Common Poisons

Prof Anura Weerasinghe

MBBS(Col), MD(Col), DCH(Col), DTM&H(Lond),
MRCP(UK), FRCP(Edin), PhD(Japan),
Fellow of the Ceylon College of Physicians
Agrochemicals Household products

Poisons

Pharmaceuticals Plant poisons

Accidental Misadventure
Poisoning

Suicide Homicide
 Organophosphate poisoning
• Acute Cholinergic syndrome
• Intermediate syndrome
• Delayed peripheral neuropathy

Recall the clinical features and pathogenesis of

Cholinergic syndrome
 Management
• Initial stabilization A, B, C
and Oxygen
• Administration of atropine (muscarinic
antagonist)
• Administration of pralidoxime (AChE
reactivator)
• Decontamination only after initial
resuscitation
 Muscarinic antagonist drugs
Atropine
0.6 – 3 mg bolus dose of atropine
depending on severity

Monitor : HR, BP, Pupil size

Respiration(including one breath
count)
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
• reactivate inhibited AChE
• Administration PAM 1grm
qid IV (injection over 2 min) or
infusion of 1 grm over 30 minutes
followed by continuous infusion of
0.5g/hour

30mg/kg bolus followed by 8mg/kg/h

Diazepam for seizures
Decontamination only after the patient
has been stabilised and treated
with oxygen, atropine, and Oxime

perform lavage only on patients who present

within two hrs of Ingesting a substantial
amount of OP and who are intubated or
conscious and willing to cooperate
Common drug overdoses
• Paracetamol
• Amphetamines
• Iron
• Tricyclic antidepressants
• Salicylate
 Metabolism of paracetamol
• In the liver, conjugated with glucuronide &
sulphate
• In addition minor metabolites are formed
N acetyl-p-benzoquinoneimine(NABQI)
Highly reactive chemically
• Made harmless by conjugation with
glutathione
• Supply of glutathione is limited
• If the amount of NABQI formed is greater than
the available glutathione
• Excess NABQI oxidises the thiol(SH)groups of
the important enzymes causing cell death
 Paracetamol: clinical features
• 0.5 – 24 hours; nausea & vomiting
• 24 – 72 h: nausea & vomiting, RHC pain,
Abnormal LFT & INR
• 72- 96 h: liver necrosis, coagulation defects,
liver failure, renal failure, hepatic
encephalopathy
• 4 days to 2 weeks: resolution of liver function
 Treatment
• Elimination: gastric lavage (if < 1 h ingestion)
• Activated charcoal (if <4h after ingestion)
both longer for SR products
• N-acetylcysteine for toxic ingestion
Risk assessment and prognosis
– History
–Single overdose of >10g or >200mg/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
Investigations 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
– 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)
Commence an antidote if an adult has
ingested a single overdose of more than
150mg/Kg or more than 10g.
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
Management of side effects
usually responds to temporarily discontinuation
or slowing the infusion
Recommence once the reaction has settled
An antihistamine is rarely needed
Amphetamines: Clinical features
• Clinical features: Hypertension, tachycardia,
arrhythmias, myocardial infarction,
vasospasm, seizures, paranoid psychosis,
tachypnoea
• Treatment: Elimination; activated charcoal
Agitation/seizures; benzodiazepines
Hypertension; control agitation, α-
antagonists(phentolamine),
vasodilators(nitroglycerin, nitroprusside,
nifedipine) Hyperthermia;
control agitation, external cooling
 Iron: Clinical features
• 0.5 – 6 h; nausea, vomiting, GI discomfort, GI
bleeding, drowsiness, hypoglycaemia,
hypotension
• 6 – 48 h; coma, seizures, coagulopathy,
acidosis, cardiac failure
• 2 – 7 d; hepatotoxicity, coagulopathy,
metabolic acidosis, renal insufficiency
 Iron; treatment
• Elimination; Gastric lavage, whole bowel
irrigation with polyethylene glycol electrolyte
solution
• Shock; intravenous fluid and blood if
haemorrhage present
• Antidote; desferoxamine to chelate iron when
iron levels > 500 mcg/dL
 Salicylate:clinical features
• Clinical features; Respiratory alkalosis
(initially), Metabolic acidosis (after substantial
absorption), pulmonary oedema, platelet
dysfunction, nausea, vomiting, hearing loss,
agitation, delirium
• Elimination; activated charcoal, haemodialysis,
alkalinization of urine IV
bicarbonate for agitation and delirium
 Gloriosa superba
Colchicine
poisoning
GI, haematological
Renal and CNS
effects
Direct irritant effect and stop normal cell division
 Datura stramonium
Attarra
moonflower
Atropine

Hallucinogenic, hyperthermia, tachycardia

mydriasis
Benzodiazepines for sedation
Antidote; physostigmine
 Yellow Oleander
(Thevetia peruviana)
All parts are poisonous
usually fruits or seeds are
used to commit suicide

Cardiotoxic:
HB, Hypotension Blocks Na/K ATPase pump
Direct irritation: Accumulation of Na hence,
Nausea & vomiting Ca within cells
CNS; xanthopsia,
Convusions & coma
 Methanol Poisoning
Methanol aldehyde
Formaldehyde dehydrogenase
alcohol
dehydrogenase Formic acid

Formic acid inhibits mitochondrial cytochrome

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

Ethanol competes with methanol for alcohol

dehydrogenase and aldehyde dehydroganase thus
prevents formation of formaldehyde and formic
acid