Toxicology Flashcards
History of poisoned patient
-The poison
=Type (drug/chemical/plant/animal)
=Duration (acute/chronic)
=Time
=Route
=Nature (deliberate/accidental)
-The patient
=Symptoms
=Signs
=Med and psych history
=Alcohol
Examination of poisoned patient
A to E
Opioid exam
-Pinpoint pupils not always that obvious), reduced respiration, reduced GCS, hypotension
=Codeine, morphine, heroin, methadone
Anticholinergic exam
-Dry mouth, mydriasis (blurred vision as dilated), urinary retention, reduced bowel sounds
SLOW DOWN
=Tricyclic antidepressants, antihistamines
Sympathomimetic/ stimulant
-Tachycardia, sweating, anxiety, seizures
=Amphetamines, cocaine, legal highs
-similar to MDMA, amphetamines and cocaine, resulting in increased levels of serotonin, dopamine and noradrenaline, resulting in a ‘high’ and feeling of euphoria
a common example is a stimulant NPS is mephedrone (‘bath salts’,’M-CAT’.’meow meow’). It is a cathinone and structurally similar to khat, a plant found in East Africa
another example is benzylpiperazine (‘Exodus’, ‘Legal X’, ‘Legal E’)
typically swallowed as a pill/powder (‘bombing’) or snorted
adverse effect profile similar to MDMA/cocaine, with the risk of serotonin syndrome
-Supportive, IV fluids active cooling ice, cooled fluids), diazepam for agitation/temperature, think about serotonin syndrome, early involvement of critical care
Sedative/ hypnotic
-Depressed conscious level, ataxia, dysarthria
-Alcohol, benzodiazepines, GHB/GBL
Cannabinoids
termed synthetic cannabinoid receptor agonists
commonly referred to as ‘spice’
typically sprayed on to herbal mixtures which are then smoked. Also available in liquid form which is then inhaled using e-cigarettes
similar adverse effects to cannabis
Hallucinogenic
can be either dissociatives and psychedelics
dissociatives produce a similar effect to ketamine, with a sense of not being connected to the physical body or time. A common dissociative NPS is methoxetamine (‘mexxy’)
psychedelics have a similar effect to LSD although NPS versions may also be a stimulant
Depressant
can be either opioid or benzodiazepine-based
usually taken as a pill or a powder
often structurally very similar to the original drug class, hence the adverse effects are similar
benzodiazepine NPS often have a significantly longer half-life
Investigations
-Obs
=Toxidrome, temp usually not sepsis and associated with poor prognosis (critical care)
-ECG
=QRS and QT intervals
-Bloods
=FBC, UE, LFT (INR, CK depending on drug)
=Assays: paracetamol, salicylate (aspirin), antiepileptic, lithium, digoxin
-Other clinical
=CXR
=Blood gases
General principles of management
-Decontamination (removal of chemical before absorbed)
=External (wash skin/ irrigation of eyes)
=GI (activated charcoal, whole bowel: large volume of polyethylene glycol administered orally/NG to flush, only used in life-threatening overdose of very toxic substance as metabolic shift and hemodynamically unstable)
Activated charcoal
-Reduced gut absorption of many drugs
-Consider inly if patient presents within 1 hour of ingestion
-Contraindicated
=Unprotected airway, intestinal obstruction
-Substance which activated charcoal does not absorb
=Iron, Lithium, ethanol/ ethanol, cyanide, acids/alkalis
Paracetamol overdose
-Clinical features
=Nausea, vomiting, abdominal pain
=Silent toxidrome: many are asymptomatic
=If untreated: liver failure 2-3 days, renal 3-5 days
-Investigations
=Paracetamol concentration ( 4 hours after ingestion, take immediately if already after 4 hours post ingestion)
=ALT (reflects liver structure if damaged)
=INR (synthetic function)
=Creatinine (renal function)
-Single acute overdose ingested in <1 hour
=Plot paracetamol against time, treat above line
=The minority of patients who present within 1 hour may benefit from activated charcoal to reduce absorption of the drug.
-Staggered overdose (therapeutic excess ingested in >1 hour
=Treat all patients
=NAC should be started, may be stopped depending on bloods
Risk factors for developing hepatotoxicity in paracetamol overdose
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days
Interestingly, acute alcohol intake, as opposed to chronic alcohol excess, is not associated with an increased risk of developing hepatotoxicity and may actually be protective.
Describe NAC
-Replenishes glutathione (mops up paracetamol metabolites)
-Most effective if administered within 8 hours
Safe to stop NAC when ALT, INR, Paracetamol, creatinine normal
-Continue if ALT raised, INR >1.3, Paracetamol still present
-Adverse reactions to NAC very common
=Anaphylactoid (pseudo-allergic) reaction as histamine mediated (non-IgE mediated mast cell release)
=Clinically identical to anaphylaxis (histamine mediated)
=Not IgE mediated; do not need prior exposure to NAC, may not have a reaction ever again
=Not a contraindicated
=Temporarily stop NAC, antihistamines (chlorphenamine), bronchodilators (nebulised salbutamol), adrenaline, steroids prevent second phase response), restart after reaction settles at slower rate)
=Acetylcysteine is now infused over 1 hour (rather than the previous 15 minutes) to reduce the number of adverse effects
