The document discusses acute exogenous poisoning, detailing its definition, common causes, and management approaches for specific types of poisoning including paracetamol, organophosphorus insecticides, and opioid poisoning. It emphasizes the importance of timely recognition and treatment, which involves supportive care, antidotes, and specific decontamination methods depending on the poison. The document also highlights the clinical features, treatment protocols, and post-exposure monitoring necessary for affected patients.

1. ACUTE EXOGENOUS
POISONING
SRISHTI GUPTA
LDK-3-18S

2. Contents
 Definition
 Etiology
 General Approach
 Specific Management
-Paracetamol Poisoning
-Organophosphorous(OP)Insecticides Poisoning
-Opiate Poisoning

3. Definition
Acute toxicity describes the adverse effects of a
substance that result either from a single exposure or from
multiple exposures in a short period of time (usually less
than 24 hours).
To be described as acute toxicity, the adverse
effects should occur within 14 days of the administration of
the substance.

4. Etiology
Acute poisoning is common. In developed
countries, the most frequent cause is intentional drug
overdose in the context of self-harm and usually involves
prescribed or “over-the-counter” medicine.
Toxicity may also occur as a result of alcohol or
recreational substance use,or other occupational or
environmental exposure.
In developing countries, the frequency of self-harm
is more difficult to estimate. Household and agricultural
products such as pesticides and herbicides,are more freely
available,and more common causes of poisoning and are
associated with a much higher case fatallity.

5. General Approach
ABC,clear airway
Consider ventilation(if the respiratory rate is <8/min or PaO2 <8kPa when
breathing 60% O2 or the airway is at risk,eg GCS<8)
Treat shock
If unconscious,nurse semi-prone

6. Further Management
Assess the patient
History from patient,friends or family is vital
Features from the examination may help
Investigations
Glucose,U&E,FBC,LFT,INR,ABG,ECG,paracetamol and
salicylate levels urine/serum toxicology,specific assays as
appropriate
Monitor -Temperature,pulse and respiratory rate,BP,O2
saturations,urine output,ECG
Treatment-Supportive measures may need catheterization
Absorption consider gastric lavage and activated charcoal
Specific measures for antidotes,consider naloxone if
conscious level and pinpoint pupil,consider pabrinex and
glucose if drowsy/confused

7. Taking a history in poisoning
 What toxins have been taken and how much?
 What time were they taken and by what route?
 Has alcohol or any drug of misuse been taken as well?
 Obtain details from witness of the circumstances of
overdose(family,friends,ambulance personnel)
 Ask the GP for background and details of prescribed
medication
 Assess suicide risk (full psychiatric evaluation)
 Assess capacity to make decisions about accepting or
refusing treatment
 Establish past medical history,drug history and
allergies,social and family history
 Record all informations carefully

8. Clinical Signs of Poisoning by
Pharmaceutical agents and drugs of misuse

9. General Management
A.Gastrointestinal decontamination
‘Single-dose activated charcoal may be considered if a patient has
ingested a potentially toxic amount of a poison (known to be adsorbed to
charcoal) up to 1 hr previously.
‘Multiple-dose’ activated charcoal should be considered only if a patient
has ingested a life-threatening amount of carbamazepine, dapsone,
phenobarbital, quinine or theophylline.
‘Gastric lavage’ should not be employed routinely, if ever, in the
management of poisoned patients.
‘Whole bowel irrigation’ should be considered for:
• poisoning with sustained-release or emetic-coated drugs
• patients who have ingested substantial amounts of iron
(as morbidity is high and other options are limited)

10. Substances poorly adsorbed by activated charcoal
Medicine
 Iron
 Lithium
Chemicals
 Acids*
 Alkalis*
 Ethanol
 Ethylene glycol
 Mercury
 Methanol
 Petroleum distillates*
*Gastric lavage is contraindicated.

11. B.Urinary alkalinisation
Urinary alkalinisation is currently recommended for
patients with clinically significant salicylate poisoning
when the criteria for haemodialysis are not met.
It is also sometimes used for poisoning with
methotrexate.
Complications include alkalaemia, hypokalaemia and
occasionally alkalotic tetany.

12. C.Haemodialysis and Haemoperfusion
These techniques can enhance the elimination of poisons
that have a small volume of distribution and a long halflife
after overdose, and are appropriate when poisoning is
sufficiently severe to justify invasive elimination methods.
The toxin must be small enough to cross the
dialysis membrane (haemodialysis) or must bind to
activated charcoal (haemoperfusion).
Haemodialysis may also correct acid–base and metabolic
disturbances associated with poisoning.

13. Poisons effectively eliminated by haemodialysis or haemoperfusion
Haemodialysis
• Ethylene glycol
• Isopropanol
• Methanol
• Salicylates
• Sodium valproate
• Lithium
Haemoperfusion
• Theophylline
• Phenytoin
• Carbamazepine
• Phenobarbital
• Amobarbital

14. D.Lipid emulsion therapy
Lipid emulsion therapy or “lipid rescue” is being
used increasingly for the management of poisoning with
lipid soluble agents such as local anathetics,tricyclic
antidepressants, calcium channel blocker and lipid soluble
beta blockers such as propranolol.
It involves intravenous infusion of 20% lipid emulsion
at a initial dose of 1.5ml/kg followed by infusion of
0.25ml/kg/min until there is clinical improvement.
It is thought that lipid soluble toxins partition into
intavenous lipid, reducing target tissue concentration.

15. E. Supportive Care
For most poisons, antidotes and methods to
accelerate elimination are inappropriate, unavailable or
incompletely effective.
Outcome is dependent on appropriate nursing and
supportive care, and on treatment of complications
Patients should be monitored carefully until the
effects of any toxins have dissipated.

16. F.Antidotes
Antidotes are available for some poisons and work by
a variety of mechanisms: for example, by specific
antagonism (isoprenaline for β-blockers), chelation
(desferrioxamine for iron) or reduction (methylene blue for
dapsone).

17. Paracetamol Poisoning
Paracetamol toxicity results in hepatic and renal failure.
Management
Activated charcoal may be used in patients presenting within 1
hour.Antidotes for paracetamol should be administered to all patients with
paracetamol concentrations above the ‘treatment line’ provided on
paracetamol poisoning nomograms.
Acetylcysteine given intravenously(or orally) is highly efficacious if
administered within 8 hours of the overdose. Administration should not be
delayed in patients presenting after 8 hours to await a paracetamol blood
concentration result.

18. The antidote can be stopped if the
paracetamol concentration is shown to be below the
nomogram treatment line.
The most important adverse effect of
acetylcysteine is related to dose-related histamine
release, the ‘anaphylactoid’ reaction, which causes
itching and urticaria, and in occasional severe cases,
bronchospasm and hypotension.
Most cases can be managed by temporary
discontinuation of acetylcysteine and administration
of an antihistamine.

19. Figure;The management of a paracetamol overdose

20. An alternative antidote is methionine 2.5 g orally
(adult dose) every 4 hours to a total of 4 doses, but this
is less effective, especially after delayed presentation.
If a patient presents more than 15 hours after
ingestion,liver function tests, prothrombin time (or
international normalised ratio – INR), renal function tests
and a venous bicarbonate should be measured, the
antidote started, and a poisons information center or local
liver unit contacted for advice if results are abnormal.

21. An arterial blood gas sample should be taken in
patients with severe liver function abnormalities; metabolic
acidosis indicates severe poisoning.
Liver transplantation should be considered in individuals
who develop life threatening liver failure due to
paracetamol poisoning.

22. Organophosphorous(OP)insecticides
Poisoning
Sequential triphasic illness follows OP intoxication
 Acute cholinergic phase
 Intermediate syndrome(IMS)
 Organophosphate-induced delayed polyneuropathy(OPIDN)

23. Clinical features
Toxic effects usually appear within 4 hours of
exposure/ingestion .Organophosphates used in agriculture
are generally the most toxic.
Miosis the most characteristic sign. SLUDGE
syndrome(Salivation, Lacrimation, Urination, Defecation, GI
distress, Emesis), bronchospasm, bronchorrhoea, diaphoresis,
bradycardia, hypotension, convulsions, ataxia, muscle
spasm, respiratory paralysis and death due to respiratory
failure.

24. Muscle fasciculation, cramps and weakness can
progress to areflexia and paralysis. Respiratory failure may
be secondary to weakness of muscle of respiration.
Hypertension, tachycardia, papillary dilatation and pallor
may result from ganglion stimulation.
Headache, giddiness, anxiety, restlessness, drowsiness,
confusion, tremors, slurred speech and generalized
weakness are early signs of mild to moderate poisoning. In
severe cases, delirium, psychosis, seizures, coma and
cardiorespiratory depression are the predominant features.

25. Treatment
Further contamination is prevented by removal from
the site of exposure and of contaminated clothing and
contact lenses.
The airway is cleared and high flow oxygen
administered. Direct mouth-to-mouth/nose resuscitation
must avoided. Contaminated clothing and contact lenses
should be double-bagged , the skin washed with soap and
water, and the eyes are irriagated.
Following ingestion, gastric lavage may be undertaken
within an hour of intake, followed by activated charcoal via
nasogastric tube, after establishing intravenous access and
airway protection.

26. Convulsions are controlled with intravenous diazepam.
Monitoring of ECGs, temperature, urea and
electrolytes, amylase and glucose is mandatory.
Severe cases should be managed in an ICU and may require supported
ventilation.
Antidote
 IV atropine
 Loading dose 1.8-3 mg(1 ampoule=0.6 mg),continue
every 5 minute until the patient is fully atropinized.
 Maintainence dose 20%-30% of loading dose given by
infusion.

27. Complete and early atropinization is essential in early
management. Speed of administration is as important as
use of sufficient doses.
Regarding intermediate syndrome, ventilator support
should be instituted before a patient develops respiratory
failure. Parenteral nutrition is often required.
For OPIDN, there is no specific therapeutic
measures. Regular physiotherapy may reduce deformity
caused by muscle wasting.

28. Opioid Poisoning
Common Causes
 Heroin
 Morphine
 Methadone
 Pethidine
 Tramadol

29. Clinical Features
 Respiration-Reduced respiration rate and ventilation
 CVS-Hypotension, relative bradycardia
 CNS-Confusion, hallucination, slurred speech,s edation, coma
 Muscle-Ataxia, reduced muscle tone
 Temperature-Hypothermia
 Eyes-Miosis
 Abdomen-Ileus
 Skin-Needle tracks

30. Management
Airway should be cleared and if necessary,respiratory support and
oxygen given.
Oxygen saturation monitoring and measurement of arterial blood gas
should be performed.
Prompt use of specific opioid antagonist naloxone
(0.4-2mg IV in adult,repeated if necessary).
Patient should be monitored at least 6 hours after last naloxone dose.