window cleaner
• Methanol is also used to fortify illicit spirits
•Almost all significant exposures occur via
ingestion, but methanol can also be absorbed via
inhalation and through the skin
Methanol Poisoning
alcohol aldehyde
dehydrogenase dehydrogenase
Methanol Formaldehyde Formic acid
Formic acid
Formic acid inhibits mitochondrial cytochrome

oxidase activity, preventing oxidative metabolism and
so producing "tissue hypoxia"

Methanol Poisoning
Antidote
Ethanol
Mechanism of action of ethanol in methanol

poisoning
Ethanol competes with methanol for alcohol

dehydrogenase and aldehyde dehydroganase
thus prevents formation of formaldehyde and
formic acid
Iron Poisoning
•Typically occurs in children

•In children, the ingestion of 2-5 tablets may cause
significant toxicity
•Causes gastrointestinal toxicity (severe
haemorrhagic gastroenteritis) followed by multi
organ failure

Iron Poisoning
Iron toxicity develops when serum iron

concentrations exceed the iron binding capacity
of transferrin in blood.
The free circulating iron damages many organs
by direct cellular toxicity.
Antidote
Desferrioxamine
THANK YOU

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Principles of Management of Poisoning

•Acute self poisoning is a major public health issue

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•The highest incidence is reported from rural

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•The type of poisoning is influenced by

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Patient should be resuscitated and stabilized

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

–Gastric aspiration and lavage

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Gastric aspiration and lavage

•If conscious obtain consent

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Technique- Gastric aspiration and lavage

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

3. Insert a large bore orogastric tube

4. Aspirate stomach contents

5. Use a small cycle lavage of 50-100 mL (and then

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•Corrosive ingestions (concentrated acids, alkali etc)

•Should not be performed in individuals where the

•These patients can be lavaged following intubation with a

•Gastric lavage may potentially increase gastric

•Aspiration of gastric contents occurs in about 3%

•Laryngospasms and hypoxia

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•Fluid and electrolyte imbalance

•Oesophageal rupture is a very rare but potentially

•Profound bradycardia, cardiac arrest

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Induced by giving syrup of ipecacuanha

•Should only be given to conscious and alert

•Prior significant vomiting - ipecac induced emesis is no

•Any patient who is comatose,seizing,hypotensive,or has

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

•The patient who is presently awake, but may be

•Caustic agents may cause additional injury during

•Need for rapid administration of oral antidotes,

•Hypertensive crisis or intracranial hypertension

•Intractable vomiting (rare)

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Activated charcoal is made from material burnt in a

Toxic compounds that are not effectively absorbed by

Indications for charcoal

–Drug ingested is adsorbed by charcoal and has

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Indications for charcoal

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Contraindications for activated charcoal

•If patients consciousness is impaired

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015

Whole Bowel Irrigation

•A technique that uses large volumes of an iso-

• It has been shown the most efficient means of

•Medications not absorbed by charcoal (e.g. iron

•Sustained release preparations (e.g. theophylline

Principles of Management of Poisoning, Pradeepa Jayawardane, 21112015