Poisoning Flashcards
What groups are most commonly affected by poisoning?
- Young children
- Adolescents and young adults
What substances are most commonly used to poison?
- Paracetamol
- Ibuprofen
- Citalopram
What substances carry the highest mortality?
- Paracetamol
- TCAs
- Opiates
- Carbon monoxide
What are the components of an initial assessment of somebody with suspected poisoning?
Obs - temp, RR, BP, HR
GCS
Pupils, tone, reflexes
Inspection for needle marks, blisters, lacerations
What are the 4 components of management of poisoning?
- Prevent absorption
- Increased drug elimination
- Specific antidotes/chelating agents
- Supportive care
What tools can be used if you dont have enough information about the poisoning?
Toxibase
Ring NPIS
What are the 3 main methods of prevention of absorption of drug?
- Activated charcoal - adsorbs poison in the GI tract
- Gastric lavage - only use in very large overdoses and ensure to protect the airway
- Induced emesis - rarely used
What are the indications and contraindications for activated charcoal?
I - <1hr since ingestion, alert, most poisons
CI - ileus, impaired gag reflex, unsafe swallow
Which poisons will activated charcoal not adsorb?
Elemental salts eg. lithium, iron Insecticides Cyanides Strong acids/alkalis Alcohols Hydrocarbons
What are the indications and contraindications for gastric lavage?
I - Iron overdose
CI - hydrocarbons, caustic substance ingestion (due to risk of aspiration and perforation)
What are the main methods of drug elimination in poison management?
- Multiple dose activated charcoal - give 50g at start followed by 25g every 2 hours, with a laxative ‘GI dialysis’
- Haemodialysis/haemoperfusion
- Haemofiltration
- Combined methods
What are the indications for haemodialysis/haemoperfusion?
Only drugs that have a small volume of distribution and low clearance rate
eg. theophylline, phenytoin, carbamazepine
HD only - methanol, valproate, lithium
What is the specific antidote to:
a) paracetamol
b) salicyclate
c) opiate
d) iron
e) TCAs
f) benzos
a) NAC
b) sodium bicarbonate
c) naloxone
d) desferrioxamine (chelating agent)
e) sodium bicarbonate
f) flumazenil
How can the following aspects of poisoning be managed (supportive care):
a) hypotension
b) fits
c) vomiting
d) acidosis
e) renal failure
a) IV fluids
b) lorazepam/diazepam
c) antiemetics
d) sodium bicarbonate
e) dialysis
What is the number one cause of fulminant hepatic failure?
Paracetamol overdose
How does paracetamol OD present?
Early - non-specific, N&V, abdo pain
Delated (2-3 days) - hepatic necrosis, jaundice, RUQ pain, encephalopathy, coagulopathy
Death (3-6 days)
What are the complications of paracetamol OD?
Liver failure Renal failure Pancreatitis Death Hypoglycaemia Metabolic acidosis
What is the mechanism behind paracetamol OD?
Normal glucaronide pathway is saturated so large amounts of NAPQI are produced.
Liver reserves of glutathione are depleted so the NAPQI, instead of being converted to a detoxified product, leads to hepatocellular injury.
What investigations should be done for someone with suspected paracetamol OD?
Blood paracetamol levels - ideally 4 hr after
Clotting (PT/INR increased due to liver failure)
ALT (massively increased)
U&E (creatinine elevated in renal damage)
ABGs (look for metabolic acidosis - indicates poor prognosis)
How is paracetamol OD treated?
- Prevent absorption - activated charcoal ASAP
- Administer NAC (if paracetamol level over 100), ideally within 8 hours, give IV over 21 hours.
- Supportive - vit K, FFP, monitor ICP, dialysis
- Monitor - falling INR is a good sign
What is an anaphylactoid reaction? How is it managed?
Urticaria, wheeze etc in response to admin of NAC - due to release of histamine from mast cells.
This is not a true anaphlactic reaction so you can give anti-histamine and continue the infusion but reduce rate.
What are some poor prognostic features of paracetamol OD?
- Creatinine >300
- PT/INR still high after day 3
- PT >180s
- Bilirubin >70
- Metabolic acidosis
- Encephalopathy
- Raised lactate
How does salicylate/aspirin OD present?
TINNITUS, HYPERVENTILATION, dizziness, sweating, vomiting, agitation, delirium
Coma (in kids especially)
What are the complications of salicylate OD?
Brain swelling
Seizures
Cardiac arrest
What is the mechanism behind salicylate OD?
in terms of ABG
- Initially you get respiratory alkalosis due to hyperventilation
- After 24 hours you get metabolic acidosis due to uncoupled oxidative phosphorylation
What investigations should be done if you suspect salicylate OD?
- Blood salicylate levels
- U&Es (expect hypokalemia)
- Blood glucose (expect hypo)
- ABGd (resp alkalosis then metabolic acidosis)
How is salicylate OD treated?
- Prevent absorption - activated charcoal within 1 hr
- Prevent CNS penetration - sodium bicarb
- Enhance eliminiation - sodium bicarb, MDAC, haemodialysis
- Supportive - airway, fluids, ventilation, glucose, K
What are the indications for haemodialysis in salicylate OD?
pH<7.3
>700mg/l aspirin
Renal failure