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
How does an opiate OD present?
- Pin prick pupils
- Respiratory depression
- Hypotension
- Hallucinations
- Rhabdomyolysis
- Non cardiac pulmonary oedema
What is the mechanism of opiate OD?
Overstimulation of MU receptors in the CNS
How is an opiate OD managed?
- ABCDE
- Administer naloxone if RR<10, GCS<10
- Supportive care
How is naloxone administered?
Adults - start 400 micrograms and titrate up
Kids - 0.1mg/kg???
What is the half life of naloxone?
60 mins
What are the complications of naloxone administration?
- Withdrawal may precipitate leave from hospital
- Hypertension
- Behavioural disturbance
- Pain unmasking
ONLY GIVE ENOUGH TO RESTORE BREATHING BUT MAINTAIN SEDATION
Give 2 examples of TCAs
Amitriptylline
Dosulepin
(-ine is often a TCA)
How does a TCA OD present?
Anticholinergic effects - dry skin, dilated pupils, tachycardia, agitation, fits, delirium , hypertonia, hyperreflexia
Na channel blockade - arrhythmias, prolonged QRS/QT interval
Alpha blockade - hypotension
What is the mechanism behind TCA OD?
Blocks certain receptors - sodium channel, alpha receptors, cholinergic receptors
What investigations should be done if you suspect TCA OD?
- U&E
- Blood glucose
- ABG (acidosis)
- ECG - look for long QRS/QT ‘sigmoid shape’
- Constant CVS monitoring for arrhythmias
What are the complications of TCA OD?
- Cardiac arrest
- Life threatening seizures
- Bowel obstruction
How is TCA OD treated?
- Prevent absoption - activated charcoal within 1h
- Enhance elimination - MDAC every 2 hrs
- Prevent arrhythmias - sodium bicarbonate, consider DC cardioversion, DONT GIVE ANTI-ARRHYTHMIA DRUGS
- Prevent fits - diazepam, lorazepam
- Supportive care
How does an iron overdose present?
Early (0-6hrs) - N&V, abdo pain, bloody diarrhoea
Delayed (2-72 hours) - black stools, fits, circulatory collapse, coma
Late (2-4 days) - acute liver necrosis, renal failure
Very late (2-5 weeks) - gastric strictures
What investigations should be done if you suspect iron overdose?
- Iron levels (repeat every 2/3hrs)
- Blood count (leucocytosis)
- U&E
- ABG (monitor bicarb)
- Glucose (hyper)
- LFTs
How is iron overdose treated?
- Prevent absorption - NOT ACTIVATED CHARCOAL, do gastric lavage or induced emesis in small children
- Chelating agent - DESFERRIOXAMINE, will be excreted in urine (red)
- Supportive care
What if the indications and contraindications for desferrioxamine?
I - severe toxicity with fits, coma, GI symptoms, leucocytosis
CI - renal failure
What are the side effects of desferrioxamine?
Hypotension
Pulmonary oedema
How does benzo overdose present?
CNS depression -drowsiness, impaired balance, ataxia, slurred speech
What is the mechanism behind benzo overdose?
Enhanced GABA effect, causing CNA depression and potential coma
What are the complications of benzo overdose?
Cardiac arrest
Deep coma
How is benzo OD diagnosed?
Clinically - use plasma conc to confirm the diagnosis but not as a prognostic marker as it does not correlate with severity
How is benzo OD treated?
- Prevent absorption - only use charcoal if OD is in combo with other drugs
- Specific antidote - FLUMENAZIL
- Supportive care - this is the mainstay of treatment
What are the contraindications for flumenazil?
- Long term benzo use
- Wide QRS complex
- Seizure history
- Anything that lowers the seizure threshold
What are the signs of alcohol withdrawal? What meds are used for addiction and withdrawal?
Increased pulse, low BP, terror, confusion fits and hallucinations, 10-72 hours after drinking
Addiction - acamprosate, disulfiram
Withdrawal - chlordiazepoxide, diazepam
What are some general side effects of antipsychotics?
- Antimuscarinic (dry mouth, blurred vision, urinary retention)
- EPS - Parkinsonism (tardive dyskinesia)
- Sedation and weight gain
- Raised prolactin
- Neuroleptic malignant syndrome
- Reduced seizure threshold
- Prolonged QT interval (haliperidol)
Name 3 typical/first generation antipsychotics
Haloperidol, perphenazine, chlorpromazine
Name 5 atypical/second generation antipsychotics
Olanzapine, risperidone, quetiapine, aripiprazole, clozapine
What are the advantages of atypical over typical antipsychotics?
- Lower risk of extrapyramidal side effects as they have a lower affinity for D2 receptors (so fewer nigrostriatal side effects)
- Affinity for 5-HT receptors aswell, so dual action
What are the advantages of typical over atypical antipsychotics?
- Lower risk of metabolic side effects (nausea, ado pain, indigestion) and weight gain
What is the risk of using clozapine?
Agranulocytosis
A patient experiences muscle stiffness, increased temperature, confusion and increased heartbeat after using an antipsychotic. What is the name of the antipsychotic and the syndrome?
Risperidone - neuroleptic malignant syndrome
Risperidone is used in schizophrenia and aggressive behaviour in Alzhemiers. It is a D2, A1 and H1 receptor antagonist
What EPS are associated with typical antipsychotics?
Tardive dyskinesia, dystonia, parkinsonism, akinesia, neuroleptic malingnant syndrome
NB some of these remain even after drug withdrawal
What are the ICD 10 criteria for depression?
3 core symptoms:
- Low mood
- Low energy
- Loss of enjoyment in things
Plus...GAPES Guilt Appetite loss Attention loss Pessimism Esteem (low) Suicidal intent Sleep disturbance
What is the monoamine theory of depression?
Depression is due to depletion in the levels of serotonin, norepinephrine, and/or dopamine in the central nervous system.
Name 6 classes of drug used to treat depression, accompanied by examples
SSRI - fluoxetine, citalopram, sertraline (1st line) SNRI - venlafaxine, duloxetine TCAs - amitriptyline, clomiparime NaSSA - mirtazapine NDRI - bupropion MAOI - phenlzine
Why are TCAs used less these days?
They have antimuscarinic side effects (ABCDS): Anorexia Blurry vision Constipation/ Confusion Dry Mouth Sedation/ Stasis of urine
They are dangerous in overdose:
Hallucinations
Arrhythmia
What are the side effects of SSRIs/SNRIs?
- Nausea
- Dry mouth
- Constipation
- Headache
- Sexual dysfunction
What is serotonin syndrome?
Fever, agitation, hypertonia, dilate pupils and hyperreflexia.
Caused by admin of two or more serotonergic drugs (SSRIs, SNRIs, MAOIs, triptans, TCAs, tramadol)
Which mood stabilisers are used for mania?
Lithium Anticonvulsants: - Lamotrigine - Carbemazepine - Sodium valproate Atypical antipsychotics (quietapine)
When should mood stabilisers not be prescribed?
Pregnancy - teratogenic
What is the SE of using carbamazepine, rarely?
Agranulocytosis
What is used to treat anxiety?
Benzodiazepines (anxiolytic)- diazepam, lorazepam
Zopiclone (hypnotic)
