Poisoning Flashcards
What are the features of accidental poisoning
Usually when a young child is found playing with tablets or household/garden substances or with some in their mouths
Peak age 30 months (just over 2 years)
Serious harm is uncommon as many household items and medications are of low toxicity and children usually ingest only small amounts
Which substances can be potentially fatal
Antihypertensives
Antidepressants
Lamp oil
Button batteries: Can discharge a small electrical current and erode through gastric tissue to cause bleeding and strictures
Magnets: Can clamp together with bowel wall trapped between them, causing ischaemia and perforation → requires urgent surgical referral for >1 magnet
What would the signs be for a patient with a deliberate anticholinergic (TCAs, antihistamines) overdose
Raised HR and BP
RR normal
Temperature raised
Pupils dilated
Reduced sweating
What would the signs be for a patient with a deliberate opioid overdose
Reduced HR and BP
Reduced RR
Reduced temperature
Constricted pupils
Reduced sweating
What would the signs be for a patient with a deliberate sympathomimetic (cocaine, amphetamines) overdose
HR and BP raised
RR raised
Temperature raised
pupils dilated
Sweating increased
What would the signs be for a patient with a deliberate sedative-hypnotic (anticonvulsant/benzo) overdose
Reduced HR and BP
Reduced RR
Reduced temp
Pupils normal
Reduced sweating
What is the management for a child with poisoning
- Identify the agent (ask patient, parents, look for clinical signs)
- Determine toxicity of agent - use ToxBase, report dose, symptoms, time since ingestino
- Within 1 hour of ingestion → consider reduction of absorption using activated charcoal
- Investigations
- Management as according to agent ingested
If low-toxicity + asymptomatic → reassure and discharge ± health visitor for risk assessment and health promotion advice for safe storage
What investigations should be done for poisoning
FBC
Renal screen
Liver function
ECG (drug has cardiovascular toxicity)
Specific blood concentrations (paracetamol, iron, salicylates, alcohol)
Urine toxicology screen
Paracetamol poisoning: mechanism, symptoms, management
Gastric irritation, saturation of liver metabolism → toxic metabolite NAPQI
Early: abdo pain + vomiting
Late: liver failure (12-24h)
Measure plasma paracetamol
IV N-Acetylcysteine
Button battery poisoning: mechanism, symptoms, management
Electrical circuit production from caustic hydroxide → corrosion of gut wall
Abdo pain, gut perforation and stricture formation
CXR/AXR: identify position
In the oesophagus, fails to pass, symptoms present → Endoscopic removal
Carbon monoxide poisoning: mechanism, symptoms, management
Binds to Hb → tissue hypoxia
Early: headache, nausea
Late: confusion, drowsiness, coma
High flow oxygen (hasten CO dissociation)
Salicylates poisoning: mechanism, symptoms, management
Direct stimulation of the resp. centre
Uncouples oxidative phosphorylation → metabolic acidosis + hypoglycaemia
Early: vomiting, tinnitus
Late: resp. alkalosis → met. acidosis
Measure plasma salicylate concentration 2-4h after ingestion
Alkalinisation of urine (increased salicylate excretion)
Haemodialysis
Tricyclic antidepressant poisoning: mechanism, symptoms, management
Anti-cholinergic, interferes with cardiac conduction pathways
Early: tachycardia, drowsiness, dry mouth
Later: arrhythmias, seizures
Arrhythmia →. Sodium bicarbonate
Support breathing
Ethylene glycol poisoning: mechanism, symptoms, management
Produces toxic metabolites that interferes with intracellular energy production
Early: intoxication
Later: tachycardia, metabolic acidosis → renal failure
Fomepizole
Haemodialysis
Alcohol poisoning: mechanism, symptoms, management
Inhibitory effect on glycolysis in the liver + brain neurotransmission
Hypoglycaemia, coma, respiratory failure
Monitor blood glucose, correct if necessary
Support ventilation
Iron poisoning: mechanism, symptoms, management
Local corrosion to gut mucosa + disruption of oxidative phosphorylation in the mitochondria → free radicals, lipid peroxidation, metabolic acidosis
Initial: vomiting, diarrhoea, haematemesis, melaena, acute gastric ulceration
→ latent period of improvement
6-12h later: drowsiness, coma, shock, liver failure + hypoglycaemia, convulsions
Long term: gut strictures
Serum iron level 4 hours after ingestion
IV deferoxamine (iron chelation)
Hydrocarbons e.g. paraffin, kerosene poisoning: mechanism, symptoms, management
Facilitates aspiration → lung toxicity
Direct inhibitory effect on neurotransmission in the brain
Supportive treatment
Organophosphorus poisoning: mechanism, symptoms, management
Inhibition of acetylcholinesterase → ACh accumulation in the nervous system
Salivation, lacrimation, urination, diarrhoea, vomiting, muscle weakness, cramps and paralysis, bradycardia and hypotension
Seizures and coma
Atropin
Supportive care
Pralidoxime (reactivates acetylcholinesterase)
What are the most common causes of chronic environmental poisoning
Lead
Pesticides
What are the symptoms of chronic lead exposure
Behavioural changes
Hyperactivity OR decreased activity
Developmental delay or loss of developmental milestones
Chronic lead nephropathy
Abdominal pain, vomiting, constipation
Headache and ataxia
Lethargy, seizures, and coma
What is the management for lead environmental poisoning
Chelation therapy to reverse acute symptoms (encephalopathy)
However treatment is complex as lead is deposited in the bone and has a long half life
